Dental health diseases such as dental caries are among the most widespread diseases in the world. Dental caries will eventually lead to pain and tooth loss if untreated. The present study was carried out to find prevalence of dental caries and its relationship with some epidemiological factors. The present study was cross sectional study which included 916 school children from 3 villages. Prevalence of dental caries in the present study was 48.14%. Higher prevalence of dental caries was associated with low education status of mother, consuming sweet articles in between meals, cleaning teeth once daily or occasionally. Due to high prevalence of dental caries in school children, health care system should ensure periodic dental health checkup and early detection and promt treatment of dental caries
1. Report of WHO expert committee Technical report series 1984
2. World health organization day 7th april 1994 Oral health for healthy life information material no WHO 94.
3. World health organization: oral health surveys, basic methods 4th edition 1997, Geneva PP 1-55.
4. Mathur HN Jain TP and Jain ML. Dental caries in school girls Indian Journal of paediatrics Vol. 46 No. 373 P 43-48
5. Singh D.K. Prevalence of dental caries in school going children of Patna: Journal of Indian dental association Vol. 53 No.3 1981 PP 267
6. Jawadekar SJ etal: Epidemiological approach to dental caries the Indian practitioner Vol.39 No12 1986 PP 1037-1041
7. Gill PS, Prasad BJ Dental health suveys of primary school children in rural area of Lukhnow, Journal of Indian dental association vol.40 no. 91968 PP 227-283
8. Bajaj M, Blah BC Hoyam metal: Prevalence of dental problems in school children – a study in rural community in Haryana Indain journal of community medicine vol.14 no 3 1989 PP 30.
9. Gupta P. Indurkar M. oral cleaning habits of school children Journal of Indian dental association vol 67 no.3 1996 pp 88-89.
10. Jalili VP, Neema HC. Dental awareness in school going children. Journal of Indian dental association vol 58 no 11 1988 pp 451- 455.
A clinicopathological study of colorectal carcinomas
Objectives: To study the clinicopathological correlation of colorectal carcinoma and its histopathological typing. Materials and Methods: Retrospective study of one year duration from Jan 2013-Dec 2013 was done in Yenepoya Medical College Hospital, Mangalore. Hematoxylin and eosin stained slides were retrieved from pathology archives and light microscopic diagnosis and typing was done according to the WHO classification. Correlation was done with the clinical findings obtained from clinical records. Histochemistry and immunohistochemistry were done wherever indicated. Results: There were a total of 24 cases of colorectal cancer, majority being adenocarcinomas (87.5%), with age range of 26 to 75 years and almost equal sex ratio. One case was associated with familial adenomatous polyposis coli (FAP). Majority were well differentiated (66.6%) followed by moderately differentiated (28.6%) and poorly differentiated type(4.8%) About 67% of adenocarcinomas occurred in the rectum followed by rectosigmoid junction (17%) and sigmoid colon(8%). Other three rare tumours (12.5%) were neuroendocrine tumour of transverse colon, leiomyosarcoma and mixed adenocarcinoma and neuroendocrine tumour. Conclusion: The diagnosis and management of colorectal carcinomas require a team perspective. The pathological assessment of colorectal carcinoma is of critical importance to know the type and extent of tumour, grade and stage, and important prognostic factors, which are of crucial value in patient treatment and predicting the prognosis.
1. Ferlay J, Soerjomataram I, Ervik M, Dikshit R, Eser S, Mathers C, Rebelo M, Parkin DM, Forman D, Bray, F.GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 11 [Internet].Lyon, France: International Agency for Research on Cancer; 2013.
2. Nooyi SC, Murthy NS, Shivananjaiah S, Sreekantaiah P, Mathew A. Trends in rectal cancer incidence-- Indian scenario. Asian Pac J Cancer Prev. 2011; 12(8):2001-6.
3. Pathology and Genetics of Tumours of the Digestive System. In WHO Classification of Tumors. Hamilton.SR, Aaltonen.LA, eds. IARC Press Lyon 2000 ,103-143.
4. Mohan H. The gastrointestinal l tract. In :Mohan H, Mohan P, Mohan T, eds.Text book of Pathology. New Delhi: Jaypee Brothers Medical Publishres (P) Ltd, 2005, 601-605.
5. Guraya YS, Eltinay OE .Higher prevalence in young population and rightward shift of colorectal carcinoma. Saudi Med J2006;27(9):1391-1393.
6. Aljebreen AM. Clinicopathological patterns of colorecral cancer in Saudi Arabia:Younger with an Advaced stage presentation. The Saudi journal of gastroenterology 2007;13(2):84-7.
7. Shen SS, Haupt BX, Ro JY, Zhu J, Bailey HR, Schwartz MR. Number of lymphnodes examined and associated clinicopathological factors in colorectal carcinoma 2009;133(5):781-6.
8. Yeh C Y, Chen HH, Tang R, Tasi WS, Lin PY, Wang JY. Surgical outcome after curative resection of rectal leiomyosarcoma. Dis Colon Rectum 2000; 43(11):1517-21.
Head and neck cancer in Bihar has distinct demographic profiles, risk factor, food habits and personal family history. The term head and neck cancer refers to a group of biological similar cancers originating from the upper aerodigestive tract, including lip, oral cavity, nasal cavity, paranasal sinuses, pharynx and larynx. Head and neck cancers can cause varying degree of structural deformities and functional handicaps, depending on site, size and patterns of spread, thereby compromising well being and self esteem.
1. Mishra A, Singh VP, Verma V. Environmental effects on head and neck cancer India. J Coin Oncon 2009:27
2. Sankarnarayan R, Masuyer E, Swaminatam R, Ferlay J, Whelan S head and neck cancer: A global perspective on epidemiology and and prognosis. Anticancer Res 1998;18:4779-86
3. Sanghvi LD, Rao DN, Joshi S epidemiology of head andneck cancer. Semin sung oncol 1989;5:305-9
4. Chaturvedi P.Head and neck surgery. J can Res Ther 2009; 5:143.
5. Applebaum KM, Furniss CS, Zeka A, Posner MR, Smith JF, Bryan J, et al. Lack of association of alcohol and tobaco with HPV16-associated head and neck cancer. J Natl cancer inst 2007;99(23):1801-10
6. Reuter CW, Morgan MA, Eckardt A. Targeting EGF-receptor-signalling in squamous cell carcinoma of the head and neck. Be J cancer 2007; 96:408-16.
7. Chaukar DA, Das AK, Deshpande MS, Pak PS, et al. Quality of life of head and neck cancer patient: Validation of the European organization for research and treatment of cancer QLQ-C30 and European organization for research and treatment of cancer QLQ-HandN35 in Indian J cancer 2005 Oct-Dec;42(4):178-84.
Study of nutritional status of primary school children in an urban field practice area of Pune
Sayyad Tajmul, Arun Bansode, Akshay Salgar, N S Inamdar
Childhood years constitutes the most crucial period in life, when the foundations are laid for cognitive, social and emotional language, physical and motor development and cumulative lifelong learning. The young child is most vulnerable to the vicious cycles of malnutrition, infection and resultant disability all of which influence the present condition of a child at micro level and the future human resource development of the nation at the macro level. The present study was a cross sectional study which was carried out in two randomly selected municipal schools of an urban area. The Study consisted of 400 school children from 6 - 9 yrs age group, in which 75 (18.75%) children were found to be stunted and 114 (28.5%) children were underweight. Prevalence of Malnutrition in the form of stunting, and underweight significantly associated with socioeconomic status, educational status of mother, type of family and high birth order. Health education, personal hygiene education, nutrition education may be made as part of the school curriculum.
1. Introduction. Nutrition and physical performance in school age children, Nutrition Foundation of India, New Delhi; July 2009.
2. The state of food insecurity in the world – 2012 Available from: URL: http: //www.fao.org/docrep/016/i3027e/i3027e.pdf‎.
3. Saluja N. et al.Nutritional Status of urban primary school children in Meerut. The Internet Journal of Epidemiology. 2010; 8 (1).
4. Nutrition. (cited on 30th sept.2013). Available from: URL: http:// www.unicef.org/india/children.
5. Registrar General of India: Population Projections. Available from: URL: http://www.censusindia.net/Projection_Report.pdf.
6. Government of India. Ministry of Labour. Index no. page. Available from: URL http://www.labourbureau.nic.in
7. Park K. Socioeconomic status scale. Textbook of Preventive and Social Medicine. 22nd ed. Jabalpur: Banarsidas Bhanot; 2013. P.640, 641.
8. Training course on child growth assessment: WHO child growth standards, A- introduction:8 [cited 2013 Nov 22]; Available from: URL: http://whqlibdoc.who.int/publications/2008/9789241595070_A_eng.pdf
9. WHO Child Growth Standards Length/height-for-age, weight-for-age, weight-for-length, weight-for-height and body mass index-for-age Methods and development. Available from: URL: http://www.who.int/childgrowth/publications/technical_report_pub/en/index.html
10. Training course on child growth assessment: WHO child growth standards, A-introduction: 9 [cited on 2013 NOV 4]; Available from: URL: http://whqlibdoc.who.int/publications/2008/9789241595070_A_eng.pdf
11. WHO Growth Reference Data for 5 -19 yrs. Length/height-for-age, weight-for- age, weight-for-length, weight-for-height and body mass index-for-age. Available from URL: http:// www.who.int/growthref/‎
12. Maj Mukherjee R, Lt Col Chaturvedi S, Col Bhalwar R. Determinants of Nutritional Status of School Children. MJAFI 2008; 64: 227-231.
13. Dr. Renubala Sharma and Dr. Mukta Trivedi. A Study of Nutritional Status of Children of Sagar City (M.p.). Sociology. June 2013; 2(6).
14. Sunil Pal Singh C. Ravi Babu D. Nutritional status of primary school children in urban area of Hyderabad, Andhra Pradesh, India. Journal of community nutrition and Health. 2013; 2(1): 36-39
15. Das P, Basu M, Dhar G, et al. Nutritional status and morbidity pattern of government primary school children in north Kolkata of West Bengal, India. South East Asia Journal of Public Health. 2012; 2(1):13-17.
16. Chandna S. and Salll Sehgal. Prevalence of Deficiency Diseases among school Children. Health arid Population- Perspectives and Issues. 1994; 17(1and2): 108 -113.
17. Shakya SR, Bhandary S, Pokharel PK. Nutritional status and morbidity pattern among governmental primary school children in the Eastern Nepal Kathmandu University Medical Journal. 2004; 2(8): 307-314.
A cross sectional study on iodized salt usage at household level in Ulagankulam Panchayat of Tirunelveli district Tamil Nadu
P Getrude Banumathi, D Jaiganesh, P Parameshwari, R Dharani Sri, P Ravishankar
Background: Iodine deficiency disorders (IDD) still remains a major public health problems in many countries including India. Thus the Iodised salt is most economical, convenient and effective means of mass prophylaxis against Iodine Deficiency Disorders. Objectives: To estimate the prevalence of iodized salt usage at household level and to find out the iodine content of edible salt with MBI spot testing kit among women at household level in Ulagankulam panchayat of Tirunelveli. Materials and Methods: A community based cross sectional study among 306 women in households of Ulagankulam Panchayat, Thirunelveli District. A standardized, semi-structured questionnaire was applied to the women household who is in charge of kitchen to estimate the usage regarding iodized salt. Cooking salt was tested with MBI Spot testing kit for iodine content. Iodine content ≥ 15ppm was considered as adequately iodised salt. Appropriate statistical tests used and analysis done using SPSS 18 software. Results: Among the 306 salt samples tested, 123 (40.2%) were using adequately iodized salt (> 15ppm), 66 (21.6%) – inadequate iodized salt, 117 (38.2) – uniodized salt. 135 (44.1%) were buying salt from street vendors, 102 (33.3%) from nearby petty shops, 66 (21.6%) from General provisional store and 3 (1%) from Public distribution system (PDS). 54 (52.9%) and 54 (78.3%) of salt samples from nearby Petty shops and General provisional store were adequately iodized. Conclusion and recommendation: Based on this study, only 40.2% were using adequately iodised salt. This is well below the WHO recommended level (90%). Iodized salt should be manufactured in small pockets and made available at low cost even in petty shops and public distribution systems of rural areas and legal measures to ban crystallized non iodized salt to be strengthened. Increased awareness and frequent inspection by health staffs to be done.
1. J.kishore, National health programes of India 9th edition page number
2. Govt of india annual report 1997-1999, Ministry of health and family welfare
3. De Benoist B, McLean E, Andersson M, Rogers L. Iodine deficiency in 2007: global progress since 2003. Food Nutr Bull 2008; 29 : 195-202.
4. "Citizen Charter" National Iodine deficiency disorder control program and nutrition. Available from: http://www.negahealth.nic.in.
5. WHO/UNICEF/ICCIDD.Indicators for assessing iodine deficiency disorders and their control through salt iodization. Geneva, World Health Organization, 1994: 29–31.
6. Sundar lal et al. Textbook of community medicine.1st edition;p 180-181
7. Salt Department, Ministry of Industry. Universal Salt Iodisation (USI) – India: progress and current status. New Delhi, 1996: 8.
8. Chandrakant S. Pandav, Narendra K. Arora, Anand Krishnan, Rajan Sankar, Smita Pandav & and Madhu G. Karmarkar. Validation of spot-testing kits to determine iodine content in salt. Bulletin of the World Health Organization, 2000; 78(8):975-80.
9. Summary report iodized salt coverage study 2010 conducted across eight states in India
10. Unicef an assessment of the household use and adequacy of iodized salt in the republic of kazakhstan аlmaty, 2005.
A study of rhinolith as detected by CT scan paranasal air sinuses at tertiary health care centre
Introduction: Rhinoliths are calcareous concretions around calcinated intranasal foreign bodies within the nasal cavity. They are commonly seen in the anterior part of the nasal cavity. The incidence of adult rhinolith is very low. Rhinoliths are generally single, exogenous or endogenous, unilateral, and asymptomatic. Aims and Objectives: To Study Rhinolith as Detected by CT Scan Paranasal Air Sinuses at tertiary health care center. Methodology: It was a retrospective study of 2860 CT scans of paranasal sinuses during the period of June 2013 to August 2015 was done to detect Rhinoliths. The observations of CT scan were made and the results were statistically analyzed. Result: The majority of the Patients were from 30-40 age group i.e. 50.00% followed by 20-30-33.33% and 40+- 16.67%. Majority of the Patients were Female i.e. 66.67% followed by Male 33.33%. Conclusion: Rhinoliths are quite rare cases of the nose, which may show clinical and radiological similarities with each other and benign and malignant diseases of the region so in the nose diseases clinical suspicion of a rhinolith should always be considered, in order to lead to the right diagnosis
1. Orhan K, Kocyigit D, Kisnisci R. Rhinolithiasis: An uncommon entity of the nasal cavity. Oral Surg Oral Med Oral Pathol Oral RadiolEndod 2006; 101:e28-32.
2. Carder HM, Hiel JJ (1966) Asymptomaticrhinolith: a brief review of the literature and case report. Laryngoscope 76: 524-530.
3. Varley EWB (1964) Rhinolith: an incidental finding. Br J Oral Surg 2: 40-43.
4. Dib GC, Tangerina RP, Abreu CE, Santos RP, Gregorio LC. Rhinolithiasis as a cause of oronasal fistula. Rev Bras Otorhinolaryngol (Eng Ed). 2005; 71:101-103.
5. Celikkanat S, Turgut S, Ozcan I, Balyan FR, Ozdem C (1997) Rhinolithiasis. Rhinology 35:39-40.
6. Polson CJ (1943) Onrhinoliths. J LaryngolOtol 58: 79-116.
7. Orhan K, Kocyigit D, Kisnisci R, Paksoy CS. Rhinolithiasis: an uncommon entity of the nasal cavity. Oral Surg Oral Med Oral Pathol Oral RadiolEndod.2006; 101: 28-32.
8. Mustafa A, Nishori S. Rhinolith caused from the undetected foreign body: A case report. Kosova Journal of Surgery. 2008; 2(1):32-35.
9. Appleton SS, Kimbrough RE, Engstrom HIM (1988) Rhinolithiasis: a review. Oral Surg 65: 693-698.
10. Eliachar I, Schalit M (1970) Rhinolithiasis: report of eight cases. Arch Otolaryngol 91: 88-90.
11. Flood TR (1988) Rhinolith: an unusual cause of palatal perforation. Br J Oral Maxillofacial Surg 26: 486-490.
12. Varley EWB (1964) Rhinolith: an incidental finding. Br J Oral Surg 2: 40-43.
13. Hsiao JC, Tai CF, Lee KWl. Giant rhinolith: A case report. Kaohsiung J Med Sci 2005; 21:582-5.
14. Keck T, Liener K, Strater J, Rozsasi A. Rhinolith of the nasal septum. Int. J Pediatrhinolaryngol 2000; 53; 225-228.
15. Royal SA, Gardner RE. Rhinolithiasis: An unusual pediatric nasal mass. PediatrRediol 1998; 28:54-55.
16. Carder HM, Hiel JJ (1966) Asymptomaticrhinolith: a brief review of the literature and case report. Laryngoscope 76: 524-530
Study of comparison of yield of bronchial brushing and broncho-alveolar lavage in diagnosis of lung cancer
Vijaykumar R Kapse, Dilip G Mhaisekar, Dattatray Totewad, Mithilesh Kulkarni
Flexible fiber-optic bronchoscope revolutionized respiratory cytology, as techniques like bronchial brushings, broncho-alveolar lavage and bronchial biopsy became more easy, accessible and popular, shifting the emphasis from diagnosis of advanced malignancy in operable patients to the use of cytology as a first line diagnostic and management tool. Objective: To compare the yield of bronchial brushing and bronchoalveolar lavage cytology in lung cancer. Methodology: the present study was carried out at dr. S.C.G.M.C. Nanded, Maharashtra. In patients having lung cancer, bronchoscopy done and bal, bronchial brushing and endobronchial biopsy samples were collected. Comparison of yield of bronchial brushing and bronchoalveolar lavage cytology was done, in patients, in whome biopsy samples are positive for malignant cells. The statistical test( chi-square test) was applied to test the significance. Results: out of 56 patients bronchial brushing yielded 45 (80.35%) to be malignant as compared to bal cytology which yielded 15(26.78%) to be malignant. the difference in yield by both techniques was found to be statistically significant (p < 0.05). Conclusion: bronchial brushing has better diagnostic yield as compared to broncho Alveolar Lavage cytology in patients having lung cancer.
1. Fishman’s Pulmonary Diseases and Disorders. Fourth Edition. Page No. 630.
2. Prakash UB, Offord KP, Stubbs SE. Bronchoscopy in North America: the ACCP survey. Chest. 1991 Dec; 100(6):1668-75.
3. Rabahi MF, Fereira AA, Reciputti BP, et al. The description of bronchoscopic findings from patients with lung cancer. Am J Respir Crit Care Med. 2012; 185:A5917
4. TG. Manickam, S Rajasekaran and PJ Vasantham. Carcinomatous pulmonary Consolidations.. lnd .J. Tub.1995, 42, 9.
5. Jindal SK, Behera D. Clinical spectrum of primary lung cancer: review of Chandigarh experience of 10 years. Lung India 1990; 8:94-98.
6. Jadish Rawat. Girish Sindhwani, Dushyant Gaur, Ruchi Dua, Sunil Saini. Clinicopathological profile of lung cancer in Uttarakhand. Lung India Vol 26 issue 3juI-sep 2009.
7. DS Gaur, S Kishore, VP Pathak, NC Thapliyal Journal of Cytology, Vol. 24, No. 2, April-June, 2007, pp. 73-77
8. Husain AN. The lung. In: Kumar V, Abbas AK, Fausto N, editors. Robbins and Cotran pathologic basis of disease. 7th ed. India: Saunders; 2004. p. 711-72
9. Johnston WW, Elson CE. Respiratory tract. In: Bibbo M, editor. Comprehensive cytopathology. 2nd ed. Philadelphia: W.B. Saunders Company; 1997. p. 325-401.
10. Truong LD, Underwood RD, Greenberg SD, McLarty JW. Diagnosis and typing of lung carcinomas by cytopathologic methods. A review of 108 cases. Acta Cytol 1985; 29:379-84JAPI. 1985; 33;64-5.
Introduction: Tuberculosis is still one of the most common granulomatous diseases of the larynx. In the past, it commonly followed pulmonary tuberculosis. Among the risk factors identified are the consumption of tobacco, alcohol, malnutrition, immunodeficiency and being homeless. Aims and Objectives: To study Laryngeal Tuberculosis and its Outcome. Methodology: This was a hospital based cross- sectional study carried out at tertiary health care Centre with the patients diagnosed as Laryngeal tuberculosis by Otolaryngology department were admitted to ward and managed accordingly medical and necessary surgical management like tracheal dilation and Tracheostomy procedure were performed as per the protocols during the year June 2014 to June 2015 there were 45 patients studied during this time. Tabulations and Percentages used for the Presenting the Data. Result: We have found that the majority of the Patients were from >50- 35.55% followed by 40-50-20.00%, 30-40-15.55%, 20-30-13.33%, 10-20-8.88%, 1-10- 6.66%. Majority of the patients were Male 75.55% and Female 24.45%.The majority of the Patients presented with Stridor-35.55% followed by Dysphonia -17.77%. Dysphagia and odynophagia -15.55%, Throat pain -13.33%, Otalgia-8.88%, Fever-8.88%.The Majority of the Patients improved i.e. of 77.78% and 17.77% referred to Higher Centre for the further surgical management and prosthetic surgeries and Death occurred in 2 patient i.e. 4.44% mortality the reasons for the death was severe stridor. Conclusion: The majority of the Patients presented with complaining of Stridorfollowed by Dysphonia, Dysphagia and odynophagia, Throat pain, Otalgia, Fever. The Majority of the Patients improved i.e. of 77.78% and 4.44% mortality found in our study the reasons for mortality was severe stridor.
1. Bailey CM, Windle-Taylor PC. Tuberculous laryngitis: a series of 37 patients, Laryngoscope1981; 91:93-100.
2. Levenson MJ. Laryngeal tuberculosis: review of twenty cases, Laryngoscope 1984; 94:1094-1097.
3. Ramandan HH, Tarayi AE, Baroudy FM. Laryngeal tuberculosis: presentation of 16 cases and review of the literature, J Otolaryngol 1993; 22:39-42.
4. Thaller SR. Laryngeal tuberculosis as manifested in the decades 1963–1983, Laryngoscope 1987; 97:848-850.
5. Soda A. Tuberculosis of the larynx: clinical aspects in 19 patients, Laryngoscope 1989; 99:1147-1150.
6. Shin JE, Nam SY, Yoo SJ, Kim SY. Changing trends in clinical manifestations of laryngeal tuberculosis. Laryngoscope 2000; 110:1950-1953.
7. Lin CJ, Kang BH, Wang HW.Laryngeal tuberculosis masquerading as carcinoma.Eur Arch Otorhinolaryngol 2002; 259:521-523.
8. Tuberculosis. In: Benenson AS, ed. Control of communicable diseases manual. 15th ed. Washington, D.C.: American Public Health Association, 1990; 459.
9. Riley EC, Amundson DE. Laryngeal tuberculosis revisited. AmFamPhys 1992; 46:759-762.
10. Nishiike S, Irifune M, Sawada T, Doi K, Kubo T
11. Ramadan HH, Tarazi AE, Baroudy FM. Laryngeal tuberculosis: presentation of 16 cases and review of the literature. J Otolaryngol 1993; 22:39-41.
12. Horowitz G, Kaslow R, Friedland G. Infectiousness of laryngeal tuberculosis. Am Rev Respir Dis 1976; 114:241-244.
13. Soda A, Rubio H, Salazar M, Ganem J, Berlanga D, Sanchez A. Tuberculosis of the larynx: clinical aspects in 19 patients. Laryngoscope 1989; 99:1147-1150.
14. Diktaban T, Lucente FE. Laryngeal tuberculosis: A hazard to the Otolaryngologist. Ear Nose Throat J 1980; 59:488-494.
15. Hunter AM, Millar JW, Wightman AJA, Horne NW. The changing pattern of laryngeal tuberculosis.J LaryngolOtol 1981; 95:393-398.
Alvarado score and ultrasonographic criteria to diagnose acute appendicitis: A clinical study of 100 cases
Acute appendicitis is one of the most common surgical emergencies around the world with a life time prevalence of approximately one in seven. It's incidence is 1.5-1.9/1000 in male and female population. Scoring systems are valuable and valid instruments for discriminating between acute appendicitis and nonspecific pain abdomen. Alvarado scoring is one of them and is purely based on history, clinical examination and few laboratory tests and is very easy to apply. Advent of cross sectional computer based imaging modalities (USG, CT and MRI) in early eighties opened up new methods for diagnosis of acute appendicitis. It was also found that ultrasound was able to establish alternative diagnosis in up to one-third cases of right iliac pain like ureteric colic and gynaecological disorders. Statistical analysis of data in our study gave sensitivity of Alvarado score as 94.9%, specificity 61.9%, positive 90.3% and negative predictive value 76.4% while sensitivity of ultrasonography was 91.9%, specificity 85%, positive 95% and negative predictive value 77.2%.When both modalities were positive for acute appendicitis, no false positive result obtained. So it is concluded that the combination of Alvarado score and ultrasonography increases the sensitivity and specificity for the diagnosis of acute appendicitis.
1. Stephens PL, Mazzucco JJ. Et al. Comparison of ultrasound and the Alvarado score for the diagnosis of acute appendicitis. Conn Med. 1999 mar; 63(3): 137-40.
2. Cuschieri a. The small intestine and vermiform appendix; in: cuschieri A, GR Giles, AR Mossa. (ed). Essential Surgical Practice, 3rded.
3. Fenyo G, Lindberg G, Blind P, Enochsson L, Oberg A. Diagnostic decision support in suspected acute appendicitis, validation of a simplified scoring system. Eur J Surg 1997; 163: 831-8.
4. Pal K M, Khan A. Appendicitis, a continuing challenge. J Pak Med Assoc 1999; 48: 189-92.
5. Kumar V, Cotran RS, Robbins SL. Appendix; in Robbins Basic pathology. 5th ed. London: W.b. Saunders 1992; 520.
6. Barnes, BA. Treatment of appendicitis at the Massachussets General Hospital. 1939-1959. JAMA 1962; 180: 122.
7. Dunn EL, Moore EF, Elerding SC, Murphy JR et al. The unnecessary laparotomy for appendicitis- Can it be decreased? Am. Surg. 1982; 48:320-323.
8. Marshall E. Sonography of appendicitis and diverticulitis. Radiologic clinics of North Am. 1994; 32: (sept).
9. Alvarado A. A practical score for acute appendicitis. Ann Emerg Med. 1986 may; 15(5) 557-64.
10. Z Tarzan and T Winlernitz. Impact of USG visualization of normal and abnormal appendix. BJR 1998; 85:2.
11. H W AOoms, R K J Koumans, P J Ho Kang You and J B C M Puylaert. Ultrasonography in the diagnosis of acute appendicitis. Br. J Surg. 1991; 78: 315-318.
12. Julian BCM, Puylaert acute appendicitis: US evaluation using graded compression. Radiology 1986: 158: 355-360.
13. Campbell JA, Mephail DC. Appendicitis. B.M.J. 1958; I 852.
14. Anderson WAD, Pathology, ED. 4th, The C.V. Mosby and company Japan P. 803-806, 1961.
15. Illingworth CF W and Bick BM. Text book of surgical pathology. J and A Churchill Ltd.
16. Reid MR, Poer DH and Messel P. J Am Med Asso. 1936; 106: 655.
17. Fitz R. et al. Perforating inflammation of the vermiform appendix with specific reference to its early diagnosis and treatment. T.R.A. Am Phys. 1886; 1: 107-44 (cited by Boyce, 1949).
18. Collins DC. Etiological factors in acute appendicitis based upon a study of 100 cases. Surg. 1939; 5: 267-70.
19. Molony GE, Russel WT and Wilson DC. BJS 1950; 38:52-64.
20. Agarwal SK and Nan AK. Appendicectomy, A surgicopathological study of 100 cases. J. Ind. Med. Asso. 1968; 51:59-62.
21. Kazarian KK, Werner J Roeder, Walter L Mercheimer. Decreasing mortality and increasing morbidity in acute appendicitis. B.J.S. 1970; vol. 119: 681-685.
22. Ganesh Roy, Ray SC, Das MM and AK Ghosh. Acute appendicitis, A clinical appraisal of 500 cases. JIMA 1969; 52: 509-513.
23. Chan MY, Ten BS, Ng BL et al. The Alvarado score and acute appendicitis Ann. Acad Med Singapore 2001 Sept; 30(5):510-2.
24. IKramullah Khan, Ata urRehman et al. Application of Alvarado scoring system in diagnosis of acute appendicitis. J Ayub Med CollAbbotabad 2005; 17(3).
25. Ohmann C, Yang Q, Franke C: The abdominal pain study group. Diagnostic scores for acute appendicitis. Eur J Surg 1995; 161: 273-81.
26. Arian GM, Sohu KM, Ahmad E, Haider W, Naqi SA. Role of Alvarado score in diagnosis of acute appendicitis. Pak J Surg 2001; 17: 41-6.
27. Denizbasi, Arzu: Unleur, ErolErden. Et al. The role of emergency medicine residents using the Alvarado score in the diagnosis of acute appendicitis compared with general surgery resident. European journal of emergency medicine 10(4): 296-301 December 2003.
A study of metabolic syndrome in newly diagnosed patients of type 2 diabetes mellitus in the tertiary care centre of Kumaun region
Introduction: Diabetes mellitus is the commonest metabolic abnormality in the world. Prevalence of type 2 diabetes is especially increasing in developing countries. The metabolic syndrome (Syndrome X) consists of a constellation of metabolic abnormalities that increase the risk of micro and macrovascular complications of type 2 diabetes mellitus. The major features of metabolic syndrome include central obesity, hypertriglyceridemia, low HDL cholesterol, hyperglycaemia, and hypertension. The metabolic dysregulation associated with diabetes mellitus and metabolic syndrome cause secondary pathophysiologic changes in multiple organ system that impose a tremendous burden on the individual with diabetes and on the health care system. Material and Methods: - 100 Patients of age group 20-60 years with newly diagnosed type 2 diabetes mellitus were included in the study. Detailed physical and anthropometric examinations were done in all patients. Estimation of extended lipid profile including Apo B, KFT and microalbuminuria were done. Results: Of the 100 patients studied, 58 patients had metabolic syndrome according to the International Diabetes Federation criteria 2006. 85% of the patients with metabolic syndrome were either overweight or obese (calculated by their body mass index) as compared to 15% of patients without metabolic syndrome. Waist hip ratio was increased in 33% of males with metabolic syndrome and 100% of females with metabolic syndrome. Serum triglyceride (p< 0.009), VLDLc (p< 0.007) and microalbuminuria (p< 0.01) levels were significantly elevated in patients of metabolic syndrome as compared to those without metabolic syndrome. Conclusion: The present study shows that metabolic syndrome is increasingly present in patients with type 2 diabetes mellitus in the Kumaun region of Uttarakhand. Physicians treating type 2 diabetics should consider metabolic syndrome with greater emphasis in their patients and advice early intervention, to delay the development of micro and macrovascular complications of diabetes mellitus.
Patient care in a tertiary care centre is a holistic and comprehensive task and cannot get desired outcomes if various aspects of patient care like physical, psychological, mental, social and personal are not properly integrated. The study was planned to provide necessary awareness to the patients and caregivers regarding their illness and treatment outcomes. This was supposed to alleviate unnecessary apprehension and help in healing of patients. By using psychological tools of management in improving patient care, study derives various results that help in understanding the intricate mechanism of patient’s response on treatment. Study demonstrates comparatively better response on added psychological interventions of study group as compared to control group.
Patient care in a tertiary care centre is a holistic and comprehensive task and cannot get desired outcomes if various aspects of patient care like physical, psychological, mental, social and personal are not properly integrated. The study was planned to provide necessary awareness to the patients and caregivers regarding their illness and treatment outcomes. This was supposed to alleviate unnecessary apprehension and help in healing of patients. By using psychological tools of management in improving patient care, study derives various results that help in understanding the intricate mechanism of patient’s response on treatment. Study demonstrates comparatively better response on added psychological interventions of study group as compared to control group.
A comparative study of venous and capillary blood glucose levels by semi auto analyser and glucometer
Supriya Shete, Humaira Khan, A M Siddiqui, Amol Shinde
Introduction: Diabetes Mellitus(DM) is a non communicable disease and most common metabolic disorder reaching epidemic proportions globally. Both type 1 and type 2 diabetes show direct relationship between the glycemic control and the risk of systemic complications. Blood glucose estimation is the mainstay of diagnosis and management of diabetes mellitus. Aim: To compare the blood glucose estimation methods from capillary blood by glucometer and venous plasma glucose estimation by Semi auto analyser and to find out variation percentages in results. Material and Methods: 80 patients attending Outpatient department of a tertiary care level hospital who were advised blood glucose estimation were selected. Finger prick (capillary) blood glucose was measured by glucometer and venous plasma glucose estimation was measured by Semi auto analyser in central laboratory. Results and Conclusion: Capillary blood glucose estimation by glucometer is better alternative to venous plasma glucose estimation for diagnosis follow up and in emergency conditions in diabetic as well as non- diabetic patients.
1. Longo, Casper, Fauci. Hauser, Jameson, Loscalzo, Harrison principles of Medicine. Diabetes Mellitus. 18th ed. Mc grow Hill 2011; (2), 2969-70.
2. Arend, Armitage, Clemmons , Drazen, Griggs, Landry, Levison, Rustgi,Scheld Goldman's Cecil Medicine 2nd edition, Chapter 237, 1491.
3. Longo, Casper, Fauci. Hauser, Jameson, Loscalzo, Harrison principles of Medicine. Diabetes Mellitus. 18th ed. Mcgrow Hill 2011; (2), 2970-71.
4. Risaiah B., Can Med Assoc J.1985 Jun 15; 132(12): 1357-1359, 1361. Self monitering of blood glucose level: potential sources of inaccuracy. PMCID: PMC1346098.
5. American Diabetes association, Standard of Medical Care in Diabetes Jan 2006; vol.29 no.suppl 1 s4-s42.
6. Trinder. P Ann . clin. Biochem 1969 6.24
7. Emerson Lorg . chem. 1943.8.417
8. International Organisation for standardization. In vitro diagnostic test systems. Requirement for blood-glucose monitering system for self-testing in managing diabetes mellitus. Refernce no ISO 15197: 2013 (E). Geneva: International organisation for standardization; 2013
9. Biag A, Saddiqui l, Jabbar A, Azam SI, Sabir S, Alam S, Ghani F. Comparison between bedside testing of blood glucose by glucometer vs centralized testing in a tertiary care hospital. J Ayub Med Coll Abbottabad. 2007 Jul-Sep;19(3):25-9. Available form: http://www.ncbi.nih.gov/pubmed/18444586.
10. Colagiuri S, Sandbak A, Carstensen B, Christiansen J. Glumer C, Lauritzen T, Borch-Johnsen K. Comparibility of venous and capillary glucose measurements in blood. Diabet Med. 2003 Nov; 20(11):953-6. Available form: http://www. ncbi.nih.gov/pubmed/14632723.
11. Brad S, Gunjan Y, Gregory A, Accuracy of Roche Accuchek Inform Whole Blood Capillary, Arterial and Venous Glucose Values in Patients Receiving Intensive Intravenous Insulin Therapy After Cardiac Surgery.AmJ Clin Pathol. 2007; 127(6):919-926.
HLA-A association with psoriasis in a south Indian population
Ashwin Anandan, Krishnamoorthy R, Ravindra Prasad T, Panicker V K, Murugan S
Background: Psoriasis is a common skin disorder affecting around 3% of the population worldwide.HLA association with psoriasis is well established with very little information about Indian Population. Aim: To determine the HLA-A pattern and its association in psoriasis patients. Materials and Methods: 50 cases and 50 controls were enrolled in the study. HLA-A typing was done by PCR-SSP method and the results was analysed and interpreted. Results: The alleles that was found in higher frequency in the cases than in the controls – HLA-A*02(36%), HLA-A*11(32%), HLA-A*03 and HLA-A*24(30%). Conclusion: HLA-A*11 shows a strong association with psoriasis and HLA-A*01 shows decreased association with psoriasis in the present study.
1. Enno Christopher and Ulrich Mrowietz.Psoriasis-Braun-Falco’s Dermatology 506.
2. Kaur I, Kumar B, Sharma V.K., Kaur. S, Epidemiology of Psoriasis in a clinic from North India. Ind. J. Dermatol. Venerol. Leprol. 1986; 52:208-12.
3. Bedi.T.R,et al.Psoriasis in North India-geographical Variations.Dermatologia 1977;155:310-4.
4. Sunil Dogra,Savita Yadav,Psoriasis in India:Prevalance and Pattern.Ind J Dermatol Venerol Leprol 2010;76:595-601.
5. Gelfand J.M., Weinstein. R, Porter S.B., Berlin J.A., Margolis. D.J. Prevalence and treatment of Psoriasis in the U.K.: A population based study. Arch. Dermatol. 2005;141:1537-41.
6. Chablani U.A., Contractor N.M., Gadgil R.B.. HLA and complement C4 studies in Psoriasis Vulgaris. Natl. Med. J India. 1992;5:8-11.
7. Pictchappan et al. HLA B57 and DR7 association with psoriasis vulgaris in South India. Tissue Antigens 1989;34:133-7.
8. Rani R, Narayanan R, Fernandez M.A., Stastany. P. Role of HLA B and C allels in the development of Psoriasis in patients from North India. Tissue Antigens 1998; 51:618-22.
9. Russel T.J., Schultes. L.M., Kuban D.J., HLA antigen associated with Psoriasis. New Engl. J.Med. 1972;287:737-40.
10. White S.H., Mickey M.R., HLA antigen frequency in Psoriasis. New Engl. J.Med 1972;287:740-43.
11. Tiwari JL,Terasaki PI.HLA and Disease Association.New York;Springer 1985;16:145-48.
12. Sasazuki T,Mathushita S,Nakamizo V et al HLA and Psoriasis in Asian populations Joint Report In 1986;23:349-353.
13. Singh S,SinghU,Singh S HLA in patients with psoriasis.Ind J Dermatol Venerol Leprol 2011;77:535-37.
14. Bach F.H,Van Rood,The Major Histocompatibility Complex:Genetics and Biology.New Engl J Med 1976;295:806-813.
15. Shankarkumar Umapathy,R Mitra,Arun Pawar,K Ghosh HLA –A and HLA-B alleles associated in psoriasis patients from Western India. Ind J Dermatol Venerol Leprol 2011;56(5):497-500.
16. Ikaheimo,Silvennoinen-Kassinen S,Karvonen J.Immunogenetics profile of psoriasis vulgaris.Arch Dermatol Res 1996.288:63-67.
17. Gonzaga HF,Torres EA Both psoriasis and benign migratory glossitis are associated with HLA.Br J Dermatol 1996;135:368-370.
A study of the role of insulin resistance and iron in NAFLD associated with HFE gene mutation
Introduction: NAFLD is becoming a major public problem worldwide. NAFLD is an emerging problem in the Asia-Pacific region and its overall prevalence at present is broadly similar to west. Based on surveys using ultrasonography, the prevalence of NAFLD in the general population across Asia varies from 5% to 40% Aims and Objectives: To Assess the risk of NASH with clinical predictor score associated with HFE gene mutation. Materials and Methods: The work embodied in this study was conducted at tertiary care Hospital. All the type 2 diabetic patients attending the OPD irrespective of their sex and treatment protocol were taken; it includes both old and new cases of type 2 diabetes. All the type 2 diabetic patients were subjected to ultrasonography to rule out the fatty liver. Type 2 DM with NAFLD was taken as cases and Type 2 DM without NAFLD was taken as controls. Biochemical parameter analyzed are fasting glucose, fasting insulin, serum iron, T.I.B.C and ALT.DNA was extracted from frozen whole blood to detect Cys282Tyr mutation. Based on HAIR score, the NASH was assessed in our NAFLD patients. Result: In our study population out of 100 type 2 diabetes patients, 54 of them had fatty liver. In our study population, cases had more female patients (59.2%) than controls (36.9%) and it was statistically significant (Chi square value x2= 4.94 and p<0.02). Fasting insulin and insulin resistance were significantly higher in cases (p< 0.05).Serum Iron and transferrin saturation were significantly raised (p<0.01) in cases when compared to controls. NAFLD patients had significantly higher ALT levels. In our study, 27.8% of patients had NASH based on HAIR score. HFE gene C282Y mutation was not found in our study population. Conclusion: Based on HAIR score, 27.8% of NAFLD patients might have NASH. NAFLD patients had significantly increased serum iron and transferrin saturation when compared to controls. None of our patients had HFE mutation.
1. Kareem Harish, Varghese Thomas. Review article. Non-alcoholic fatty liver disease in Asians- an emerging problem. Calicut Medical Journal 2008; 6(3):e6.
2. Hamaguchi M, Kojima T, Takeda N et al. The metabolic syndrome as a predictor of nonalcoholic fatty liver disease. Ann. Intern. Med. 2005; 143: 72208.
3. Duseja A, Das A, Das R, Dhiman R, Chawla Y. Nonalcoholic steatohepatitis: our experience. Indian J. Gastroenterol 2004; 23 (Suppl. 1): S25.
4. Agarwal SR, Malhotra V, Sakhuja P, Sarin S. Clinical biochemical and histological profile of nonalcoholic steatohepatitis. Indian J.Gastroenterol.2001; 20: 183–6.
5. Duseja A, Chawla Y. Nonalcoholic fatty liver disease in India. How Much? How Soon. Trop Gastoenterol. 2005; 26: 1–3.
6. Buetler E. Genetic irony beyond haemochromatosis: clinical effects of HLA-H mutations. Lancet 1997; 349:296-297.
7. Brunt EM, Janney CG, Di Bisceglie AM, Neuschwander-Tetri BA, Bacon BR. Nonalcoholic steatohepatitis: a proposal for grading and staging the histological lesions. Am J Gastroenterol 1999;94:2467-74.
8. Day, C. P. and James, O. F. W., Steatohepatitis – a tale of two hits. Gastroenterology, 1998, 114, 842–845.
9. Sies, H., Biochemistry of oxidative stress. Angew. Chem. Int. Ed. Engl., 1986; 25: 1058–1071.
10. Feder JN, Gnirke A, Thomas W, et al. A novel MHC class I like gene is mutated in patients with hereditary haemochromatosis. Nat Genet 1996;13:399–408.
11. Nemeth E, Tuttle MS, Powelson J, et al. Hepcidin regulates cellular iron efflux by binding to ferroportin and inducing its internalization. Science 2004; 306: 2090-3.
12. Papanikolaou G, Samuels ME, Ludwig EH, et al. Mutations in HFE2 cause iron overload in chromosome 1q linked juvenile hemochromatosis. Nat Genet 2004; 36: 77- 82.
13. Bridle KR, Frazer DM, Wilkins SJ, et al. Disrupted hepcidin regulation in HFE-associated haemochromatosis and the liver as a regulator of body iron homoeostasis. Lancet 2003; 361: 669-73.
14. Kawabata H, Fleming RE, Gui D, et al. Expression of hepcidin is down-regulated in TfR2 mutant mice manifesting a phenotype of hereditary hemochromatosis. Blood 2005; 105: 376-81.
15. Kristin G. Monaghan, Benjamin A et al. Mutation Analysis of the HFE Gene Associated With Hereditary Hemochromatosis in African Americans. American Journal of Hematology 1998; 58:213–217.
16. Yu AS, Keetie AB. Predictors of NASH and advanced fibrosis. Reviews in Gastrointest Disorders 2002; 2(1): 11-9.
17. Gupte P, Amarapukar D, Agal S, Baijal R, Kulshreshtta P, Pramik S, et al. Non-alcoholic steato-hepatitis in type 2 diabetes mellitus. J GasteroentrolHepatol 2004;19:854-58.
18. ShobhaLuxmi, Rukhsana Abdul Sattar and Jamal Ara.Association of Non Alcoholic Fatty Liver with type 2 Diabetes Mellitus. JLUMHS 2008; 188-193.
19. Akber DH, Kawther AH. Non-alcoholic fatty liver disease in Saudi type-II diabetic subjects attending a medical outpatient clinic. Diabetes Care 2003 ;26: 3351 – 65.
20. Ludwig J, Viggiano TR, McGill DB, et al. Non alcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease. Mayo ClinProc 1980;55:434-8.
21. Bugianesi E, Manzini P, D’Antico S et al. Relative Relative Contribution of Iron Burden, HFE Mutations, and Insulin Resistance to Fibrosis in Nonalcoholic Fatty Liver. Hepatology, January 2004; Vol. 39, No. 1: 179-187.
22. Fan JG, Zhu J, Li XJ et al. Fatty liver and the metabolic syndrome among Shanghai adults. J. Gastroenterol. Hepatol. 2005; 20: 1825-32.
23. Hamaguchi M, Kojima T, Takeda N et al. The metabolic syndrome as a predictor of nonalcoholic fatty liver disease. Ann. Intern. Med. 2005; 143: 722-8.
24. Younossi ZM, Gramlich T, Bacon BR et al. Hepatic iron and nonalcoholic fatty liver disease. Hepatology 1999; 30:847–50.
25. Salonen JT, Tuomanien TP, Nyyssonen et al. Relation between iron stores and non-insulin dependent diabetes in men: case-control study. BMJ 1998; 317: 727.
26. Hanson EH, Imperatore G, Burke W 2001. HFE gene and hereditary hemochromatosis: a HuGE review. Human Genome Epidemiology. Am J Epidemiol, 154(3):193-206.
27. Christine E, McLaren, James C et al. Determinants and characteristics of mean corpuscular volume and hemoglobin concentration in white HFE C282Y homozygotes in the hemochromatosis and iron overload screening study. American Journal of Hematology 2007; 82: 898-905.
28. Joseph A .E , Saverymuttu S H , Al-Sams , Cook M G ,et al. Comparison of liver histology with USG in assessing diffuse parenchymal liver disease. Radiology 1991;43:26-31.
29. Younossi ZM, Diehl AM, Ong J P, et al. Non Alcoholic Fatty Liver Disease- an agenda for clinical research. Hepatology 2002; 35: 746-742.
Dukes treadmill score and myocardial perfusion scintigraphy - A comparative study in patients
Radionuclide myocardial perfusion imaging (MPI) can be used to demonstrate the presence of coronary heart disease and to risk stratify and guide management of patients with known disease. Treadmill test which is commonly used as screening test for CAD, and with help of DTS can to some extent accurately risk stratify the patients as well. Aim of the study was to compare Duke treadmill score and MPI in risk stratifying the patient with CAD. 130 patients were considered in the study. Most of the patients fell in moderate Dukes score (78 patients, 60%). MPI could further stratify those patients into high (28 patients, 36%) and low risk (50 patients, 64%) groups. Low and high Dukes scores correlated well with normal and severe defects in MPI respectively. Hence it is advisable to perform MPI in moderate Dukes Score patients for further risk stratification.
1. Heart Facts 1980 American Heart Association, 1979
2. Report of Joint International Society and Federation of Cardiology and World Health Organization Task Force on Standardization of Clinical Nomenclature 1979 Nomenclature and criteria for diagnosis of ischemic heart disease. Circulation 59: 607
3. Wyatt HL, Forrester JS, Tyberg JV et al 1975 Effect of graded reduction in regional coronary perfusion and total cardiac function Am J Cradiol 36:185
4. Kubler W, Katz AM 1977 Mechanism of early pump failure of the ischemic heart: possible role of adenosine triphosphate depletion and inorganic phosphate accumulation. Am J Cardiol 40: 467
5. Robb G.P, Marks M H 1974 Latent Coronary artery disease: determination of its presence and severity by the exercise electrocardiogram. Am J Cardiol 13:603
6. Goldschlager N, Selzer A, Cohn K 1976 Treadmill stress tests as indications of presence and severity of coronary artery disease. Ann Intern Med 85: 277
7. Master AM, Jaffe HL 1941 Ecltrocardiographic changes after exercise in angina pectoris. J Mount Sinai Hosp 7:629
8. AHA/ACSM Scientific Statement, Recommendation for Cardiovascular Screening, Staffing and emergency policies at Health/fitness facilities, Circulation 1998; 97: 2283-2293 doc 10.1161/01 CIR.97.22.2283.
Assessment of the insulin resistance- insulin sensitivity and β cell function in type 2 diabetes with NAFLD associated with HFE gene mutation
Introduction: Diabetes mellitus has reached pandemic proportion and in 2030, there will be approximately 366 million diabetics; of these 79 million will be from India. Diabetes mellitus is a group of metabolic diseases that includes hyperglycemia resulting from defects in insulin secretion, insulin action or both. Type 2 diabetes is characterized by insulin resistance and insulin deficiency (often relative rather than absolute). Aims and Objectives: To study Assessment of the insulin resistance- insulin sensitivity and β cell function in type 2 diabetes with NAFLD associated with HFE gene mutation. Materials and Methods: The work embodied in this study was conducted at tertiary care Hospital. It is a hospital based case control study. All the type 2 diabetic patients attending the OPD irrespective of their sex and treatment protocol were taken; it includes both old and new cases of type 2 diabetes. All the type 2 diabetic patients were subjected to ultrasonography to rule out the fatty liver. Type 2 DM with NAFLD was taken as cases and Type 2 DM without NAFLD was taken as controls. Biochemical parameters analysed were glucose, insulin, serum iron and total iron binding capacity. DNA was extracted from frozen whole blood to detect Cys282Tyr mutation.Result: In our study population out of 100 type 2 diabetes, 54 patients had fatty liver. The prevalence of fatty liver in our study group was 54%.In our study population, majority of the patients were in the age group of 51- 60 years in both cases and controls. Age distribution between cases and controls were matched (Chi square value 2.45 degree of freedom (df) is 3, p value = 0.48).NAFLD cases had more female patients (59.2%) than controls and it was statistically significant (Chi square value x2= 4.94 and p<0.02). In our study population, mean fasting glucose in cases and controls (147.8 ± 44.6 and 138.5 ± 33.9 respectively) were not significantly different (p<0.5). Whereas post prandial glucose, fasting insulin, HOMA-IR and HOMA-β were significantly(p<0.5) higher in NAFLD patients. In comparison to controls, Insulin sensitivity index (QUICK) was statistically low(p< 0.05) in NAFLD patients. Conclusion: We observed significant increase in fasting insulin, beta-cell function (HOMA-β) and insulin resistance along with decreased insulin sensitivity in NAFLD patients
1. Sarah Wild, GojkaRoglic, Anders Green et al Global Prevalence of Diabetes: Estimates for the year 2000 and projections for 2030. Diabetes Care 2004; 27:1047–1053.
2. Report of the export committee on the diagnosis and classification of diabetes mellitus. Diabetes Care Jan 2002. vol 25(1); s5-s20.
3. Yoon KH, Lee JH, Kim JW et al. Epidemic obesity and type 2 diabetes in Asia. Lancet 2006; 368: 1681–8.
4. Brunt EM. Nonalcoholic steatohepatitis: definition and pathology. Semin Liver Dis 2001;21:3–16.
5. Cairns SR, Peters TJ. Biochemical analysis of hepatic lipid in alcoholic and diabetic and control subjects. ClinSci (Lond). 1983 ; 65:645-52.
6. Farrell GC, Larter CZ. Nonalcoholic fatty liver disease: from Steatosis to cirrhosis.Hepatology 2006; 43(Suppl.1): S99 – 112.
7. Ludwig J, Viggiano TR, McGill DB, et al. Non alcoholicsteatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease. Mayo ClinProc 1980;55:434-8.
8. Braunwald E et al. Harrison’ s principles of internal medicine , 16th edition. McGraw-Hill,2005.
9. Bacon BR, Farahvash MJ, Janney CG et al. Non-alcoholic steatohepatitis: an expanded entity. Gastroenterology 1994; 107:1103.
10. Powell EE, Cooksley WGE, Hanson R et al. The natural history of nonalcoholicsteatohepatitis: a follow up study of 22 patient for up to 21 years. Hepatology 1990; 11:74.
11. Marchesini G, Bugianesi E, Forlanietal.Nonalcoholic fatty liver, steatohepatitis, the metabolic syndrome.Hepatology2003;37:917- 23.
12. Chitturi S, Abeygunasekera S, FarrellGCet al. NASH and insulin resistance: Insulin hypersecretion and specific association with the insulin resistance syndrome. Hepatology 2002;35:373-379.
13. Feder JN, Penny DM, Irrinki A, et al. The hemochromatosis gene product complexes with the transferrin receptor and lowers its affinity for ligand binding. ProcNatlAcadSci U S A 1998;95:1472–7.
14. Bridle KR, Frazer DM, Wilkins SJ, et al. Disrupted hepcidin regulation in HFE-associated haemochromatosis and the liver as a regulator of body iron homoeostasis. Lancet 2003; 361: 669-73.
15. C.ABurtis, E.R Ashwood, W.B Saunder. Tietz text book of clinical chemistry, 3rd 1999: pg 750-785
16. Robbins DC, Andersen L, Bowsher R et al. Report of the American Diabetes Association’s task force on standardization of the insulin assay.Diabetes 1996; 45: 242-256.
17. Matthews DR, Hosker JP, Rudenski AS. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentration. Diabetologia 1985; 28: 412-9.
18. Levy JC, Matthews DR, Herman MP. Correct homeostasis model assessment (HOMA) evaluation uses the computer program. Diabetes Care 1998; 21: 2191-2.
19. Katz A, Nambi SS, Mather K et al. Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans. J ClinEndocrinolMetab 2000; 85: 2402-10.
20. Kristin G. Monaghan, Benjamin A et al. Mutation Analysis of the HFE Gene Associated With Hereditary Hemochromatosis in African Americans. American Journal of Hematology 1998; 58:213–217.
21. Feder JN, Gnirke A, Thomas W, et al. A novel MHC class I like gene is mutated in patients with hereditary haemochromatosis. Nat Genet 1996;13:399–408.
22. Muhammad Khurram, Abdul Shakoor, Mian M Arshad et al. Characteristic features of 50 NAFLD patients. Rawal Med J 2004; 29: 8-12.
23. Gupte P, Amarapukar D, Agal S, Baijal R, Kulshreshtta P, Pramik S, et al. Non-alcoholic steato-hepatitis in type 2 diabetes mellitus. J GasteroentrolHepatol 2004;19:854-58.
24. ShobhaLuxmi, Rukhsana Abdul Sattar and Jamal Ara.Association of Non Alcoholic Fatty Liver with type 2 Diabetes Mellitus. JLUMHS 2008; 188-193.
25. Akber DH, Kawther AH. Non-alcoholic fatty liver disease in Saudi type-II diabetic subjects attending a medical outpatient clinic. Diabetes Care 2003 ;26: 3351 – 65.
26. Sandhya Mishra, Dharamveer, Monika Gupta et al. Hyperinsulinemia predisposes to NAFLD. Indian journal of Clinical Biochemistry, 2008; 23(2): 130-135
27. Constantine Goritsas, Konstantinos Spanos, Dimitrios Stefanopoulos et al. Non Alcoholic Fatty Liver Disease: Correlation With Clinical Hormonal and Biochemical Parameters. Hospital Chronicles 2007; 2(3): 100–103.
28. Ajay Duseja, Reena Das, Mohit Nanda, Ashim Das et al. Nonalcoholic steatohepatitis in Asian Indians is neither associated with iron overload nor with HFE gene mutations. World J Gastroenterol 2005;11(3):393-395.
A comparative study of two different doses of Gabapentin in attenuating the cardiovascular response to direct laryngoscopy and intubation
V B Gowda, Manjunath K S, Henjarappa K S, Namrata Ranganath, Arathi B H
Introduction: Direct laryngoscopy and endotracheal intubation is an integral part of anaesthesia which offers tremendous safety to administration of general anaesthesia but is associated with hemodynamic changes, due to reflex sympathetic discharge caused by epipharyngeal and laryngopharyngeal stimulation. Aims and Objectives: Tostudy the effect of two different doses of Gabapentin in attenuating the cardiovascular response to direct laryngoscopy and intubation. Materials and methods: Prospective, randomized, double blind and placebo controlled clinical study involving90 patients of kidwai memorial institute of oncology,Banglore visiting pre anaesthesia clinic scheduled for elective surgery under GA with ASA I and ASA II was designed after approval from institute ethics committee. Statistical analysis was done by Analysis of variance (ANOVA) to find the significance of study.Student t test (paired) has been used to find the significance within the same group. Result: Laryngoscopy and intubation caused a significant increase in heart rate and blood pressure in controlled group. Gabapentin can be used to attenuate pressor response to laryngoscopy and intubation. Gabapentin 800mg and 400mg attenuated the pressor response to laryngoscopy and intubation. SBP, DBP, MAP and HR were all attenuated by Gabapentin in comparison to control group. Gabapentin 800mg is more effective than 400mg for attenuation of pressor response to laryngoscopy and intubation (Statistically significant p<0.05) Conclusion: SBP, DBP, MAP and HR were all attenuated by Gabapentin in comparison to control group. Gabapentin 800mg is more effective than 400mg for attenuation of pressor response to laryngoscopy and intubation.
1. Burstein CL, Lo Pinto FJ,Newman: Electrocardiographic studies during endotracheal intubation; Effects during usual routine techniques. Anesthesiology 1950; 11:224
2. King B D, Elder J D, Procter D F, et al: Reflex circulatory responses to tracheal intubation performed during general anesthesia. Anesthesiology 1951;12: 556
3. Fox E.J, Sklar G.S, Hill C.H, Villanuera R, King BD. Complications related to the pressure response to endotracheal intubation. Anesthesiology 1977; 47: 524-5
4. Miller Forbes and F G Dally: Acute hypertension during induction of anesthesia and endotracheal intubation in normotensive men. Br J Anaesth 1970; 42: 618.
5. Asfar S N, Abdulla WY: The effects of various administration routes of lignocaine on the hemodynamics and ECG rhythm during endotracheal intubation. ActaAnesthesiologicaBelgica1990; 41: 17-24.
6. Helfman SM, Gold MI, Delisser EA, Herrington CA: Which drug prevents tachycardia and hypertension associated with tracheal intubation; Lignocaine, Fentanyl or Esmolol?Anesthesia and Analgesia 1991; 72: 482-6.
7. Lev R, Rosen P: Prophylactic lignocaine use pre intubation: A review. Journal of Emergency Medicine 1994; 12(4): 499-506.
8. James F Hamill, Robert F Bedford, David C Weaver, Austin colohan. Lignocaine before endotracheal intubation: Intravenous or laryngotracheal. Anesthesiology 1982; 55: 578-581.
9. Gold M, Brown Mand, Selem J: The effects of Esmolol on hemodynamics after ketamine induction and intubation. Anesthesiology 1982; 61-119.
10. Puri GD, Batra YD. Effects of Nifedepine on the cardiovascular responses to laryngoscopy and intubation. Br J Anaes1988; 60(5): 579-581.
11. NibeditaPani, ShovankumarRath. Regional and Topical Anaesthesia of upper Airways. Indian J of Anaesth2009; 53: 61-648.
12. Mostafa SM, Murthy B V, Barett P J, McHugh P: Comparison of the effects of lignocaine spray applied before or after induction of anesthesia on the pressor 57 response to direct laryngoscopy and inubation. Eur J Anaesthesiol1999;16: 7-10.
13. Donald Martin et al: low dose fentanyl blunts circulatory responses to tracheal ntubation. Anesthesia and Analgesia 1982; 61: 680.
14. AbouMadi M, Kelzler H, Yacoub O: A Method of prevention of cardiovascular reactions to laryngoscopy and intubation. Canadian Anaesthesia Society Journal 1975; 22: 316.
15. Bahman Venus, VenugopalPolassani , Con Gial Pham: Effects of aerolized lignocaine on circulatory responses to larynoscopy and tracheal intubation.critical care medicine 1984;12: 391-4.
16. Sklar B Z, Lurie S, Krichelli D, Savir I, Soroker D: Lignocaine inhalation attenuates the circulatory response to laryngoscopy and endotracheal intubation. Journal of Clinical Anesthesia 1992; 4(5): 382-5.
17. Kautto UM, Heinonen J: Attenuation of circulatory response to laryngoscopy and tracheal intubation: a comparison of two methods of topical anaesthesia. Actaanaesthesiology Scandinavia 1982; 26(6): 599-602.
18. Rachael K Seib, James E Paul. Pre-operative Gabapentin for post-operative analgesia: A meta analysis. Can J Anaesth2006; 53: 461-69.
19. Gilron et al. Is Gabapentin a broad spectrum analgesic? Anesthesiology 2002;97: 537-539.
20. Kong VK, Irwin MG. Gabapentin: a multimodal peri-operative drug? Br J Anaes2007; 99: 775-786
21. Rosner H, Rubin L, Kestenbaum A. Gabapentin adjunctive therapy in neuropathic pain states. ClinJ Pain 1996; 12: 56–8.
22. Menigaux C, Adam F, Guignard B, Sessler DI, Chauvin M. Preoperative gabapentin decreases anxiety and improves early functional recovery from knee surgery. AnesthAnalg2005; 100: 1394–9.
23. Memis D, Turan A, Karamanlioglu B, Seker S, Ture M. Gabapentin reduces cardiovascular responses to laryngoscopy and tracheal intubation. Eur J Anaesthesiol2006; 23: 686–90.
24. Prys-roberts C, Greene L.T, Meloche R, Forex P. Studies of anaesthesia in relation to hypertension II: Hemodynamic consequences of induction and endotracheal intubation. BrJAnaesth1971; 43:531.
25. Fassoulaki A, Melemeni A, Paraskeva A, Petropoulos G. Gabapentin attenuates the pressor response to direct laryngoscopy and tracheal intubation. Br J Anaesth2006 ; 96: 769-773.
26. Koc S, Memis D, Sut N. The preoperative use of gabapentin, dexamethasone and their combination in varicocele surgery: a randomized control study. AnaesthAnalg2007; 105(4): 1137-42.
A study of the efficacy of mifepristone with misoprostol over misoprostol alone in medical termination of pregnancy
Introduction: Misoprostol has proven its efficacy as an effective abortifacient for the second trimester termination of pregnancy. It is being successfully used through all the routes i.e. sublingual, oral and vaginal and in different regimens with the induction abortion interval varying from 12 h to as high as 33 h. Aims and Objectives: To Study the Efficacy of Mifepristone with misoprostol over misoprostol alone in medical termination of Pregnancy Methodology: This was a hospital based study in patients attending the department of Obstretics and Gynecology of teaching hospitals attached to Bangalore Medical College, Bangalore (viz. Bowring and Lady Curzon Hospital and Vanivilas Hospital) who needed MTP. Out of 100 Pregnant Women 50 pregnant women given oral mifepristone 200mg followed by vaginal misoprostol 400 microgram after 48 hours and one hour of that 200 microgram of oral misoprostol. 50 pregnant women given 600 microgram vaginal misoprostol alone at a time The statistical analysis done by unpaired t-test. Result: Complete abortion was achieved in 88% (44) of the patients in misoprostol alone regimen. Complete abortion was achieved in 96% (48) of the patinets in combination regimen. Overall complete abortion was achieved in 92 patients in our study. Failure rate was observed more in Misoprostol alone group i.e. 12.0% as compared to Misoprostol+Mifepristone group i.e. 4.0%. Mean Time to Induction to Abortion was significantly less in Mifepristone with misoprostol than misoprostol alone group. Conclusion: From our study it can be concluded that the combination of Mifepristone with misoprostol is superior to misoprostol alone with respect to less failure rate and Mean Time to Induction to Abortion in both Primi and Multi Gravidity.
1. Wong KS, Ngai CS, Yeo EL, et al. A comparison of two regimen of intravaginal misoprostol for termination of second trimester pregnancy: a randomized trial. Hum Reprod. 2000; 15:709–12.
2. Herbutya Y, Chanarchakul B, Punyavachira P. Vaginal misoprostol in the termination of second trimester pregnancy. J ObstetGynaecol Res. 2000; 26:121–5.
3. Pongsatha S, Tongsong T. Second trimester pregnancy termination with 800 mcg vaginal misoprostol.J Med Assoc Thai. 2001; 84: 859–63.
4. Herbutya Y, Chanarchakul B, Punyavachira P. Second trimester pregnancy termination: a comparison of 600 and 800 lg of intravaginal misoprostol. J ObstetGynaecol Res. 2001; 27:125–8.
5. Gilbert A, Reid R. A randomized trial of oral versus vaginal administration of misoprostol for the purpose of mid trimester termination of pregnancy.Aust N Z J ObstetGynaecol.2001; 41:407–10.
6. Ramin KD, Ogburn PL, Danilenko DR, et al. High dose oral misoprostol for mid trimester pregnancy interruption. J GynecolObstet Invest. 2002; 54:176–9.
7. Dickinson JE, Evans SF. A comparison of oral misoprostol with vaginal misoprostol administration in second-trimester pregnancy termination for fetal abnormality.Obstet Gynecol. 2003; 102: 1294–9.
8. Tang OS, Lau WNT, Chan CCW, et al. A prospective randomized comparison of sublingual and vaginal misoprostol in second trimester termination of pregnancy.Br J ObstetGyneacol. 2004; 11:1001–5.
9. Pongastha S, Tong song T. Therapeutic termination of second trimester pregnancies with intrauterine fetal death with 400 lg of oral misoprostol. J ObstetGynaecol Res. 2004; 30:217–20.
10. Baird DT, Rodger MW. Pretreatment with mifepristone (R U 486) reduces interval between prostaglandin administration and expulsion in second trimester abortion. Br J ObstetGyneacol. 1990; 97:41–5.
11. Hinshaw K, Refaey HE. Mid trimester termination for fetal abnormality: advantages of a new regimen using mifepristone and misoprostol. Br J ObstetGyneacol. 1995; 102:559–60.
12. Refaey HE, Templeton A. Induction of abortion in the second trimester by a combination of misoprostol and mifepristone: a randomized comparison between two misoprostol regimens. Hum Reprod. 1995; 10:475–8.
13. HO PC, Tsang SSK, Ma HK. Reducing the induction to abortion interval in termination of second trimester pregnancies: a comparison of mifepristone with laminaria tent.Br J ObstetGyneacol. 1995; 102:648–51.
14. Premila WA, Templeton A. Nonsurgical mid trimester termination of pregnancy; a review of 500 consecutive cases. Br J ObstetGyneacol. 1999; 106:706–10.
15. Ngai SW, Tang OS, Pak Chiung HO. Randomized comparison of vaginal (200 lg every 3 h) and oral (400 lg every 3 h) misoprostol when combined with mifepristone in termination of second trimester pregnancy. Hum Reprod. 2001; 15:2205–8.
Comparative study of bone marrow aspiration and bone marrow clot sections in various haematological disorders
Introduction: During the last two decades, bone marrow examination has become an indispensable adjuvant to diagnose the malignant diseases of the blood and other body systems. This will obviate the need for many other expensive and time-consuming investigations. When both the procedures for bone marrow examination i.e. aspiration and clot section done simultaneously, can yield a good diagnostic material which will be helpful for more accurate diagnosis. Aims and Objectives: This study was aimed to assess the diagnostic value of the BMA and Bone Marrow Clot Sections and role of both the procedures to reach final diagnosis when done simultaneously. Methods: The present study was done on 80 cases in which complete peripheral blood smears, bone marrow and cell blocks was available were included in the study. Bone marrow aspiration was performed, Cell block was prepared and stained with hematoxylin and eosin stain, smears were stained with Leishman stain. Results: Comparison was done between bone marrow aspirate smears stained by Romanowsky group of stains i.e. Leishman and paraffin embedded cell block section stained by Hematoxylin and Eosin stain. Out of 80 cases, there were 60 cases (75%) of anaemias, 9(11.2%) platelet disorders, 6(7.5%) Acute Leukaemias, 2(2.5%) Lymphoproliferative disorders, 1(1.2%) MDS, 1(1.2%) Leishmaniasis and 1(1.2%) hyperspleenism. Conclusions: The advantage of both the procedures done together provided more material and enabled us to study the cytomorphology of the cells, with the pattern of distribution of the cells depending on the cases and help in more accurate diagnosis.
1. Riley RS, Hogan TF, Pavot DR, Forysthe R, Massey D, Smith E, Wright L, Jr, Ben-Ezra JM. A pathologist’s perspective on bone marrow aspiration and biopsy; Performing a bone marrow examination. J Clin Lab Anal. 2004; 18:70–79. doi: 10.1002/jcla.2008.
2. Islam A. Bone marrow aspiration prior to bone marrow core biopsy using the same bone marrow biopsy needle. A good or bad practice. J Clin Pathol. 2007;60:212–215. doi: 10.1136/jcp.2006.037341.
3. Hyun BH, Gulati GL ,Ashton JK.Bone marrow examination :techniques and interpretation.Hematol Oncol Clin North Amer 1988;2:513-523.
4. Riley RS .Hogan TF, Pavot DR.etal .A pathologist perspective on bone marrow aspiration and biopsy: Performing a bone marrow examination .J Clin Lab Annal.2004;18 (2) :70-90.
5. Brain BJ..Bone Marrow Evaluation .J clin Pathol 2001; 54: 737-742.
6. Kuperan P,Rajshekhar swamy.Magaloblastic anaemia- A review from university hospital Kuala Lumpur.Ann Acad Med Singapore.1998;17(2):261-266.
7. Pizzuto J, Ambriz R.Therapeutic experience on 934 adults with idiopathic thrombocytopaenic purpura: Multicentric trial co-operative Latin American Group on Hemostatis and thrombosis.Blood1984;64:1179-1183.
8. Jaishree Sharma,Shobha Mohindroo.FAB classification of Leukaemia: A cytochemical study.Indian J Pathol Microbiol 2004;47(3):336-339.
9. Sitalaxmi S, Anuradha Srikrishna,Shantal Devi,Prema Damodar,Betty Alexander.The Diagnostic utility of bone marrow trephine biopsies. Indian J Pathol Microbiol 2005;48(2):173-176.
10. Rozman C ,Monserrat E,Rodriguez-Fernandez JM,Ayats R,Vallespi T ,Parody R etal. Bone marrow Histologic Pattern- The Best Single prognostic parameters in CLL:A multivariate survival analysis of 329 cases. Blood 1984; 64(3) :642-64811.
11. Alteration in cellularity of bone marrow. Bone marrow cellularity- general.Ann clin Lab Sci 2004;34:307.
12. Pasquale D, Chikkapa G. Comparative evaluation of bone marrow aspirate particle smears, biopsy imprints and biopsy sections. Am J Hematol. 1986;22:381–389. doi: 10.1002/ajh.2830220407.
13. Ozkalemkas F, Ali R, Ozkocaman V, Oscelik T, Ozanu OH, et al. The bone marrow aspirate and biopsy in the diagnosis of unsuspected non hematologic malignancy. A clinical study of 19 cases. BMC Cancer. 2005;1(5):144. doi: 10.1186/1471-2407-5-144.
14. Varma N, Dash S, Sarode R and Marwaha N. Relative efficacy of bone marrow trephine biopsy sections as compared to trephine imprints and aspiration smears in routine hematological practice. Indian J Pathol Microbiol 1993; 36(3):215-226.
15. Dee JW, Valdivieso M , Drewinko B. Comparison of the efficacies of closed trephine needle biopsy,aspirated paraffin embedded clot section, and smear preparation in the diagnosis of bone marrow involvement by lymphoma. Am J Clin Pathol 1976;65:183-94.
Phenotyphic Determination of Urinary Virulence Factors in Escherichia coli
Aim: To determine the virulence factors haemolysin production, hemagglutination and serum resistance in Escherichia coli (E.coli) of urinary isolates and Escherichia coli isolated from the other sites like blood, exudate and stool. Materials and Methods: A cross sectional study was conducted in the Department of Microbiology, Sri Ramachandra Medical College and Research Institute. A total of 120 strains of E. Coli isolated fromthe following specimens urine (50), Exudate (25), Blood (25) and Stool (20) were included in the study and assessed for the presence of Uropathogenic virulence factors such as Haemolysin production, Hemagglutination property both the Mannose Resistant Hemagglutination (MRHA) and Mannose Sensitive Hemagglutination (MSHA) and Serum Resistance factor. Results: Among the 50 urinary isolates haemolysis was observed in 10%, hemagglutinating property was seen in 20 %( MRHA 7 and MSHA 3 n=10)) and 88 % of them had serum resistance factor. Out of the 25 E.coli strains isolated from the exudate samples none of them was found to be haemolytic, 12% of them were hemagglutinating (MRHA 67% and MSHA 33%) and serum resistance factor was seen with 24% of isolates. Among the 25 E. coli isolates from the blood 8% were haemolytic, 28% of them were hemagglutinating (MRHA 100%) and serum resistance factor was observed in 72. Out of 20 E.coli strains isolated from stool, haemolysis was not seen in any of the them, 20% of them were hemagglutinating property (MRHA 100%) and serum resistance factor was positive in 20% of them. Summary and Conclusion: A total of 50 E.coli reported as significant bacteriuria (>105) was included in this study and at the same time 70 isolates of E.coli reported from other specimens (Blood, Exudates and Stool) were taken as control group. Uropathogenic virulence factor was exhibited by 45 out of 50 urinary isolates (90%). Serum Resistance is the commonest virulence factor observed in our study (88%) followed by Hemagglutination property (20%) and Haemolytic property (10%). The entire 3 virulence factor is exhibited by 3 strains of urinary isolates (6%) only. In the control group Haemolysis was observed in 2 isolates, Hemagglutination with 24 isolate, Serum Resistance in 28 E.coli isolates.
1. Mulvey M A“Adhesion and Entry of Uropathogenic Escherichia coli†Cellular Microbiology (2002) 4(5), 257–271.
2. M Douglas and Bennetts.“Principle and Practice of Infectious Diseaseâ€. 7th edition. Churchill Livingstone (2010) Vol 2 Chapter 218.
3. Seetharama S, Cavalieri S J, Snyderl I S. “Immune Response to Escherichia coli Alpha-Hemolysin in Patientsâ€. Journal of clinical microbiology, May 1988, p. 850-856
4. JOHNSON J R“Virulence Factors in Escherichia coli Urinary Tract Infectionâ€.CLINICAL MICROBIOLOGY REVIEWS, Jan. 1991, p. 80-128
5. Kausar Y, Chunchanur S K, Nadagir S D, Halesh L H and Chandrasekhar M R. “Virulence factors, Serotypes and Antimicrobial Suspectibility Pattern of Escherichia coli in Urinary Tract Infectionsâ€. Al Ameen J Med Sci. 2009; Vol 2(1): 47 -51.
6. Sharma S, Bhat GK, Shenoy S. Virulence factors and drug resistance in Escherichia coli isolated from extraintestinal infections. Indian J Med Microbiol 2007;25:369-73
7. Ranjan KP, Ranjan N, Chakraborty A, Arora DR. “An approach to uropathogenic Escherichia coli in urinary tract infectionsâ€. J Lab Physicians. 2010 Jul;2(2):70-3.
Comorbidity of recurrent depressive disorder with thyroid dysfunction and altered lipid metabolism in postmenopausal women: A case-control study
The transition to menopause represents the passage from reproductive to non-reproductive life. Most women during the menopause experience irregular menstrual periods along with fluctuation of ovarian hormones secretion during this time. Usually during the menopause and after menopause i.e. post-menopause women face physical and emotional changes. Since years various investigators have already documented an association between depression and menopause. Post-menopausal period is accompanied in a majority of women with significant somatic and psychiatric symptomatology. Objective: Since psychiatric symptomatology is a growing concern in post-menopausal women, hence we tried to examine whether a comorbidity of metabolic and psychiatric disorders occurs in this patient population or whether these disorders occur independently. The study was planned to examine comorbidity of recurrent depressive disorder with thyroid dysfunction and altered lipid metabolism in post-menopausal women (PMW). Method: To conduct this study a cross sectional, case-control study was planned. The experimental group consisted of PMW with recurrent depressive disorder (ICD-10 criteria) (n=100), and was compared with a control group (n=100) of PMW without recurrent depressive disorder. Subjects were assessed through Beck’s depressive self-rating inventory and their blood level of Thyroid Stimulating Hormone (TSH) and lipid profile was assessed. Group comparison was done with chi square test and z test. Correlation analysis was undertaken using Pearson correlation coefficients (r). Result: Results obtained depicted that serum total cholesterol, triglyceride, TSH levels were significantly higher and HDL levels were significantly lower in the depressed group.Highly significant positive correlation was found between Beck’s score and TSH levels in depressed PMW. Conclusion: Taken together, these data demonstrated that comorbidity of recurrent depressive disorder with Thyroid dysfunction and lipid metabolism abnormality in post-menopausal women is common and needs clinical attention.
1. Alexopoulas G S, Kalz I R, Reynolds C F III, Carpenter D, Doherthy J P. The expert consensus guideline series: Pharmacotherapy of depressive disorders in older patients. Post graduate medicine special report.2001
2. Anderson E, Hamburger S, Liu J H, Rebar R W. Characteristics of menopausal women seeking assistance. Am J ObstetGynecol 1987; 156: 428-33.
3. Archer J S. Relationship between estrogen, serotonin and recurrent depressive disorder. Menopause .1999; 6: 71-8.
4. Artt W.Androgen therapy in women .Eur J Endocrinol. 2006; 154:1-11.
5. Beck AT, Rial WY, Rickets K. Short form of recurrent depressive disorder inventory: cross validation. Psychol Rep.1974; 34(3):1184-6.
6. Beck, AT, Steer RA. Internal consistencies of the original and revised Beck Recurrent depressive disorder Inventory. J ClinPsychol 1984; 40(6):1365-7.
7. Beck, Ward, Mendelson, Mock and Erbaugh. An inventory for necologic care.1961; 4th ed., St. Louis:Mosby.
8. Beck, Ward, Mendelson, Mock, Erbaugh .An inventory for measuring recurrent depressive disorder. Arch Gen Psychiat 1961; 4: 561-571.
9. Bobak, IM, Jensen MD, Zalar MK. Maternity and gynecologic care 1990; 4th ed., St Louis: Mosby.
10. Bromberger, JT, Matthes KA, Schott LL. Depressive symptoms during the menopausal transition: the study of women’s health across the nation (SWAN). J Affect Disord 2007; 103: 267-72.
11. Brown, ES, Varghese, FP and McEwen, BS. Association of depression with medical illness: does cortisol play a role? Biological Psychiatry. 2004; Vol 55: 1; 1-9.
12. BuccoloG .Quantitative determination of serum triglyceride by use of enzymes. ClinChem 1973; 19(5):476-482.
13. Burger HG, Dudley EC, Robertson DM and Dennerstein L. Hormonal changes in the menopause transition. Recent Prog Horm Res. 2002; 57:257–75.
14. Burt VK and Stein K. Epidemiology of depression throughout the female life cycle. J Clin Psychiatry.2002; 63 (Suppl 7) : 9-15
15. Canaris G J, Manowitz N R and Major G. The Colorado thyroid disease prevalence study. Arch Intern Med. 2000; 160: 526 -34.
16. Chang ER. A study on factors that affect ego-identity and recurrent depressive disorder of middle-aged women. Masters thesis. 2000: Seoul Theological University, Seoul.
17. Chedraui P, Hidalgo L, Chanez D, Morocho N, Alvarado M and Huc A. Menopausal symptoms and associated risk factors among PMW screened for the metabolic syndrome. Arch Gynecol Obstet.2007;275:161-168
18. ChienChih C, Tiao Lai H. Association of serum Lipid Profiles with Depressive and Anxiety Disorders in Menopausal Women. Chang Gung Med J 2006; 29: 325-30.
19. Chowta N K, Sabastian J and Chowta M N. Comparative study of menopausal symptoms in postmenopausal and Perimenopausal women. Journal of Clinical and Diagnostic Research. 2008 Aug; (2): 959-962.
20. Das P P, Malhotra S, Chakrabarti S and Sharma S. Elevated total cholesterol in severly depressed patients: Role in cardiovascular risk? World J Biol Psychiatry. 2009.
21. De Kleijn MJ, VanderSchouw YT, Banga JD, Vander GY. The effect of menopause on risk factors for ischemic diseases. Ned TijdschrGeneeskd 1996; 140: 478–482.
22. Dennerstein L, Lehert P, Burger H G and Guthrie J R. New findings from non- linear longitudinal modelling of menopausal hormone changes. Hum Reprod Update. 2007.
23. Ellen WF, Mary DS, HuiL, Deborah BN. Association of hormones and menopausal status with depressed mood in women with no history of recurrent depressive disorder. Arch Gen Psychiatry 2006; 63 (4): 375-382.
24. Engelberg H. Low serum cholesterol and suicide. Lancet 1992; 339: 727-9.
25. Freedman M A.Quality of life and menopause: The role of estrogen. J Women Health .2002; 11:703-18.
26. Gibbs Z, Lee S, Kulkarni, J. Factors associated with depression during menopausal transition. Women’s Health Issues. 2013 Sep-Oct; 23(5):e301-7. doi: 10.1016/j.whi.2013.07.001
27. Gupta S, Saha P K and Mukhopadhyay A. Prevalance of hypothyroidism and importance of cholesterol estimation in patients suffering from major depressive disorder. J Indian Med Assoc. 2008; 106 : 240-2
28. Hadine J, Claudio NS, Lee SC. Assessment and treatment of hot flushes and menopausal mood disturbance. PsychiatrClin N Am 2003; 26: 563-580.
29. Holland WW, Detels R, Knox G, Fitxsimons B, Gardner L. Oxford textbook of public health. 1991; 2nded, Oxford university press, 170-172.
30. Huang TL. Serum Lipid profiles in major recurrent depressive disorder with clinical subtypes, suicide attempts and episodes. J Affect Disord 2005; 86: 75-9.
31. Karen AM, Elaine M, Lewis HK, Sheryl FK, Arlene WC, Rne RW. Menopause and Risk Factors for Coronary Heart Disease. N Engl J Med 1989; 321(7): 641-646.
32. Kessler RC, McGonagle KA, Zhao S, Nelson CB, Hughes M, Eshleman S, Wittchen HU, Kendler KS. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States. Results from the National Comorbidity Survey. Arch Gen Psychiatry 1994; 51: 8-19.
33. Kim SS. The associated factors with the recurrent depressive disorder of middle-aged women living in a city. Unpublished doctoral dissertation.2000; Chosun University, Kwangju.
34. Kwon SH, Kim YJ, Moon KN, Kim IS, Park KJ, Park CW, Bae JE, Song AR, Yeo JH, Jung ES, Jung HM. The climacteric symptoms and recurrent depressive disorder in middle-aged women. Korean J Women Health Nurs 1995; 2(2): 235-243.
35. Lee Y W. Recurrent depressive disorder in postmenopausal women. TaihanKanhoHakhoe Chi 2003; 33(4):471-477.
36. Lepine JP, Bouchez S. Epidemiology of recurrent depressive disorder in the elderly. IntClinPsychopharmacol 1998; 13: S7 – S12.
37. Lindberg G, Larsson G, Setterlind S, Rastam L. Serum lipids and mood in working men and women in Sweden. J EpidemiolCommun Health 1994; 48: 360-3.
38. Maes M, Smith R, Christophe A, Vandoolarghe E, Vangastle A, Neels H, Demendts P, Wauters A, Meltz HY. Lower serum high density lipoprotein cholesterol (HDL-C) in major recurrent depressive disorder and in depressed men with serious suicidal attempts: relationship with immune inflammatory markers. ActaPsychiatrica Scandinavia 1997; 95(3): 212-221.
39. Markovitz J H, Smith D, Raczynski J M, Oberman A, Williams O D, Knox S, Jacobs DR . Lack of relations of hostility, negative affect, and high-risk behavior with low plasma lipid levels in the Coronary Artery Risk Development in Young Adults Study. Arch Intern Med. 1997; 157: 1953-9.
40. McCallum J, Simons L, Simons J, Friedlander Y. Low serum cholesterol is not associated with recurrent depressive disorder in the elderly: data from an Australian community study. Aust NZ J Med. 1994; 26:561-4.
41. Milan M T, Jelena D, Sanja M, Tihomir M and Bratislava T. Influence of red clover-derived isoflavones on serum lipid profile in postmenopausal women. JObstetGynaecolRes.Dec 2009; 35(6):1091-1095.
42. Mudali S, Dobs AS, Ding J, Jingzhong D, Cauley JA, Moyses S and Golden SH. Endogenous postmenopausal hormones and serum lipids: the Atherosclerosis Risk in Communities Study. Journal of Clinical Endocrinology and Metabolism. 2005; 90: 1202–1209.
43. Naito H K: Cholestrol. Clin Chem.1984; 1194-11206.
44. Naito H K: HDL Cholestrol.Clin Chem.1984; 1207-1213.
45. Olusi S O, Fido A A. Serum Lipid Concentration in patients with major depressive disorder. Biol Psychiatry. 1996; 40:1128-31.
46. Ossewaarde ME, Bots ML, van der Schouw YT, Thijssen JHH, Westerveld T, de Jong FH and Grobbee DE. Plasma and urinary sex hormones are differently related to lipids in healthy postmenopausal women. Maturitas. 2003; 44: 181–187
47. Papakostas GI, Petersen T, Sonawalla SB, Merens W, Iosifescu DV, Alpert JE, Fawa M and Nerenberg AA. Serum cholesterol in treatment – resistant depression. Neuropsychobiology. 2003; 47(3): 146 – 51.
48. Parry B L, Meliska C J, Martinez L F, Basavaraj N and Zirpoli G G. Menopause: neuroendocrine changes and hormone replacement therapy. J Am Med Womens Assoc. 2004 Spring; 59(2): 135-45.
49. Paterson ME, Sturdee DW, Moore B and Whitehead TP. The effect of menopausal status and sequential mestranol and norethisterone on serum cholesterol, triglyceride and electrophoretic lipoprotein patterns. Br J Obstet Gynaecol. 1979 Oct; 86(10): 810-5.
50. Schindler TH, Campisi R, Dorsey D, Prior JO, Olschewski M, Sayre J, Schelbert HR. Effect of hormone replacement therapy on vasomotor function of the coronary microcirculation in post-menopausal women with medically treated cardiovascular risk factors. Eur Heart J. 2009 Apr; 30(8):978-86. Doi: 10.1093/eurheartj/ehp013. Epub 2009 Feb 26
51. Shin M H. A study on the relationship between the climacteric symptoms and recurrent depressive disorder in menopausal women who have received hormonal replacement therapy. Master thesis.2001; Soonchunhyang University, Onyang.
52. Stevenson J C, Crook D, Godsland I F. Influence of age and menopause on serum lipids and lipoproteins in healthy women. Atherosclerosis. 1993; 98:83-90.
53. Stevenson J C, David C and Ian F G. Influence of age and menopause on serum lipids and lipoproteins in healthy women. Atherosclerosis.1993; 98(1): 83-90.
54. Sung, M H. An analysis of the relationship between climacteric symptoms and recurrent depressive disorder of middle-aged women. Korean J Women Health Nurs.2000; 6(4): 465-476.
55. Soares C N. Newyork, Arlington, V A: American Phycriatic Publishing; 2004. Perimenopause related mood disturbance: An update on risk factors and novel treatment strategies available. In: meeting programs and abstracts. Psychopharmacology and reproductive transitions symposium. American psychiatric association 157th annual meeting; May 1-6, 2004; pp51-61
56. Wood N F and Mitchell E S. Patterns of depressed mood in midlife women: Observation from the Seattle midlife women’s health study. Res Nurs Health. 1996; 19: 111-123.
Incidence, risk factors and microbiological profile of Surgical Site Infections in cardiac surgery patients
Objective: To find out the incidence of surgical site infections(SSI) in cardiac surgery patients, the organisms responsible and the risk factors associated with such infections. Materials and methods: The study is conducted in 1000 consecutive adult patients who underwent cardiac surgeries between January 2011 and August 2015 in a cardiac surgical department attached to a teaching hospital in Central Kerala, India. Results: SSIs were diagnosed in 1.8% of the patients (18 of 1,000). Of these, 15 were superficial wound infections and three were mediastinitis and all got cured with conservative management without any mortality. Culture was positive in 13 cases and the most commonly isolated pathogen was Staphylococcus spp. Though age > 60 years and male sex predisposed to SSIs, these were not statistically significant. 13 of our 18 SSI patients were diabetics. Conclusion: The incidence of surgical site infections in this centre is comparable with other studies from India as well as abroad which range from 0.53% to 18.7% [1, 2, 3, 4].
1. Jonathan T Tan, Kristina Coleman, Sarah Norris, Jayashree Mapari, Satyanand Shastri, Laurent Metz. Surgical-site infection in India: A systematic review of the incidence and economic burden .htanalysts, www. htanalysts.com
2. Sanjeev Singh, Murali Chakravarthy, Victor Daniel Rosenthal, Sheila N. Myatrad, Arpita Dwivedy et al. Surgical site infection rates in 6 cities of India: findings of the
International Nosocomial Infection Control Consortium (INICC). International Health :
doi:10.1093/inthealth/ihu089
3. Lepelletier D, Perron S, Bizouarn P, Caillon J, Drugeon H, Michaud JL, Duveau D. Surgical-site infection after cardiac surgery: incidence, microbiology, and risk factors. Infect Control Hosp Epidemiol. 2005 May; 26(5):466-72.
4. Manoj Kumar Sahu, Bharat Siddharth, Arin Choudhury, Sreenivas Vishnubhatla, Sarvesh Pal Singh, Ramesh Menon, Poonam Malhotra Kapoor, Sachin Talwar, Shiv Choudhary, Balram Airan. Incidence, microbiological profile of nosocomial infections, and their antibiotic resistance patterns in a high volume Cardiac Surgical Intensive Care Unit Year: Annals of Cardiac Anaesthesia .2016 ; 19 (2): 281-287
5. Ahmed Abdulaziz Abuzaid1, Mahmood Zaki2, Habib Al Tarief Potential risk factors for surgical site infection after isolated coronary artery bypass grafting in a Bahrain Cardiac Centre: A retrospective, case-controlled study . Heart Views. 2015; 16 ( 3) : 79-84.
6. Heilmann C, Stahl R, Schneider C, Sukhodolya T, Siepe M, Olschewski M, et al. Wound complications after median sternotomy: A single-centre study. Interact Cardiovasc Thorac Surg 2013;16: 643-8.
7. Itagaki S, Cavallaro P, Adams DH, Chikwe J. Bilateral internal mammary artery grafts, mortality and morbidity: An analysis of 1 526 360 coronary bypass operations. Heart 2013;99:849-53
8. Parissis H, Al-Alao B, Soo A, Orr D, Young V. Risk analysis and outcome of mediastinal wound and deep mediastinal wound infections with specific emphasis to omental transposition. J Cardiothorac Surg 2011;6:111
9. Jonkers D, Elenbaas T, Terporten P, Nieman F, Stobberingh E. Prevalence of 90-days postoperative wound infections after cardiac surgery. Eur J Cardiothorac Surg 2003;23: 97–102.CrossRef,PubMed,Web of Science® Times Cited:
10. Sharma M, Berriel-Cass D, Baran J Jr. Sternal surgical-site infection following coronary artery bypass graft: prevalence, microbiology, and complications during a 42-month period. Infect Control Hosp Epidemiol 2004;25: 468–71.CrossRef,PubMed,Web of Science® Times Cited: 20
11. Tegnell A, Aren C, Ohman L. Coagulase-negative staphylococci and sternal infections after cardiac operation. Ann Thorac Surg 2000;69: 1104–9.
12. Gårdlund B, Bitkover CY, Vaage J. Postoperative mediastinitis in cardiac surgery –
microbiology and pathogenesis. Eur J Cardiothorac Surg 2002;21: 825–30.
13. Quenia Cristina Gonçalves da Silva; Maria Helena Barbosa .Risk factors for surgical site infection in cardiac surgery. Acta Paulista de Enfermagem On-line version ISSN 1982-0194 Acta paul. enferm.vol.25 no.spe2 São Paulo 2012 http://dx.doi.org/10.1590/S0103 21002012000900014
14. Filsoufi F, Castillo JG, Rahmanian PB, Broumand SR, Silvay G, Carpentier A, et al Epidemiology of deep sternal wound infection in cardiac surgery. J Cardiothoracic Vasc Anesth. 2009; 23(4):488-94.
15. Ennker IC, Malkoc A, Pietrowski D, Vogt PM, Ennker J, Albert A. The concept of
negative pressure wound therapy (NPWT) after poststernotomy mediastinitis – a single
center experience with 54 patients. J Cardiothorac Surg. 2009; 4:5.
16. Risnes I, Abdelnoor M, Almdahl SM, Svennevig JL. Mediastinitis after coronary artery bypass grafting risk factors and long-term survival. Ann Thorac Surg. 2010; 89(5):1502-9
17. Ahmed D, Cheema FH, Ahmed YI, Schaefle KJ, Azam SI, Sami SA, et al Incidence and predictors of infection in patients undergoing primary isolated coronary artery bypass grafting: a report from a tertiary care hospital in a developing country. J Cardiovasc Surg (Torino). 2011; 52 (1):99-104.
18. Talbot TR. Diabetes mellitus and cardiothoracic surgical site infections. Am J Infect Control 2005;33:353
19. Robinson PJ, Billah B, Leder K, Reid CM, ASCTS Database Committee. Factors
associated with deep sternal wound infection and haemorrhage following cardiac surgery in Victoria. Interact Cardiovasc Thorac Surg 2007;6:167-71.
20. Filsoufi F, Castillo JG, Rahmanian PB, Broumand SR, Silvay G, Carpentier A, et al. Epidemiology of deep sternal wound infection in cardiac surgery. J Cardiothorac Vasc Anesth 2009;23:488-94.
21. Mangram AJ, Horan TC, Pearson ML, Silver LC, Jarvis WR. Guideline for prevention of surgical site infection, 1999. Hospital Infection Control Practices Advisory Committee. Infect Control Hosp Epidemiol. 1999; 20(4):247-78.
Issue details
Study of dental caries in primary school children of rural area
Arun Bansode, Sayyad Tajmul, N S Inamdar
Dental health diseases such as dental caries are among the most widespread diseases in the world. Dental caries will eventually lead to pain and tooth loss if untreated. The present study was carried out to find prevalence of dental caries and its relationship with some epidemiological factors. The present study was cross sectional study which included 916 school children from 3 villages. Prevalence of dental caries in the present study was 48.14%. Higher prevalence of dental caries was associated with low education status of mother, consuming sweet articles in between meals, cleaning teeth once daily or occasionally. Due to high prevalence of dental caries in school children, health care system should ensure periodic dental health checkup and early detection and promt treatment of dental caries
1. Report of WHO expert committee Technical report series 1984 2. World health organization day 7th april 1994 Oral health for healthy life information material no WHO 94. 3. World health organization: oral health surveys, basic methods 4th edition 1997, Geneva PP 1-55. 4. Mathur HN Jain TP and Jain ML. Dental caries in school girls Indian Journal of paediatrics Vol. 46 No. 373 P 43-48 5. Singh D.K. Prevalence of dental caries in school going children of Patna: Journal of Indian dental association Vol. 53 No.3 1981 PP 267 6. Jawadekar SJ etal: Epidemiological approach to dental caries the Indian practitioner Vol.39 No12 1986 PP 1037-1041 7. Gill PS, Prasad BJ Dental health suveys of primary school children in rural area of Lukhnow, Journal of Indian dental association vol.40 no. 91968 PP 227-283 8. Bajaj M, Blah BC Hoyam metal: Prevalence of dental problems in school children – a study in rural community in Haryana Indain journal of community medicine vol.14 no 3 1989 PP 30. 9. Gupta P. Indurkar M. oral cleaning habits of school children Journal of Indian dental association vol 67 no.3 1996 pp 88-89. 10. Jalili VP, Neema HC. Dental awareness in school going children. Journal of Indian dental association vol 58 no 11 1988 pp 451- 455.
A clinicopathological study of colorectal carcinomas
Farzana T
Objectives: To study the clinicopathological correlation of colorectal carcinoma and its histopathological typing. Materials and Methods: Retrospective study of one year duration from Jan 2013-Dec 2013 was done in Yenepoya Medical College Hospital, Mangalore. Hematoxylin and eosin stained slides were retrieved from pathology archives and light microscopic diagnosis and typing was done according to the WHO classification. Correlation was done with the clinical findings obtained from clinical records. Histochemistry and immunohistochemistry were done wherever indicated. Results: There were a total of 24 cases of colorectal cancer, majority being adenocarcinomas (87.5%), with age range of 26 to 75 years and almost equal sex ratio. One case was associated with familial adenomatous polyposis coli (FAP). Majority were well differentiated (66.6%) followed by moderately differentiated (28.6%) and poorly differentiated type(4.8%) About 67% of adenocarcinomas occurred in the rectum followed by rectosigmoid junction (17%) and sigmoid colon(8%). Other three rare tumours (12.5%) were neuroendocrine tumour of transverse colon, leiomyosarcoma and mixed adenocarcinoma and neuroendocrine tumour. Conclusion: The diagnosis and management of colorectal carcinomas require a team perspective. The pathological assessment of colorectal carcinoma is of critical importance to know the type and extent of tumour, grade and stage, and important prognostic factors, which are of crucial value in patient treatment and predicting the prognosis.
1. Ferlay J, Soerjomataram I, Ervik M, Dikshit R, Eser S, Mathers C, Rebelo M, Parkin DM, Forman D, Bray, F.GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 11 [Internet].Lyon, France: International Agency for Research on Cancer; 2013. 2. Nooyi SC, Murthy NS, Shivananjaiah S, Sreekantaiah P, Mathew A. Trends in rectal cancer incidence-- Indian scenario. Asian Pac J Cancer Prev. 2011; 12(8):2001-6. 3. Pathology and Genetics of Tumours of the Digestive System. In WHO Classification of Tumors. Hamilton.SR, Aaltonen.LA, eds. IARC Press Lyon 2000 ,103-143. 4. Mohan H. The gastrointestinal l tract. In :Mohan H, Mohan P, Mohan T, eds.Text book of Pathology. New Delhi: Jaypee Brothers Medical Publishres (P) Ltd, 2005, 601-605. 5. Guraya YS, Eltinay OE .Higher prevalence in young population and rightward shift of colorectal carcinoma. Saudi Med J2006;27(9):1391-1393. 6. Aljebreen AM. Clinicopathological patterns of colorecral cancer in Saudi Arabia:Younger with an Advaced stage presentation. The Saudi journal of gastroenterology 2007;13(2):84-7. 7. Shen SS, Haupt BX, Ro JY, Zhu J, Bailey HR, Schwartz MR. Number of lymphnodes examined and associated clinicopathological factors in colorectal carcinoma 2009;133(5):781-6. 8. Yeh C Y, Chen HH, Tang R, Tasi WS, Lin PY, Wang JY. Surgical outcome after curative resection of rectal leiomyosarcoma. Dis Colon Rectum 2000; 43(11):1517-21.
Head and neck cancer in Bihar
Rajat Rohan, Damandeep Kaur Mundi, Arup Sengupta
Head and neck cancer in Bihar has distinct demographic profiles, risk factor, food habits and personal family history. The term head and neck cancer refers to a group of biological similar cancers originating from the upper aerodigestive tract, including lip, oral cavity, nasal cavity, paranasal sinuses, pharynx and larynx. Head and neck cancers can cause varying degree of structural deformities and functional handicaps, depending on site, size and patterns of spread, thereby compromising well being and self esteem.
1. Mishra A, Singh VP, Verma V. Environmental effects on head and neck cancer India. J Coin Oncon 2009:27 2. Sankarnarayan R, Masuyer E, Swaminatam R, Ferlay J, Whelan S head and neck cancer: A global perspective on epidemiology and and prognosis. Anticancer Res 1998;18:4779-86 3. Sanghvi LD, Rao DN, Joshi S epidemiology of head andneck cancer. Semin sung oncol 1989;5:305-9 4. Chaturvedi P.Head and neck surgery. J can Res Ther 2009; 5:143. 5. Applebaum KM, Furniss CS, Zeka A, Posner MR, Smith JF, Bryan J, et al. Lack of association of alcohol and tobaco with HPV16-associated head and neck cancer. J Natl cancer inst 2007;99(23):1801-10 6. Reuter CW, Morgan MA, Eckardt A. Targeting EGF-receptor-signalling in squamous cell carcinoma of the head and neck. Be J cancer 2007; 96:408-16. 7. Chaukar DA, Das AK, Deshpande MS, Pak PS, et al. Quality of life of head and neck cancer patient: Validation of the European organization for research and treatment of cancer QLQ-C30 and European organization for research and treatment of cancer QLQ-HandN35 in Indian J cancer 2005 Oct-Dec;42(4):178-84.
Study of nutritional status of primary school children in an urban field practice area of Pune
Sayyad Tajmul, Arun Bansode, Akshay Salgar, N S Inamdar
Childhood years constitutes the most crucial period in life, when the foundations are laid for cognitive, social and emotional language, physical and motor development and cumulative lifelong learning. The young child is most vulnerable to the vicious cycles of malnutrition, infection and resultant disability all of which influence the present condition of a child at micro level and the future human resource development of the nation at the macro level. The present study was a cross sectional study which was carried out in two randomly selected municipal schools of an urban area. The Study consisted of 400 school children from 6 - 9 yrs age group, in which 75 (18.75%) children were found to be stunted and 114 (28.5%) children were underweight. Prevalence of Malnutrition in the form of stunting, and underweight significantly associated with socioeconomic status, educational status of mother, type of family and high birth order. Health education, personal hygiene education, nutrition education may be made as part of the school curriculum.
1. Introduction. Nutrition and physical performance in school age children, Nutrition Foundation of India, New Delhi; July 2009. 2. The state of food insecurity in the world – 2012 Available from: URL: http: //www.fao.org/docrep/016/i3027e/i3027e.pdf‎. 3. Saluja N. et al.Nutritional Status of urban primary school children in Meerut. The Internet Journal of Epidemiology. 2010; 8 (1). 4. Nutrition. (cited on 30th sept.2013). Available from: URL: http:// www.unicef.org/india/children. 5. Registrar General of India: Population Projections. Available from: URL: http://www.censusindia.net/Projection_Report.pdf. 6. Government of India. Ministry of Labour. Index no. page. Available from: URL http://www.labourbureau.nic.in 7. Park K. Socioeconomic status scale. Textbook of Preventive and Social Medicine. 22nd ed. Jabalpur: Banarsidas Bhanot; 2013. P.640, 641. 8. Training course on child growth assessment: WHO child growth standards, A- introduction:8 [cited 2013 Nov 22]; Available from: URL: http://whqlibdoc.who.int/publications/2008/9789241595070_A_eng.pdf 9. WHO Child Growth Standards Length/height-for-age, weight-for-age, weight-for-length, weight-for-height and body mass index-for-age Methods and development. Available from: URL: http://www.who.int/childgrowth/publications/technical_report_pub/en/index.html 10. Training course on child growth assessment: WHO child growth standards, A-introduction: 9 [cited on 2013 NOV 4]; Available from: URL: http://whqlibdoc.who.int/publications/2008/9789241595070_A_eng.pdf 11. WHO Growth Reference Data for 5 -19 yrs. Length/height-for-age, weight-for- age, weight-for-length, weight-for-height and body mass index-for-age. Available from URL: http:// www.who.int/growthref/‎ 12. Maj Mukherjee R, Lt Col Chaturvedi S, Col Bhalwar R. Determinants of Nutritional Status of School Children. MJAFI 2008; 64: 227-231. 13. Dr. Renubala Sharma and Dr. Mukta Trivedi. A Study of Nutritional Status of Children of Sagar City (M.p.). Sociology. June 2013; 2(6). 14. Sunil Pal Singh C. Ravi Babu D. Nutritional status of primary school children in urban area of Hyderabad, Andhra Pradesh, India. Journal of community nutrition and Health. 2013; 2(1): 36-39 15. Das P, Basu M, Dhar G, et al. Nutritional status and morbidity pattern of government primary school children in north Kolkata of West Bengal, India. South East Asia Journal of Public Health. 2012; 2(1):13-17. 16. Chandna S. and Salll Sehgal. Prevalence of Deficiency Diseases among school Children. Health arid Population- Perspectives and Issues. 1994; 17(1and2): 108 -113. 17. Shakya SR, Bhandary S, Pokharel PK. Nutritional status and morbidity pattern among governmental primary school children in the Eastern Nepal Kathmandu University Medical Journal. 2004; 2(8): 307-314.
A cross sectional study on iodized salt usage at household level in Ulagankulam Panchayat of Tirunelveli district Tamil Nadu
P Getrude Banumathi, D Jaiganesh, P Parameshwari, R Dharani Sri, P Ravishankar
Background: Iodine deficiency disorders (IDD) still remains a major public health problems in many countries including India. Thus the Iodised salt is most economical, convenient and effective means of mass prophylaxis against Iodine Deficiency Disorders. Objectives: To estimate the prevalence of iodized salt usage at household level and to find out the iodine content of edible salt with MBI spot testing kit among women at household level in Ulagankulam panchayat of Tirunelveli. Materials and Methods: A community based cross sectional study among 306 women in households of Ulagankulam Panchayat, Thirunelveli District. A standardized, semi-structured questionnaire was applied to the women household who is in charge of kitchen to estimate the usage regarding iodized salt. Cooking salt was tested with MBI Spot testing kit for iodine content. Iodine content ≥ 15ppm was considered as adequately iodised salt. Appropriate statistical tests used and analysis done using SPSS 18 software. Results: Among the 306 salt samples tested, 123 (40.2%) were using adequately iodized salt (> 15ppm), 66 (21.6%) – inadequate iodized salt, 117 (38.2) – uniodized salt. 135 (44.1%) were buying salt from street vendors, 102 (33.3%) from nearby petty shops, 66 (21.6%) from General provisional store and 3 (1%) from Public distribution system (PDS). 54 (52.9%) and 54 (78.3%) of salt samples from nearby Petty shops and General provisional store were adequately iodized. Conclusion and recommendation: Based on this study, only 40.2% were using adequately iodised salt. This is well below the WHO recommended level (90%). Iodized salt should be manufactured in small pockets and made available at low cost even in petty shops and public distribution systems of rural areas and legal measures to ban crystallized non iodized salt to be strengthened. Increased awareness and frequent inspection by health staffs to be done.
1. J.kishore, National health programes of India 9th edition page number 2. Govt of india annual report 1997-1999, Ministry of health and family welfare 3. De Benoist B, McLean E, Andersson M, Rogers L. Iodine deficiency in 2007: global progress since 2003. Food Nutr Bull 2008; 29 : 195-202. 4. "Citizen Charter" National Iodine deficiency disorder control program and nutrition. Available from: http://www.negahealth.nic.in. 5. WHO/UNICEF/ICCIDD.Indicators for assessing iodine deficiency disorders and their control through salt iodization. Geneva, World Health Organization, 1994: 29–31. 6. Sundar lal et al. Textbook of community medicine.1st edition;p 180-181 7. Salt Department, Ministry of Industry. Universal Salt Iodisation (USI) – India: progress and current status. New Delhi, 1996: 8. 8. Chandrakant S. Pandav, Narendra K. Arora, Anand Krishnan, Rajan Sankar, Smita Pandav & and Madhu G. Karmarkar. Validation of spot-testing kits to determine iodine content in salt. Bulletin of the World Health Organization, 2000; 78(8):975-80. 9. Summary report iodized salt coverage study 2010 conducted across eight states in India 10. Unicef an assessment of the household use and adequacy of iodized salt in the republic of kazakhstan аlmaty, 2005.
A study of rhinolith as detected by CT scan paranasal air sinuses at tertiary health care centre
Anil G Joshi
Introduction: Rhinoliths are calcareous concretions around calcinated intranasal foreign bodies within the nasal cavity. They are commonly seen in the anterior part of the nasal cavity. The incidence of adult rhinolith is very low. Rhinoliths are generally single, exogenous or endogenous, unilateral, and asymptomatic. Aims and Objectives: To Study Rhinolith as Detected by CT Scan Paranasal Air Sinuses at tertiary health care center. Methodology: It was a retrospective study of 2860 CT scans of paranasal sinuses during the period of June 2013 to August 2015 was done to detect Rhinoliths. The observations of CT scan were made and the results were statistically analyzed. Result: The majority of the Patients were from 30-40 age group i.e. 50.00% followed by 20-30-33.33% and 40+- 16.67%. Majority of the Patients were Female i.e. 66.67% followed by Male 33.33%. Conclusion: Rhinoliths are quite rare cases of the nose, which may show clinical and radiological similarities with each other and benign and malignant diseases of the region so in the nose diseases clinical suspicion of a rhinolith should always be considered, in order to lead to the right diagnosis
1. Orhan K, Kocyigit D, Kisnisci R. Rhinolithiasis: An uncommon entity of the nasal cavity. Oral Surg Oral Med Oral Pathol Oral RadiolEndod 2006; 101:e28-32. 2. Carder HM, Hiel JJ (1966) Asymptomaticrhinolith: a brief review of the literature and case report. Laryngoscope 76: 524-530. 3. Varley EWB (1964) Rhinolith: an incidental finding. Br J Oral Surg 2: 40-43. 4. Dib GC, Tangerina RP, Abreu CE, Santos RP, Gregorio LC. Rhinolithiasis as a cause of oronasal fistula. Rev Bras Otorhinolaryngol (Eng Ed). 2005; 71:101-103. 5. Celikkanat S, Turgut S, Ozcan I, Balyan FR, Ozdem C (1997) Rhinolithiasis. Rhinology 35:39-40. 6. Polson CJ (1943) Onrhinoliths. J LaryngolOtol 58: 79-116. 7. Orhan K, Kocyigit D, Kisnisci R, Paksoy CS. Rhinolithiasis: an uncommon entity of the nasal cavity. Oral Surg Oral Med Oral Pathol Oral RadiolEndod.2006; 101: 28-32. 8. Mustafa A, Nishori S. Rhinolith caused from the undetected foreign body: A case report. Kosova Journal of Surgery. 2008; 2(1):32-35. 9. Appleton SS, Kimbrough RE, Engstrom HIM (1988) Rhinolithiasis: a review. Oral Surg 65: 693-698. 10. Eliachar I, Schalit M (1970) Rhinolithiasis: report of eight cases. Arch Otolaryngol 91: 88-90. 11. Flood TR (1988) Rhinolith: an unusual cause of palatal perforation. Br J Oral Maxillofacial Surg 26: 486-490. 12. Varley EWB (1964) Rhinolith: an incidental finding. Br J Oral Surg 2: 40-43. 13. Hsiao JC, Tai CF, Lee KWl. Giant rhinolith: A case report. Kaohsiung J Med Sci 2005; 21:582-5. 14. Keck T, Liener K, Strater J, Rozsasi A. Rhinolith of the nasal septum. Int. J Pediatrhinolaryngol 2000; 53; 225-228. 15. Royal SA, Gardner RE. Rhinolithiasis: An unusual pediatric nasal mass. PediatrRediol 1998; 28:54-55. 16. Carder HM, Hiel JJ (1966) Asymptomaticrhinolith: a brief review of the literature and case report. Laryngoscope 76: 524-530
Study of comparison of yield of bronchial brushing and broncho-alveolar lavage in diagnosis of lung cancer
Vijaykumar R Kapse, Dilip G Mhaisekar, Dattatray Totewad, Mithilesh Kulkarni
Flexible fiber-optic bronchoscope revolutionized respiratory cytology, as techniques like bronchial brushings, broncho-alveolar lavage and bronchial biopsy became more easy, accessible and popular, shifting the emphasis from diagnosis of advanced malignancy in operable patients to the use of cytology as a first line diagnostic and management tool. Objective: To compare the yield of bronchial brushing and bronchoalveolar lavage cytology in lung cancer. Methodology: the present study was carried out at dr. S.C.G.M.C. Nanded, Maharashtra. In patients having lung cancer, bronchoscopy done and bal, bronchial brushing and endobronchial biopsy samples were collected. Comparison of yield of bronchial brushing and bronchoalveolar lavage cytology was done, in patients, in whome biopsy samples are positive for malignant cells. The statistical test( chi-square test) was applied to test the significance. Results: out of 56 patients bronchial brushing yielded 45 (80.35%) to be malignant as compared to bal cytology which yielded 15(26.78%) to be malignant. the difference in yield by both techniques was found to be statistically significant (p < 0.05). Conclusion: bronchial brushing has better diagnostic yield as compared to broncho Alveolar Lavage cytology in patients having lung cancer.
1. Fishman’s Pulmonary Diseases and Disorders. Fourth Edition. Page No. 630. 2. Prakash UB, Offord KP, Stubbs SE. Bronchoscopy in North America: the ACCP survey. Chest. 1991 Dec; 100(6):1668-75. 3. Rabahi MF, Fereira AA, Reciputti BP, et al. The description of bronchoscopic findings from patients with lung cancer. Am J Respir Crit Care Med. 2012; 185:A5917 4. TG. Manickam, S Rajasekaran and PJ Vasantham. Carcinomatous pulmonary Consolidations.. lnd .J. Tub.1995, 42, 9. 5. Jindal SK, Behera D. Clinical spectrum of primary lung cancer: review of Chandigarh experience of 10 years. Lung India 1990; 8:94-98. 6. Jadish Rawat. Girish Sindhwani, Dushyant Gaur, Ruchi Dua, Sunil Saini. Clinicopathological profile of lung cancer in Uttarakhand. Lung India Vol 26 issue 3juI-sep 2009. 7. DS Gaur, S Kishore, VP Pathak, NC Thapliyal Journal of Cytology, Vol. 24, No. 2, April-June, 2007, pp. 73-77 8. Husain AN. The lung. In: Kumar V, Abbas AK, Fausto N, editors. Robbins and Cotran pathologic basis of disease. 7th ed. India: Saunders; 2004. p. 711-72 9. Johnston WW, Elson CE. Respiratory tract. In: Bibbo M, editor. Comprehensive cytopathology. 2nd ed. Philadelphia: W.B. Saunders Company; 1997. p. 325-401. 10. Truong LD, Underwood RD, Greenberg SD, McLarty JW. Diagnosis and typing of lung carcinomas by cytopathologic methods. A review of 108 cases. Acta Cytol 1985; 29:379-84JAPI. 1985; 33;64-5.
Laryngeal tuberculosis and its outcome
Ashok Purohit, Shashikant Dorkar
Introduction: Tuberculosis is still one of the most common granulomatous diseases of the larynx. In the past, it commonly followed pulmonary tuberculosis. Among the risk factors identified are the consumption of tobacco, alcohol, malnutrition, immunodeficiency and being homeless. Aims and Objectives: To study Laryngeal Tuberculosis and its Outcome. Methodology: This was a hospital based cross- sectional study carried out at tertiary health care Centre with the patients diagnosed as Laryngeal tuberculosis by Otolaryngology department were admitted to ward and managed accordingly medical and necessary surgical management like tracheal dilation and Tracheostomy procedure were performed as per the protocols during the year June 2014 to June 2015 there were 45 patients studied during this time. Tabulations and Percentages used for the Presenting the Data. Result: We have found that the majority of the Patients were from >50- 35.55% followed by 40-50-20.00%, 30-40-15.55%, 20-30-13.33%, 10-20-8.88%, 1-10- 6.66%. Majority of the patients were Male 75.55% and Female 24.45%.The majority of the Patients presented with Stridor-35.55% followed by Dysphonia -17.77%. Dysphagia and odynophagia -15.55%, Throat pain -13.33%, Otalgia-8.88%, Fever-8.88%.The Majority of the Patients improved i.e. of 77.78% and 17.77% referred to Higher Centre for the further surgical management and prosthetic surgeries and Death occurred in 2 patient i.e. 4.44% mortality the reasons for the death was severe stridor. Conclusion: The majority of the Patients presented with complaining of Stridorfollowed by Dysphonia, Dysphagia and odynophagia, Throat pain, Otalgia, Fever. The Majority of the Patients improved i.e. of 77.78% and 4.44% mortality found in our study the reasons for mortality was severe stridor.
1. Bailey CM, Windle-Taylor PC. Tuberculous laryngitis: a series of 37 patients, Laryngoscope1981; 91:93-100. 2. Levenson MJ. Laryngeal tuberculosis: review of twenty cases, Laryngoscope 1984; 94:1094-1097. 3. Ramandan HH, Tarayi AE, Baroudy FM. Laryngeal tuberculosis: presentation of 16 cases and review of the literature, J Otolaryngol 1993; 22:39-42. 4. Thaller SR. Laryngeal tuberculosis as manifested in the decades 1963–1983, Laryngoscope 1987; 97:848-850. 5. Soda A. Tuberculosis of the larynx: clinical aspects in 19 patients, Laryngoscope 1989; 99:1147-1150. 6. Shin JE, Nam SY, Yoo SJ, Kim SY. Changing trends in clinical manifestations of laryngeal tuberculosis. Laryngoscope 2000; 110:1950-1953. 7. Lin CJ, Kang BH, Wang HW.Laryngeal tuberculosis masquerading as carcinoma.Eur Arch Otorhinolaryngol 2002; 259:521-523. 8. Tuberculosis. In: Benenson AS, ed. Control of communicable diseases manual. 15th ed. Washington, D.C.: American Public Health Association, 1990; 459. 9. Riley EC, Amundson DE. Laryngeal tuberculosis revisited. AmFamPhys 1992; 46:759-762. 10. Nishiike S, Irifune M, Sawada T, Doi K, Kubo T 11. Ramadan HH, Tarazi AE, Baroudy FM. Laryngeal tuberculosis: presentation of 16 cases and review of the literature. J Otolaryngol 1993; 22:39-41. 12. Horowitz G, Kaslow R, Friedland G. Infectiousness of laryngeal tuberculosis. Am Rev Respir Dis 1976; 114:241-244. 13. Soda A, Rubio H, Salazar M, Ganem J, Berlanga D, Sanchez A. Tuberculosis of the larynx: clinical aspects in 19 patients. Laryngoscope 1989; 99:1147-1150. 14. Diktaban T, Lucente FE. Laryngeal tuberculosis: A hazard to the Otolaryngologist. Ear Nose Throat J 1980; 59:488-494. 15. Hunter AM, Millar JW, Wightman AJA, Horne NW. The changing pattern of laryngeal tuberculosis.J LaryngolOtol 1981; 95:393-398.
Alvarado score and ultrasonographic criteria to diagnose acute appendicitis: A clinical study of 100 cases
Arvind
Acute appendicitis is one of the most common surgical emergencies around the world with a life time prevalence of approximately one in seven. It's incidence is 1.5-1.9/1000 in male and female population. Scoring systems are valuable and valid instruments for discriminating between acute appendicitis and nonspecific pain abdomen. Alvarado scoring is one of them and is purely based on history, clinical examination and few laboratory tests and is very easy to apply. Advent of cross sectional computer based imaging modalities (USG, CT and MRI) in early eighties opened up new methods for diagnosis of acute appendicitis. It was also found that ultrasound was able to establish alternative diagnosis in up to one-third cases of right iliac pain like ureteric colic and gynaecological disorders. Statistical analysis of data in our study gave sensitivity of Alvarado score as 94.9%, specificity 61.9%, positive 90.3% and negative predictive value 76.4% while sensitivity of ultrasonography was 91.9%, specificity 85%, positive 95% and negative predictive value 77.2%.When both modalities were positive for acute appendicitis, no false positive result obtained. So it is concluded that the combination of Alvarado score and ultrasonography increases the sensitivity and specificity for the diagnosis of acute appendicitis.
1. Stephens PL, Mazzucco JJ. Et al. Comparison of ultrasound and the Alvarado score for the diagnosis of acute appendicitis. Conn Med. 1999 mar; 63(3): 137-40. 2. Cuschieri a. The small intestine and vermiform appendix; in: cuschieri A, GR Giles, AR Mossa. (ed). Essential Surgical Practice, 3rded. 3. Fenyo G, Lindberg G, Blind P, Enochsson L, Oberg A. Diagnostic decision support in suspected acute appendicitis, validation of a simplified scoring system. Eur J Surg 1997; 163: 831-8. 4. Pal K M, Khan A. Appendicitis, a continuing challenge. J Pak Med Assoc 1999; 48: 189-92. 5. Kumar V, Cotran RS, Robbins SL. Appendix; in Robbins Basic pathology. 5th ed. London: W.b. Saunders 1992; 520. 6. Barnes, BA. Treatment of appendicitis at the Massachussets General Hospital. 1939-1959. JAMA 1962; 180: 122. 7. Dunn EL, Moore EF, Elerding SC, Murphy JR et al. The unnecessary laparotomy for appendicitis- Can it be decreased? Am. Surg. 1982; 48:320-323. 8. Marshall E. Sonography of appendicitis and diverticulitis. Radiologic clinics of North Am. 1994; 32: (sept). 9. Alvarado A. A practical score for acute appendicitis. Ann Emerg Med. 1986 may; 15(5) 557-64. 10. Z Tarzan and T Winlernitz. Impact of USG visualization of normal and abnormal appendix. BJR 1998; 85:2. 11. H W AOoms, R K J Koumans, P J Ho Kang You and J B C M Puylaert. Ultrasonography in the diagnosis of acute appendicitis. Br. J Surg. 1991; 78: 315-318. 12. Julian BCM, Puylaert acute appendicitis: US evaluation using graded compression. Radiology 1986: 158: 355-360. 13. Campbell JA, Mephail DC. Appendicitis. B.M.J. 1958; I 852. 14. Anderson WAD, Pathology, ED. 4th, The C.V. Mosby and company Japan P. 803-806, 1961. 15. Illingworth CF W and Bick BM. Text book of surgical pathology. J and A Churchill Ltd. 16. Reid MR, Poer DH and Messel P. J Am Med Asso. 1936; 106: 655. 17. Fitz R. et al. Perforating inflammation of the vermiform appendix with specific reference to its early diagnosis and treatment. T.R.A. Am Phys. 1886; 1: 107-44 (cited by Boyce, 1949). 18. Collins DC. Etiological factors in acute appendicitis based upon a study of 100 cases. Surg. 1939; 5: 267-70. 19. Molony GE, Russel WT and Wilson DC. BJS 1950; 38:52-64. 20. Agarwal SK and Nan AK. Appendicectomy, A surgicopathological study of 100 cases. J. Ind. Med. Asso. 1968; 51:59-62. 21. Kazarian KK, Werner J Roeder, Walter L Mercheimer. Decreasing mortality and increasing morbidity in acute appendicitis. B.J.S. 1970; vol. 119: 681-685. 22. Ganesh Roy, Ray SC, Das MM and AK Ghosh. Acute appendicitis, A clinical appraisal of 500 cases. JIMA 1969; 52: 509-513. 23. Chan MY, Ten BS, Ng BL et al. The Alvarado score and acute appendicitis Ann. Acad Med Singapore 2001 Sept; 30(5):510-2. 24. IKramullah Khan, Ata urRehman et al. Application of Alvarado scoring system in diagnosis of acute appendicitis. J Ayub Med CollAbbotabad 2005; 17(3). 25. Ohmann C, Yang Q, Franke C: The abdominal pain study group. Diagnostic scores for acute appendicitis. Eur J Surg 1995; 161: 273-81. 26. Arian GM, Sohu KM, Ahmad E, Haider W, Naqi SA. Role of Alvarado score in diagnosis of acute appendicitis. Pak J Surg 2001; 17: 41-6. 27. Denizbasi, Arzu: Unleur, ErolErden. Et al. The role of emergency medicine residents using the Alvarado score in the diagnosis of acute appendicitis compared with general surgery resident. European journal of emergency medicine 10(4): 296-301 December 2003.
A study of metabolic syndrome in newly diagnosed patients of type 2 diabetes mellitus in the tertiary care centre of Kumaun region
Taukeer Ahmad, Sangeeta Singh, Basant Joshi, Suman Pandey
Introduction: Diabetes mellitus is the commonest metabolic abnormality in the world. Prevalence of type 2 diabetes is especially increasing in developing countries. The metabolic syndrome (Syndrome X) consists of a constellation of metabolic abnormalities that increase the risk of micro and macrovascular complications of type 2 diabetes mellitus. The major features of metabolic syndrome include central obesity, hypertriglyceridemia, low HDL cholesterol, hyperglycaemia, and hypertension. The metabolic dysregulation associated with diabetes mellitus and metabolic syndrome cause secondary pathophysiologic changes in multiple organ system that impose a tremendous burden on the individual with diabetes and on the health care system. Material and Methods: - 100 Patients of age group 20-60 years with newly diagnosed type 2 diabetes mellitus were included in the study. Detailed physical and anthropometric examinations were done in all patients. Estimation of extended lipid profile including Apo B, KFT and microalbuminuria were done. Results: Of the 100 patients studied, 58 patients had metabolic syndrome according to the International Diabetes Federation criteria 2006. 85% of the patients with metabolic syndrome were either overweight or obese (calculated by their body mass index) as compared to 15% of patients without metabolic syndrome. Waist hip ratio was increased in 33% of males with metabolic syndrome and 100% of females with metabolic syndrome. Serum triglyceride (p< 0.009), VLDLc (p< 0.007) and microalbuminuria (p< 0.01) levels were significantly elevated in patients of metabolic syndrome as compared to those without metabolic syndrome. Conclusion: The present study shows that metabolic syndrome is increasingly present in patients with type 2 diabetes mellitus in the Kumaun region of Uttarakhand. Physicians treating type 2 diabetics should consider metabolic syndrome with greater emphasis in their patients and advice early intervention, to delay the development of micro and macrovascular complications of diabetes mellitus.
1. Ramachandran A, Snehalatha C. Type 2 diabetes mellitus-the epidemic of the 21st century, the Indian scenario. Int J. Diab. Dev. Countries 1999; 19: 158-164. 2. American Diabetes Association. (2008). Clinical practice recommenda-tion: Standards of medical care. Diabetes Care, 31. (Suppl. 1), S14. 3. Reaven GM. Role of insulin resistance in human disease. Diabetes. 1988; 37: 1595-607. 4. Reilly MP, Rader DJ. The metabolic syndrome: more than the sum of its parts? Circulation 2003; 108:1546–51. 5. Kylin E: Studienueber das Hypertonie-Hyperglyka†mie-Hyperurika†miesyndrom. ZeufralblattFuerInnereMedizin 1923, 44: 105-127. 6. Ardern CI, Katzmarzyk PT, Janssen I, Ross R. Discrimination of health risk by combined body mass index and waist circumference. Obes Res 2003; 11(1):135-42. 7. Lea Duvnjak et al, Hypertension and the Metabolic Syndrome, DiabetologyCroatica 37-4, 2008. 8. Han TS, Sattar N, Williams K, et al. Prospective study of C-reactive protein in relation to the development of diabetes and metabolic syndrome in the Mexico City Diabetes Study. Diabetes Care. 2002; 25: 2016–2021. 9. Yudkin JS, Forrest RD, Johnson CA. Microalbuminuria as predictor of vascular disease in non‑diabetic subjects. Lancet 1988; 2:530‑3. 10. Malik, VS; Popkin, BM; Bray, GA; Després, JP; Willett, WC; Hu, FB. (2010). "Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis". Diabetes Care 33 (11): 2477–2483. Doi:10. 2337/dc10-1079. PMC 2963518. PMID 20693348. 11. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: finding from the third National Health and Nutrition Examination Survey. JAMA 2002; 287: 356-359. 12. Shinji Tabata, Shinichiro Yoshimitsu(2009): Tadamichi Hamachi Department of Preventive Medicine and Self-Defense Force Fukuoka Hospital, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan. BMC Endocrine Disorders: 1doi. 10. 1186/1472-6823-9-1. 9. 13. Oscar H. M. Franco, Joseph. Massaro, Jacky Civil, R. Mark. Cobain (2009): Form Unilever Corporate Research, Sharnbrook, UK (O. H. F., J. C., M. R. C., B. O. ); University of Warwick, Warwick Medical School, Health Sciences Research Institute, Coventry, UK (O. H. F. ); Department of Mathematics/Statistics and Biostatistics, Boston University, Boston, Mass (J. M. M. ); and the National, Heart, Lung and Blood Institute's Framingham Heart Study, Framingham, Mass ( R. B. D. ). Circulation. ; 120:1943-1950. 14. Bjorntorp P. Fat cell distribution and metabolism. Annals of the New York Academy of Sciences, 1987, 499:66â€72. 15. Seidell JC, Cigolini M, Deslypere JP, Charzewska J, Ellsinger BM, Cruz A. Body fat distribution in relation to physical activity and smoking habits in 38-year old European men: the European Fat Distribution Study. Am J Epidemiol 1991; 133:257-65. 16. Gupta R, Rastogi S, Panwar RB, Soangra MR, Gupta VP, Gupta KD. Major coronary risk factors and coronary heart disease epidemic in India. South Asian J PrevCardiol2003; 7:11-40. 17. Osei K, Rhinesmith S, Gaillard T, Schuster D. Is glycosylated hemoglobin A1c a surrogate for metabolic syndrome in nondiabetic, first-degree relatives of African-American patients with type 2 diabetes? J ClinEndocrinolMetab2003; 88: 4596–4601. 18. Matsuura F, et al. Effect of visceral fat accumulation on uric acid metabolism in male obese subjects: visceral fat obesity is linked more closely to overproduction of uric acid than subcutaneous fat obesity. Metabolism: clinical and experimental. 1998; 47:929–933. [PubMed: 9711987] 19. Sui X, Church TS, Meriwether RA, Lobelo F, Blair SN. Uric acid and the development of metabolic syndrome in women and men. Metabolism: clinical and experimental. 2008; 57:845– 852. [PubMed: 18502269] 20. Kodama S, et al. Association Between Serum Uric Acid and Development of Type 2 Diabetes. Diabetes care. 2009; 32:1737–1742. [PubMed: 19549729] 21. Niskanen LK, Laaksonen DE, Nyyssonen K, Alfthan G, Lakka HM, Lakka TA, Salonen JT: Uric acid level as a risk factor for cardiovascular and all-cause mortality in middle-aged men: a prospective cohort study. Arch Intern Med 2004, 164(14):1546-1551. PubMed HYPERLINK "http://www. nutritionandmetabolism. com/pubmed/15277287" Abstract | Publisher Full Text Return to text 22. Kannel WB, Castelli WP, McNamara PM: The coronary profile: 12-year follow-up in the Framingham study. J Occup Med 1967, 9(12):611-619. PubMed HYPERLINK "http://www. nutritionandmetabolism. com/pubmed/ 6065137" Abstract Return to text 23. Lin CC, Liu CS, Li TC, et al: Microalbuminuria and the metabolic syndrome and its components in the Chinese population. Eur J Clin Invest 2007, 37:783–790. 24. Kundu D, A Roy et ai, Relation of microalbuminuria to glycosylated haemoglobin and duration of type 2 diabetes 2012-22; 700-037. 25. Klausen K. P, Parving H. -H. Et al, The association between metabolic syndrome, microalbuminuria and impaired renal function in the general population: impact on cardiovascular disease and mortality. 2007 journal of Internal Medicine 262; 470-478. 26. Marsh JB. Lipoprotein metabolism in obesity and diabetes: insights from stable isotope kinetic studies in humans. Nutr Rev. 2003; 61:363–375. 27. ValluriSatya Prasad, et al, “The Prevalence of Metabolic Syndrome in Newly Diagnosed Type 2 Diabetes Mellitusâ€. Journal of Evidence based Medicine and Healthcare; Volume 2, 2015; Page:2500-2507. 28. Faraj M, Messier L, Bastard JP, et al. Apolipoprotein B: a predictor of inflammatory status in postmenopausal overweight and obese women. Diabetologia 2006; 49:1637-46. 29. Lim JS, Lee DH, Park JY, Jin SH, Jacobs DR (2011). "Reliability of low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B measurement". Journal of Clinical Lipidology 5 (4): 264–272. doi:10. 1016/j. jacl. 2011. 05. 004. PMID 17478563. 30. Ryoo JH, Park SK. Association of apolipoprotein B and in¬cidence of metabolic syndrome in Korean men: a 5-years’ follow-up study. Atherosclerosis 2013; 226:496-501. 31. Pfützner A, Standl E, Strotmann HJ, et al. Association of high-sensitive C-reactive protein with advanced stage beta-cell dysfunction and insulin resistance in patients with type 2 diabetes mellitus. ClinChem Lab Med 2006; 44(5):556-60. 32. Sattar N, Gaw A, Scherbakova O, et al. Metabolic syndrome with and without C-reactive protein as a predictor of coronary heart disease and diabetes in the West of Scotland Coronary Prevention Study. Circulation. 2003; 108:414–419. 33. Fared F et al. (2011): Waist circumference in metabolic syndrome in the Egyption Population. 2011; 7 (12): 1257-1265. 34. Tamakoshi K, H Yatsuyaet al, metabolic syndrome; C-reactive protein; systemiclow- grade inflammation; obesity; intenational journal of obesity 2002 -27, 443-449. 35. Mendall MA, Patel P, Ballam L, et al. C reactive protein and its relation to cardiovascular risk factors: a population based cross sectional study. BMJ. 1996; 312:1061–1065. 36. Esteghamati et al. (2010): Diabetologyand Metabolic Syndrome. 2010; 2:36. 37. SudhaVidyasagar et al, Highly sensitive C-reactive protein in metabolic syndrome. Journal, Indian Academy of Clinical Medicine. Vol. No. 3-4. 2013. 38. Tracy RP, Lemaitre RN, Psaty BM, Ives DG, Evans RW, Cushman M, Meilahn EN, Kuller LH. Relationship of C-reactive protein to risk of cardiovascular disease in the elderly. Results from the Cardiovascular Health Study and the Rural Health Promotion Project. ArteriosclerThrombVascBiol 1997; 17: 1121–1127.
Use of psychological principles of management for improved performance in patients care in a tertiary care centre - A randomised control study
Nasir Mahmood Khan
Patient care in a tertiary care centre is a holistic and comprehensive task and cannot get desired outcomes if various aspects of patient care like physical, psychological, mental, social and personal are not properly integrated. The study was planned to provide necessary awareness to the patients and caregivers regarding their illness and treatment outcomes. This was supposed to alleviate unnecessary apprehension and help in healing of patients. By using psychological tools of management in improving patient care, study derives various results that help in understanding the intricate mechanism of patient’s response on treatment. Study demonstrates comparatively better response on added psychological interventions of study group as compared to control group.
Patient care in a tertiary care centre is a holistic and comprehensive task and cannot get desired outcomes if various aspects of patient care like physical, psychological, mental, social and personal are not properly integrated. The study was planned to provide necessary awareness to the patients and caregivers regarding their illness and treatment outcomes. This was supposed to alleviate unnecessary apprehension and help in healing of patients. By using psychological tools of management in improving patient care, study derives various results that help in understanding the intricate mechanism of patient’s response on treatment. Study demonstrates comparatively better response on added psychological interventions of study group as compared to control group.
A comparative study of venous and capillary blood glucose levels by semi auto analyser and glucometer
Supriya Shete, Humaira Khan, A M Siddiqui, Amol Shinde
Introduction: Diabetes Mellitus(DM) is a non communicable disease and most common metabolic disorder reaching epidemic proportions globally. Both type 1 and type 2 diabetes show direct relationship between the glycemic control and the risk of systemic complications. Blood glucose estimation is the mainstay of diagnosis and management of diabetes mellitus. Aim: To compare the blood glucose estimation methods from capillary blood by glucometer and venous plasma glucose estimation by Semi auto analyser and to find out variation percentages in results. Material and Methods: 80 patients attending Outpatient department of a tertiary care level hospital who were advised blood glucose estimation were selected. Finger prick (capillary) blood glucose was measured by glucometer and venous plasma glucose estimation was measured by Semi auto analyser in central laboratory. Results and Conclusion: Capillary blood glucose estimation by glucometer is better alternative to venous plasma glucose estimation for diagnosis follow up and in emergency conditions in diabetic as well as non- diabetic patients.
1. Longo, Casper, Fauci. Hauser, Jameson, Loscalzo, Harrison principles of Medicine. Diabetes Mellitus. 18th ed. Mc grow Hill 2011; (2), 2969-70. 2. Arend, Armitage, Clemmons , Drazen, Griggs, Landry, Levison, Rustgi,Scheld Goldman's Cecil Medicine 2nd edition, Chapter 237, 1491. 3. Longo, Casper, Fauci. Hauser, Jameson, Loscalzo, Harrison principles of Medicine. Diabetes Mellitus. 18th ed. Mcgrow Hill 2011; (2), 2970-71. 4. Risaiah B., Can Med Assoc J.1985 Jun 15; 132(12): 1357-1359, 1361. Self monitering of blood glucose level: potential sources of inaccuracy. PMCID: PMC1346098. 5. American Diabetes association, Standard of Medical Care in Diabetes Jan 2006; vol.29 no.suppl 1 s4-s42. 6. Trinder. P Ann . clin. Biochem 1969 6.24 7. Emerson Lorg . chem. 1943.8.417 8. International Organisation for standardization. In vitro diagnostic test systems. Requirement for blood-glucose monitering system for self-testing in managing diabetes mellitus. Refernce no ISO 15197: 2013 (E). Geneva: International organisation for standardization; 2013 9. Biag A, Saddiqui l, Jabbar A, Azam SI, Sabir S, Alam S, Ghani F. Comparison between bedside testing of blood glucose by glucometer vs centralized testing in a tertiary care hospital. J Ayub Med Coll Abbottabad. 2007 Jul-Sep;19(3):25-9. Available form: http://www.ncbi.nih.gov/pubmed/18444586. 10. Colagiuri S, Sandbak A, Carstensen B, Christiansen J. Glumer C, Lauritzen T, Borch-Johnsen K. Comparibility of venous and capillary glucose measurements in blood. Diabet Med. 2003 Nov; 20(11):953-6. Available form: http://www. ncbi.nih.gov/pubmed/14632723. 11. Brad S, Gunjan Y, Gregory A, Accuracy of Roche Accuchek Inform Whole Blood Capillary, Arterial and Venous Glucose Values in Patients Receiving Intensive Intravenous Insulin Therapy After Cardiac Surgery.AmJ Clin Pathol. 2007; 127(6):919-926.
HLA-A association with psoriasis in a south Indian population
Ashwin Anandan, Krishnamoorthy R, Ravindra Prasad T, Panicker V K, Murugan S
Background: Psoriasis is a common skin disorder affecting around 3% of the population worldwide.HLA association with psoriasis is well established with very little information about Indian Population. Aim: To determine the HLA-A pattern and its association in psoriasis patients. Materials and Methods: 50 cases and 50 controls were enrolled in the study. HLA-A typing was done by PCR-SSP method and the results was analysed and interpreted. Results: The alleles that was found in higher frequency in the cases than in the controls – HLA-A*02(36%), HLA-A*11(32%), HLA-A*03 and HLA-A*24(30%). Conclusion: HLA-A*11 shows a strong association with psoriasis and HLA-A*01 shows decreased association with psoriasis in the present study.
1. Enno Christopher and Ulrich Mrowietz.Psoriasis-Braun-Falco’s Dermatology 506. 2. Kaur I, Kumar B, Sharma V.K., Kaur. S, Epidemiology of Psoriasis in a clinic from North India. Ind. J. Dermatol. Venerol. Leprol. 1986; 52:208-12. 3. Bedi.T.R,et al.Psoriasis in North India-geographical Variations.Dermatologia 1977;155:310-4. 4. Sunil Dogra,Savita Yadav,Psoriasis in India:Prevalance and Pattern.Ind J Dermatol Venerol Leprol 2010;76:595-601. 5. Gelfand J.M., Weinstein. R, Porter S.B., Berlin J.A., Margolis. D.J. Prevalence and treatment of Psoriasis in the U.K.: A population based study. Arch. Dermatol. 2005;141:1537-41. 6. Chablani U.A., Contractor N.M., Gadgil R.B.. HLA and complement C4 studies in Psoriasis Vulgaris. Natl. Med. J India. 1992;5:8-11. 7. Pictchappan et al. HLA B57 and DR7 association with psoriasis vulgaris in South India. Tissue Antigens 1989;34:133-7. 8. Rani R, Narayanan R, Fernandez M.A., Stastany. P. Role of HLA B and C allels in the development of Psoriasis in patients from North India. Tissue Antigens 1998; 51:618-22. 9. Russel T.J., Schultes. L.M., Kuban D.J., HLA antigen associated with Psoriasis. New Engl. J.Med. 1972;287:737-40. 10. White S.H., Mickey M.R., HLA antigen frequency in Psoriasis. New Engl. J.Med 1972;287:740-43. 11. Tiwari JL,Terasaki PI.HLA and Disease Association.New York;Springer 1985;16:145-48. 12. Sasazuki T,Mathushita S,Nakamizo V et al HLA and Psoriasis in Asian populations Joint Report In 1986;23:349-353. 13. Singh S,SinghU,Singh S HLA in patients with psoriasis.Ind J Dermatol Venerol Leprol 2011;77:535-37. 14. Bach F.H,Van Rood,The Major Histocompatibility Complex:Genetics and Biology.New Engl J Med 1976;295:806-813. 15. Shankarkumar Umapathy,R Mitra,Arun Pawar,K Ghosh HLA –A and HLA-B alleles associated in psoriasis patients from Western India. Ind J Dermatol Venerol Leprol 2011;56(5):497-500. 16. Ikaheimo,Silvennoinen-Kassinen S,Karvonen J.Immunogenetics profile of psoriasis vulgaris.Arch Dermatol Res 1996.288:63-67. 17. Gonzaga HF,Torres EA Both psoriasis and benign migratory glossitis are associated with HLA.Br J Dermatol 1996;135:368-370.
A study of the role of insulin resistance and iron in NAFLD associated with HFE gene mutation
K Ponsuganthi, R Sudha
Introduction: NAFLD is becoming a major public problem worldwide. NAFLD is an emerging problem in the Asia-Pacific region and its overall prevalence at present is broadly similar to west. Based on surveys using ultrasonography, the prevalence of NAFLD in the general population across Asia varies from 5% to 40% Aims and Objectives: To Assess the risk of NASH with clinical predictor score associated with HFE gene mutation. Materials and Methods: The work embodied in this study was conducted at tertiary care Hospital. All the type 2 diabetic patients attending the OPD irrespective of their sex and treatment protocol were taken; it includes both old and new cases of type 2 diabetes. All the type 2 diabetic patients were subjected to ultrasonography to rule out the fatty liver. Type 2 DM with NAFLD was taken as cases and Type 2 DM without NAFLD was taken as controls. Biochemical parameter analyzed are fasting glucose, fasting insulin, serum iron, T.I.B.C and ALT.DNA was extracted from frozen whole blood to detect Cys282Tyr mutation. Based on HAIR score, the NASH was assessed in our NAFLD patients. Result: In our study population out of 100 type 2 diabetes patients, 54 of them had fatty liver. In our study population, cases had more female patients (59.2%) than controls (36.9%) and it was statistically significant (Chi square value x2= 4.94 and p<0.02). Fasting insulin and insulin resistance were significantly higher in cases (p< 0.05).Serum Iron and transferrin saturation were significantly raised (p<0.01) in cases when compared to controls. NAFLD patients had significantly higher ALT levels. In our study, 27.8% of patients had NASH based on HAIR score. HFE gene C282Y mutation was not found in our study population. Conclusion: Based on HAIR score, 27.8% of NAFLD patients might have NASH. NAFLD patients had significantly increased serum iron and transferrin saturation when compared to controls. None of our patients had HFE mutation.
1. Kareem Harish, Varghese Thomas. Review article. Non-alcoholic fatty liver disease in Asians- an emerging problem. Calicut Medical Journal 2008; 6(3):e6. 2. Hamaguchi M, Kojima T, Takeda N et al. The metabolic syndrome as a predictor of nonalcoholic fatty liver disease. Ann. Intern. Med. 2005; 143: 72208. 3. Duseja A, Das A, Das R, Dhiman R, Chawla Y. Nonalcoholic steatohepatitis: our experience. Indian J. Gastroenterol 2004; 23 (Suppl. 1): S25. 4. Agarwal SR, Malhotra V, Sakhuja P, Sarin S. Clinical biochemical and histological profile of nonalcoholic steatohepatitis. Indian J.Gastroenterol.2001; 20: 183–6. 5. Duseja A, Chawla Y. Nonalcoholic fatty liver disease in India. How Much? How Soon. Trop Gastoenterol. 2005; 26: 1–3. 6. Buetler E. Genetic irony beyond haemochromatosis: clinical effects of HLA-H mutations. Lancet 1997; 349:296-297. 7. Brunt EM, Janney CG, Di Bisceglie AM, Neuschwander-Tetri BA, Bacon BR. Nonalcoholic steatohepatitis: a proposal for grading and staging the histological lesions. Am J Gastroenterol 1999;94:2467-74. 8. Day, C. P. and James, O. F. W., Steatohepatitis – a tale of two hits. Gastroenterology, 1998, 114, 842–845. 9. Sies, H., Biochemistry of oxidative stress. Angew. Chem. Int. Ed. Engl., 1986; 25: 1058–1071. 10. Feder JN, Gnirke A, Thomas W, et al. A novel MHC class I like gene is mutated in patients with hereditary haemochromatosis. Nat Genet 1996;13:399–408. 11. Nemeth E, Tuttle MS, Powelson J, et al. Hepcidin regulates cellular iron efflux by binding to ferroportin and inducing its internalization. Science 2004; 306: 2090-3. 12. Papanikolaou G, Samuels ME, Ludwig EH, et al. Mutations in HFE2 cause iron overload in chromosome 1q linked juvenile hemochromatosis. Nat Genet 2004; 36: 77- 82. 13. Bridle KR, Frazer DM, Wilkins SJ, et al. Disrupted hepcidin regulation in HFE-associated haemochromatosis and the liver as a regulator of body iron homoeostasis. Lancet 2003; 361: 669-73. 14. Kawabata H, Fleming RE, Gui D, et al. Expression of hepcidin is down-regulated in TfR2 mutant mice manifesting a phenotype of hereditary hemochromatosis. Blood 2005; 105: 376-81. 15. Kristin G. Monaghan, Benjamin A et al. Mutation Analysis of the HFE Gene Associated With Hereditary Hemochromatosis in African Americans. American Journal of Hematology 1998; 58:213–217. 16. Yu AS, Keetie AB. Predictors of NASH and advanced fibrosis. Reviews in Gastrointest Disorders 2002; 2(1): 11-9. 17. Gupte P, Amarapukar D, Agal S, Baijal R, Kulshreshtta P, Pramik S, et al. Non-alcoholic steato-hepatitis in type 2 diabetes mellitus. J GasteroentrolHepatol 2004;19:854-58. 18. ShobhaLuxmi, Rukhsana Abdul Sattar and Jamal Ara.Association of Non Alcoholic Fatty Liver with type 2 Diabetes Mellitus. JLUMHS 2008; 188-193. 19. Akber DH, Kawther AH. Non-alcoholic fatty liver disease in Saudi type-II diabetic subjects attending a medical outpatient clinic. Diabetes Care 2003 ;26: 3351 – 65. 20. Ludwig J, Viggiano TR, McGill DB, et al. Non alcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease. Mayo ClinProc 1980;55:434-8. 21. Bugianesi E, Manzini P, D’Antico S et al. Relative Relative Contribution of Iron Burden, HFE Mutations, and Insulin Resistance to Fibrosis in Nonalcoholic Fatty Liver. Hepatology, January 2004; Vol. 39, No. 1: 179-187. 22. Fan JG, Zhu J, Li XJ et al. Fatty liver and the metabolic syndrome among Shanghai adults. J. Gastroenterol. Hepatol. 2005; 20: 1825-32. 23. Hamaguchi M, Kojima T, Takeda N et al. The metabolic syndrome as a predictor of nonalcoholic fatty liver disease. Ann. Intern. Med. 2005; 143: 722-8. 24. Younossi ZM, Gramlich T, Bacon BR et al. Hepatic iron and nonalcoholic fatty liver disease. Hepatology 1999; 30:847–50. 25. Salonen JT, Tuomanien TP, Nyyssonen et al. Relation between iron stores and non-insulin dependent diabetes in men: case-control study. BMJ 1998; 317: 727. 26. Hanson EH, Imperatore G, Burke W 2001. HFE gene and hereditary hemochromatosis: a HuGE review. Human Genome Epidemiology. Am J Epidemiol, 154(3):193-206. 27. Christine E, McLaren, James C et al. Determinants and characteristics of mean corpuscular volume and hemoglobin concentration in white HFE C282Y homozygotes in the hemochromatosis and iron overload screening study. American Journal of Hematology 2007; 82: 898-905. 28. Joseph A .E , Saverymuttu S H , Al-Sams , Cook M G ,et al. Comparison of liver histology with USG in assessing diffuse parenchymal liver disease. Radiology 1991;43:26-31. 29. Younossi ZM, Diehl AM, Ong J P, et al. Non Alcoholic Fatty Liver Disease- an agenda for clinical research. Hepatology 2002; 35: 746-742.
Dukes treadmill score and myocardial perfusion scintigraphy - A comparative study in patients
Harish B, Sowmya H E
Radionuclide myocardial perfusion imaging (MPI) can be used to demonstrate the presence of coronary heart disease and to risk stratify and guide management of patients with known disease. Treadmill test which is commonly used as screening test for CAD, and with help of DTS can to some extent accurately risk stratify the patients as well. Aim of the study was to compare Duke treadmill score and MPI in risk stratifying the patient with CAD. 130 patients were considered in the study. Most of the patients fell in moderate Dukes score (78 patients, 60%). MPI could further stratify those patients into high (28 patients, 36%) and low risk (50 patients, 64%) groups. Low and high Dukes scores correlated well with normal and severe defects in MPI respectively. Hence it is advisable to perform MPI in moderate Dukes Score patients for further risk stratification.
1. Heart Facts 1980 American Heart Association, 1979 2. Report of Joint International Society and Federation of Cardiology and World Health Organization Task Force on Standardization of Clinical Nomenclature 1979 Nomenclature and criteria for diagnosis of ischemic heart disease. Circulation 59: 607 3. Wyatt HL, Forrester JS, Tyberg JV et al 1975 Effect of graded reduction in regional coronary perfusion and total cardiac function Am J Cradiol 36:185 4. Kubler W, Katz AM 1977 Mechanism of early pump failure of the ischemic heart: possible role of adenosine triphosphate depletion and inorganic phosphate accumulation. Am J Cardiol 40: 467 5. Robb G.P, Marks M H 1974 Latent Coronary artery disease: determination of its presence and severity by the exercise electrocardiogram. Am J Cardiol 13:603 6. Goldschlager N, Selzer A, Cohn K 1976 Treadmill stress tests as indications of presence and severity of coronary artery disease. Ann Intern Med 85: 277 7. Master AM, Jaffe HL 1941 Ecltrocardiographic changes after exercise in angina pectoris. J Mount Sinai Hosp 7:629 8. AHA/ACSM Scientific Statement, Recommendation for Cardiovascular Screening, Staffing and emergency policies at Health/fitness facilities, Circulation 1998; 97: 2283-2293 doc 10.1161/01 CIR.97.22.2283.
Assessment of the insulin resistance- insulin sensitivity and β cell function in type 2 diabetes with NAFLD associated with HFE gene mutation
K Ponsuganthi, R Sudha
Introduction: Diabetes mellitus has reached pandemic proportion and in 2030, there will be approximately 366 million diabetics; of these 79 million will be from India. Diabetes mellitus is a group of metabolic diseases that includes hyperglycemia resulting from defects in insulin secretion, insulin action or both. Type 2 diabetes is characterized by insulin resistance and insulin deficiency (often relative rather than absolute). Aims and Objectives: To study Assessment of the insulin resistance- insulin sensitivity and β cell function in type 2 diabetes with NAFLD associated with HFE gene mutation. Materials and Methods: The work embodied in this study was conducted at tertiary care Hospital. It is a hospital based case control study. All the type 2 diabetic patients attending the OPD irrespective of their sex and treatment protocol were taken; it includes both old and new cases of type 2 diabetes. All the type 2 diabetic patients were subjected to ultrasonography to rule out the fatty liver. Type 2 DM with NAFLD was taken as cases and Type 2 DM without NAFLD was taken as controls. Biochemical parameters analysed were glucose, insulin, serum iron and total iron binding capacity. DNA was extracted from frozen whole blood to detect Cys282Tyr mutation.Result: In our study population out of 100 type 2 diabetes, 54 patients had fatty liver. The prevalence of fatty liver in our study group was 54%.In our study population, majority of the patients were in the age group of 51- 60 years in both cases and controls. Age distribution between cases and controls were matched (Chi square value 2.45 degree of freedom (df) is 3, p value = 0.48).NAFLD cases had more female patients (59.2%) than controls and it was statistically significant (Chi square value x2= 4.94 and p<0.02). In our study population, mean fasting glucose in cases and controls (147.8 ± 44.6 and 138.5 ± 33.9 respectively) were not significantly different (p<0.5). Whereas post prandial glucose, fasting insulin, HOMA-IR and HOMA-β were significantly(p<0.5) higher in NAFLD patients. In comparison to controls, Insulin sensitivity index (QUICK) was statistically low(p< 0.05) in NAFLD patients. Conclusion: We observed significant increase in fasting insulin, beta-cell function (HOMA-β) and insulin resistance along with decreased insulin sensitivity in NAFLD patients
1. Sarah Wild, GojkaRoglic, Anders Green et al Global Prevalence of Diabetes: Estimates for the year 2000 and projections for 2030. Diabetes Care 2004; 27:1047–1053. 2. Report of the export committee on the diagnosis and classification of diabetes mellitus. Diabetes Care Jan 2002. vol 25(1); s5-s20. 3. Yoon KH, Lee JH, Kim JW et al. Epidemic obesity and type 2 diabetes in Asia. Lancet 2006; 368: 1681–8. 4. Brunt EM. Nonalcoholic steatohepatitis: definition and pathology. Semin Liver Dis 2001;21:3–16. 5. Cairns SR, Peters TJ. Biochemical analysis of hepatic lipid in alcoholic and diabetic and control subjects. ClinSci (Lond). 1983 ; 65:645-52. 6. Farrell GC, Larter CZ. Nonalcoholic fatty liver disease: from Steatosis to cirrhosis.Hepatology 2006; 43(Suppl.1): S99 – 112. 7. Ludwig J, Viggiano TR, McGill DB, et al. Non alcoholicsteatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease. Mayo ClinProc 1980;55:434-8. 8. Braunwald E et al. Harrison’ s principles of internal medicine , 16th edition. McGraw-Hill,2005. 9. Bacon BR, Farahvash MJ, Janney CG et al. Non-alcoholic steatohepatitis: an expanded entity. Gastroenterology 1994; 107:1103. 10. Powell EE, Cooksley WGE, Hanson R et al. The natural history of nonalcoholicsteatohepatitis: a follow up study of 22 patient for up to 21 years. Hepatology 1990; 11:74. 11. Marchesini G, Bugianesi E, Forlanietal.Nonalcoholic fatty liver, steatohepatitis, the metabolic syndrome.Hepatology2003;37:917- 23. 12. Chitturi S, Abeygunasekera S, FarrellGCet al. NASH and insulin resistance: Insulin hypersecretion and specific association with the insulin resistance syndrome. Hepatology 2002;35:373-379. 13. Feder JN, Penny DM, Irrinki A, et al. The hemochromatosis gene product complexes with the transferrin receptor and lowers its affinity for ligand binding. ProcNatlAcadSci U S A 1998;95:1472–7. 14. Bridle KR, Frazer DM, Wilkins SJ, et al. Disrupted hepcidin regulation in HFE-associated haemochromatosis and the liver as a regulator of body iron homoeostasis. Lancet 2003; 361: 669-73. 15. C.ABurtis, E.R Ashwood, W.B Saunder. Tietz text book of clinical chemistry, 3rd 1999: pg 750-785 16. Robbins DC, Andersen L, Bowsher R et al. Report of the American Diabetes Association’s task force on standardization of the insulin assay.Diabetes 1996; 45: 242-256. 17. Matthews DR, Hosker JP, Rudenski AS. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentration. Diabetologia 1985; 28: 412-9. 18. Levy JC, Matthews DR, Herman MP. Correct homeostasis model assessment (HOMA) evaluation uses the computer program. Diabetes Care 1998; 21: 2191-2. 19. Katz A, Nambi SS, Mather K et al. Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans. J ClinEndocrinolMetab 2000; 85: 2402-10. 20. Kristin G. Monaghan, Benjamin A et al. Mutation Analysis of the HFE Gene Associated With Hereditary Hemochromatosis in African Americans. American Journal of Hematology 1998; 58:213–217. 21. Feder JN, Gnirke A, Thomas W, et al. A novel MHC class I like gene is mutated in patients with hereditary haemochromatosis. Nat Genet 1996;13:399–408. 22. Muhammad Khurram, Abdul Shakoor, Mian M Arshad et al. Characteristic features of 50 NAFLD patients. Rawal Med J 2004; 29: 8-12. 23. Gupte P, Amarapukar D, Agal S, Baijal R, Kulshreshtta P, Pramik S, et al. Non-alcoholic steato-hepatitis in type 2 diabetes mellitus. J GasteroentrolHepatol 2004;19:854-58. 24. ShobhaLuxmi, Rukhsana Abdul Sattar and Jamal Ara.Association of Non Alcoholic Fatty Liver with type 2 Diabetes Mellitus. JLUMHS 2008; 188-193. 25. Akber DH, Kawther AH. Non-alcoholic fatty liver disease in Saudi type-II diabetic subjects attending a medical outpatient clinic. Diabetes Care 2003 ;26: 3351 – 65. 26. Sandhya Mishra, Dharamveer, Monika Gupta et al. Hyperinsulinemia predisposes to NAFLD. Indian journal of Clinical Biochemistry, 2008; 23(2): 130-135 27. Constantine Goritsas, Konstantinos Spanos, Dimitrios Stefanopoulos et al. Non Alcoholic Fatty Liver Disease: Correlation With Clinical Hormonal and Biochemical Parameters. Hospital Chronicles 2007; 2(3): 100–103. 28. Ajay Duseja, Reena Das, Mohit Nanda, Ashim Das et al. Nonalcoholic steatohepatitis in Asian Indians is neither associated with iron overload nor with HFE gene mutations. World J Gastroenterol 2005;11(3):393-395.
A comparative study of two different doses of Gabapentin in attenuating the cardiovascular response to direct laryngoscopy and intubation
V B Gowda, Manjunath K S, Henjarappa K S, Namrata Ranganath, Arathi B H
Introduction: Direct laryngoscopy and endotracheal intubation is an integral part of anaesthesia which offers tremendous safety to administration of general anaesthesia but is associated with hemodynamic changes, due to reflex sympathetic discharge caused by epipharyngeal and laryngopharyngeal stimulation. Aims and Objectives: Tostudy the effect of two different doses of Gabapentin in attenuating the cardiovascular response to direct laryngoscopy and intubation. Materials and methods: Prospective, randomized, double blind and placebo controlled clinical study involving90 patients of kidwai memorial institute of oncology,Banglore visiting pre anaesthesia clinic scheduled for elective surgery under GA with ASA I and ASA II was designed after approval from institute ethics committee. Statistical analysis was done by Analysis of variance (ANOVA) to find the significance of study.Student t test (paired) has been used to find the significance within the same group. Result: Laryngoscopy and intubation caused a significant increase in heart rate and blood pressure in controlled group. Gabapentin can be used to attenuate pressor response to laryngoscopy and intubation. Gabapentin 800mg and 400mg attenuated the pressor response to laryngoscopy and intubation. SBP, DBP, MAP and HR were all attenuated by Gabapentin in comparison to control group. Gabapentin 800mg is more effective than 400mg for attenuation of pressor response to laryngoscopy and intubation (Statistically significant p<0.05) Conclusion: SBP, DBP, MAP and HR were all attenuated by Gabapentin in comparison to control group. Gabapentin 800mg is more effective than 400mg for attenuation of pressor response to laryngoscopy and intubation.
1. Burstein CL, Lo Pinto FJ,Newman: Electrocardiographic studies during endotracheal intubation; Effects during usual routine techniques. Anesthesiology 1950; 11:224 2. King B D, Elder J D, Procter D F, et al: Reflex circulatory responses to tracheal intubation performed during general anesthesia. Anesthesiology 1951;12: 556 3. Fox E.J, Sklar G.S, Hill C.H, Villanuera R, King BD. Complications related to the pressure response to endotracheal intubation. Anesthesiology 1977; 47: 524-5 4. Miller Forbes and F G Dally: Acute hypertension during induction of anesthesia and endotracheal intubation in normotensive men. Br J Anaesth 1970; 42: 618. 5. Asfar S N, Abdulla WY: The effects of various administration routes of lignocaine on the hemodynamics and ECG rhythm during endotracheal intubation. ActaAnesthesiologicaBelgica1990; 41: 17-24. 6. Helfman SM, Gold MI, Delisser EA, Herrington CA: Which drug prevents tachycardia and hypertension associated with tracheal intubation; Lignocaine, Fentanyl or Esmolol?Anesthesia and Analgesia 1991; 72: 482-6. 7. Lev R, Rosen P: Prophylactic lignocaine use pre intubation: A review. Journal of Emergency Medicine 1994; 12(4): 499-506. 8. James F Hamill, Robert F Bedford, David C Weaver, Austin colohan. Lignocaine before endotracheal intubation: Intravenous or laryngotracheal. Anesthesiology 1982; 55: 578-581. 9. Gold M, Brown Mand, Selem J: The effects of Esmolol on hemodynamics after ketamine induction and intubation. Anesthesiology 1982; 61-119. 10. Puri GD, Batra YD. Effects of Nifedepine on the cardiovascular responses to laryngoscopy and intubation. Br J Anaes1988; 60(5): 579-581. 11. NibeditaPani, ShovankumarRath. Regional and Topical Anaesthesia of upper Airways. Indian J of Anaesth2009; 53: 61-648. 12. Mostafa SM, Murthy B V, Barett P J, McHugh P: Comparison of the effects of lignocaine spray applied before or after induction of anesthesia on the pressor 57 response to direct laryngoscopy and inubation. Eur J Anaesthesiol1999;16: 7-10. 13. Donald Martin et al: low dose fentanyl blunts circulatory responses to tracheal ntubation. Anesthesia and Analgesia 1982; 61: 680. 14. AbouMadi M, Kelzler H, Yacoub O: A Method of prevention of cardiovascular reactions to laryngoscopy and intubation. Canadian Anaesthesia Society Journal 1975; 22: 316. 15. Bahman Venus, VenugopalPolassani , Con Gial Pham: Effects of aerolized lignocaine on circulatory responses to larynoscopy and tracheal intubation.critical care medicine 1984;12: 391-4. 16. Sklar B Z, Lurie S, Krichelli D, Savir I, Soroker D: Lignocaine inhalation attenuates the circulatory response to laryngoscopy and endotracheal intubation. Journal of Clinical Anesthesia 1992; 4(5): 382-5. 17. Kautto UM, Heinonen J: Attenuation of circulatory response to laryngoscopy and tracheal intubation: a comparison of two methods of topical anaesthesia. Actaanaesthesiology Scandinavia 1982; 26(6): 599-602. 18. Rachael K Seib, James E Paul. Pre-operative Gabapentin for post-operative analgesia: A meta analysis. Can J Anaesth2006; 53: 461-69. 19. Gilron et al. Is Gabapentin a broad spectrum analgesic? Anesthesiology 2002;97: 537-539. 20. Kong VK, Irwin MG. Gabapentin: a multimodal peri-operative drug? Br J Anaes2007; 99: 775-786 21. Rosner H, Rubin L, Kestenbaum A. Gabapentin adjunctive therapy in neuropathic pain states. ClinJ Pain 1996; 12: 56–8. 22. Menigaux C, Adam F, Guignard B, Sessler DI, Chauvin M. Preoperative gabapentin decreases anxiety and improves early functional recovery from knee surgery. AnesthAnalg2005; 100: 1394–9. 23. Memis D, Turan A, Karamanlioglu B, Seker S, Ture M. Gabapentin reduces cardiovascular responses to laryngoscopy and tracheal intubation. Eur J Anaesthesiol2006; 23: 686–90. 24. Prys-roberts C, Greene L.T, Meloche R, Forex P. Studies of anaesthesia in relation to hypertension II: Hemodynamic consequences of induction and endotracheal intubation. BrJAnaesth1971; 43:531. 25. Fassoulaki A, Melemeni A, Paraskeva A, Petropoulos G. Gabapentin attenuates the pressor response to direct laryngoscopy and tracheal intubation. Br J Anaesth2006 ; 96: 769-773. 26. Koc S, Memis D, Sut N. The preoperative use of gabapentin, dexamethasone and their combination in varicocele surgery: a randomized control study. AnaesthAnalg2007; 105(4): 1137-42.
A study of the efficacy of mifepristone with misoprostol over misoprostol alone in medical termination of pregnancy
Pushpee Sinha
Introduction: Misoprostol has proven its efficacy as an effective abortifacient for the second trimester termination of pregnancy. It is being successfully used through all the routes i.e. sublingual, oral and vaginal and in different regimens with the induction abortion interval varying from 12 h to as high as 33 h. Aims and Objectives: To Study the Efficacy of Mifepristone with misoprostol over misoprostol alone in medical termination of Pregnancy Methodology: This was a hospital based study in patients attending the department of Obstretics and Gynecology of teaching hospitals attached to Bangalore Medical College, Bangalore (viz. Bowring and Lady Curzon Hospital and Vanivilas Hospital) who needed MTP. Out of 100 Pregnant Women 50 pregnant women given oral mifepristone 200mg followed by vaginal misoprostol 400 microgram after 48 hours and one hour of that 200 microgram of oral misoprostol. 50 pregnant women given 600 microgram vaginal misoprostol alone at a time The statistical analysis done by unpaired t-test. Result: Complete abortion was achieved in 88% (44) of the patients in misoprostol alone regimen. Complete abortion was achieved in 96% (48) of the patinets in combination regimen. Overall complete abortion was achieved in 92 patients in our study. Failure rate was observed more in Misoprostol alone group i.e. 12.0% as compared to Misoprostol+Mifepristone group i.e. 4.0%. Mean Time to Induction to Abortion was significantly less in Mifepristone with misoprostol than misoprostol alone group. Conclusion: From our study it can be concluded that the combination of Mifepristone with misoprostol is superior to misoprostol alone with respect to less failure rate and Mean Time to Induction to Abortion in both Primi and Multi Gravidity.
1. Wong KS, Ngai CS, Yeo EL, et al. A comparison of two regimen of intravaginal misoprostol for termination of second trimester pregnancy: a randomized trial. Hum Reprod. 2000; 15:709–12. 2. Herbutya Y, Chanarchakul B, Punyavachira P. Vaginal misoprostol in the termination of second trimester pregnancy. J ObstetGynaecol Res. 2000; 26:121–5. 3. Pongsatha S, Tongsong T. Second trimester pregnancy termination with 800 mcg vaginal misoprostol.J Med Assoc Thai. 2001; 84: 859–63. 4. Herbutya Y, Chanarchakul B, Punyavachira P. Second trimester pregnancy termination: a comparison of 600 and 800 lg of intravaginal misoprostol. J ObstetGynaecol Res. 2001; 27:125–8. 5. Gilbert A, Reid R. A randomized trial of oral versus vaginal administration of misoprostol for the purpose of mid trimester termination of pregnancy.Aust N Z J ObstetGynaecol.2001; 41:407–10. 6. Ramin KD, Ogburn PL, Danilenko DR, et al. High dose oral misoprostol for mid trimester pregnancy interruption. J GynecolObstet Invest. 2002; 54:176–9. 7. Dickinson JE, Evans SF. A comparison of oral misoprostol with vaginal misoprostol administration in second-trimester pregnancy termination for fetal abnormality.Obstet Gynecol. 2003; 102: 1294–9. 8. Tang OS, Lau WNT, Chan CCW, et al. A prospective randomized comparison of sublingual and vaginal misoprostol in second trimester termination of pregnancy.Br J ObstetGyneacol. 2004; 11:1001–5. 9. Pongastha S, Tong song T. Therapeutic termination of second trimester pregnancies with intrauterine fetal death with 400 lg of oral misoprostol. J ObstetGynaecol Res. 2004; 30:217–20. 10. Baird DT, Rodger MW. Pretreatment with mifepristone (R U 486) reduces interval between prostaglandin administration and expulsion in second trimester abortion. Br J ObstetGyneacol. 1990; 97:41–5. 11. Hinshaw K, Refaey HE. Mid trimester termination for fetal abnormality: advantages of a new regimen using mifepristone and misoprostol. Br J ObstetGyneacol. 1995; 102:559–60. 12. Refaey HE, Templeton A. Induction of abortion in the second trimester by a combination of misoprostol and mifepristone: a randomized comparison between two misoprostol regimens. Hum Reprod. 1995; 10:475–8. 13. HO PC, Tsang SSK, Ma HK. Reducing the induction to abortion interval in termination of second trimester pregnancies: a comparison of mifepristone with laminaria tent.Br J ObstetGyneacol. 1995; 102:648–51. 14. Premila WA, Templeton A. Nonsurgical mid trimester termination of pregnancy; a review of 500 consecutive cases. Br J ObstetGyneacol. 1999; 106:706–10. 15. Ngai SW, Tang OS, Pak Chiung HO. Randomized comparison of vaginal (200 lg every 3 h) and oral (400 lg every 3 h) misoprostol when combined with mifepristone in termination of second trimester pregnancy. Hum Reprod. 2001; 15:2205–8.
Comparative study of bone marrow aspiration and bone marrow clot sections in various haematological disorders
Upasana Uniya, Yogesh Patle, Hanisha Jain
Introduction: During the last two decades, bone marrow examination has become an indispensable adjuvant to diagnose the malignant diseases of the blood and other body systems. This will obviate the need for many other expensive and time-consuming investigations. When both the procedures for bone marrow examination i.e. aspiration and clot section done simultaneously, can yield a good diagnostic material which will be helpful for more accurate diagnosis. Aims and Objectives: This study was aimed to assess the diagnostic value of the BMA and Bone Marrow Clot Sections and role of both the procedures to reach final diagnosis when done simultaneously. Methods: The present study was done on 80 cases in which complete peripheral blood smears, bone marrow and cell blocks was available were included in the study. Bone marrow aspiration was performed, Cell block was prepared and stained with hematoxylin and eosin stain, smears were stained with Leishman stain. Results: Comparison was done between bone marrow aspirate smears stained by Romanowsky group of stains i.e. Leishman and paraffin embedded cell block section stained by Hematoxylin and Eosin stain. Out of 80 cases, there were 60 cases (75%) of anaemias, 9(11.2%) platelet disorders, 6(7.5%) Acute Leukaemias, 2(2.5%) Lymphoproliferative disorders, 1(1.2%) MDS, 1(1.2%) Leishmaniasis and 1(1.2%) hyperspleenism. Conclusions: The advantage of both the procedures done together provided more material and enabled us to study the cytomorphology of the cells, with the pattern of distribution of the cells depending on the cases and help in more accurate diagnosis.
1. Riley RS, Hogan TF, Pavot DR, Forysthe R, Massey D, Smith E, Wright L, Jr, Ben-Ezra JM. A pathologist’s perspective on bone marrow aspiration and biopsy; Performing a bone marrow examination. J Clin Lab Anal. 2004; 18:70–79. doi: 10.1002/jcla.2008. 2. Islam A. Bone marrow aspiration prior to bone marrow core biopsy using the same bone marrow biopsy needle. A good or bad practice. J Clin Pathol. 2007;60:212–215. doi: 10.1136/jcp.2006.037341. 3. Hyun BH, Gulati GL ,Ashton JK.Bone marrow examination :techniques and interpretation.Hematol Oncol Clin North Amer 1988;2:513-523. 4. Riley RS .Hogan TF, Pavot DR.etal .A pathologist perspective on bone marrow aspiration and biopsy: Performing a bone marrow examination .J Clin Lab Annal.2004;18 (2) :70-90. 5. Brain BJ..Bone Marrow Evaluation .J clin Pathol 2001; 54: 737-742. 6. Kuperan P,Rajshekhar swamy.Magaloblastic anaemia- A review from university hospital Kuala Lumpur.Ann Acad Med Singapore.1998;17(2):261-266. 7. Pizzuto J, Ambriz R.Therapeutic experience on 934 adults with idiopathic thrombocytopaenic purpura: Multicentric trial co-operative Latin American Group on Hemostatis and thrombosis.Blood1984;64:1179-1183. 8. Jaishree Sharma,Shobha Mohindroo.FAB classification of Leukaemia: A cytochemical study.Indian J Pathol Microbiol 2004;47(3):336-339. 9. Sitalaxmi S, Anuradha Srikrishna,Shantal Devi,Prema Damodar,Betty Alexander.The Diagnostic utility of bone marrow trephine biopsies. Indian J Pathol Microbiol 2005;48(2):173-176. 10. Rozman C ,Monserrat E,Rodriguez-Fernandez JM,Ayats R,Vallespi T ,Parody R etal. Bone marrow Histologic Pattern- The Best Single prognostic parameters in CLL:A multivariate survival analysis of 329 cases. Blood 1984; 64(3) :642-64811. 11. Alteration in cellularity of bone marrow. Bone marrow cellularity- general.Ann clin Lab Sci 2004;34:307. 12. Pasquale D, Chikkapa G. Comparative evaluation of bone marrow aspirate particle smears, biopsy imprints and biopsy sections. Am J Hematol. 1986;22:381–389. doi: 10.1002/ajh.2830220407. 13. Ozkalemkas F, Ali R, Ozkocaman V, Oscelik T, Ozanu OH, et al. The bone marrow aspirate and biopsy in the diagnosis of unsuspected non hematologic malignancy. A clinical study of 19 cases. BMC Cancer. 2005;1(5):144. doi: 10.1186/1471-2407-5-144. 14. Varma N, Dash S, Sarode R and Marwaha N. Relative efficacy of bone marrow trephine biopsy sections as compared to trephine imprints and aspiration smears in routine hematological practice. Indian J Pathol Microbiol 1993; 36(3):215-226. 15. Dee JW, Valdivieso M , Drewinko B. Comparison of the efficacies of closed trephine needle biopsy,aspirated paraffin embedded clot section, and smear preparation in the diagnosis of bone marrow involvement by lymphoma. Am J Clin Pathol 1976;65:183-94.
Phenotyphic Determination of Urinary Virulence Factors in Escherichia coli
Vidhya J, Senita Samuel, Kennedy Kumar P, KopulaSridharan S, Uma Sekar
Aim: To determine the virulence factors haemolysin production, hemagglutination and serum resistance in Escherichia coli (E.coli) of urinary isolates and Escherichia coli isolated from the other sites like blood, exudate and stool. Materials and Methods: A cross sectional study was conducted in the Department of Microbiology, Sri Ramachandra Medical College and Research Institute. A total of 120 strains of E. Coli isolated fromthe following specimens urine (50), Exudate (25), Blood (25) and Stool (20) were included in the study and assessed for the presence of Uropathogenic virulence factors such as Haemolysin production, Hemagglutination property both the Mannose Resistant Hemagglutination (MRHA) and Mannose Sensitive Hemagglutination (MSHA) and Serum Resistance factor. Results: Among the 50 urinary isolates haemolysis was observed in 10%, hemagglutinating property was seen in 20 %( MRHA 7 and MSHA 3 n=10)) and 88 % of them had serum resistance factor. Out of the 25 E.coli strains isolated from the exudate samples none of them was found to be haemolytic, 12% of them were hemagglutinating (MRHA 67% and MSHA 33%) and serum resistance factor was seen with 24% of isolates. Among the 25 E. coli isolates from the blood 8% were haemolytic, 28% of them were hemagglutinating (MRHA 100%) and serum resistance factor was observed in 72. Out of 20 E.coli strains isolated from stool, haemolysis was not seen in any of the them, 20% of them were hemagglutinating property (MRHA 100%) and serum resistance factor was positive in 20% of them. Summary and Conclusion: A total of 50 E.coli reported as significant bacteriuria (>105) was included in this study and at the same time 70 isolates of E.coli reported from other specimens (Blood, Exudates and Stool) were taken as control group. Uropathogenic virulence factor was exhibited by 45 out of 50 urinary isolates (90%). Serum Resistance is the commonest virulence factor observed in our study (88%) followed by Hemagglutination property (20%) and Haemolytic property (10%). The entire 3 virulence factor is exhibited by 3 strains of urinary isolates (6%) only. In the control group Haemolysis was observed in 2 isolates, Hemagglutination with 24 isolate, Serum Resistance in 28 E.coli isolates.
1. Mulvey M A“Adhesion and Entry of Uropathogenic Escherichia coli†Cellular Microbiology (2002) 4(5), 257–271. 2. M Douglas and Bennetts.“Principle and Practice of Infectious Diseaseâ€. 7th edition. Churchill Livingstone (2010) Vol 2 Chapter 218. 3. Seetharama S, Cavalieri S J, Snyderl I S. “Immune Response to Escherichia coli Alpha-Hemolysin in Patientsâ€. Journal of clinical microbiology, May 1988, p. 850-856 4. JOHNSON J R“Virulence Factors in Escherichia coli Urinary Tract Infectionâ€.CLINICAL MICROBIOLOGY REVIEWS, Jan. 1991, p. 80-128 5. Kausar Y, Chunchanur S K, Nadagir S D, Halesh L H and Chandrasekhar M R. “Virulence factors, Serotypes and Antimicrobial Suspectibility Pattern of Escherichia coli in Urinary Tract Infectionsâ€. Al Ameen J Med Sci. 2009; Vol 2(1): 47 -51. 6. Sharma S, Bhat GK, Shenoy S. Virulence factors and drug resistance in Escherichia coli isolated from extraintestinal infections. Indian J Med Microbiol 2007;25:369-73 7. Ranjan KP, Ranjan N, Chakraborty A, Arora DR. “An approach to uropathogenic Escherichia coli in urinary tract infectionsâ€. J Lab Physicians. 2010 Jul;2(2):70-3.
Comorbidity of recurrent depressive disorder with thyroid dysfunction and altered lipid metabolism in postmenopausal women: A case-control study
Aditi Ranawat, Maheep Sinha, Ram Kumar Solanki
The transition to menopause represents the passage from reproductive to non-reproductive life. Most women during the menopause experience irregular menstrual periods along with fluctuation of ovarian hormones secretion during this time. Usually during the menopause and after menopause i.e. post-menopause women face physical and emotional changes. Since years various investigators have already documented an association between depression and menopause. Post-menopausal period is accompanied in a majority of women with significant somatic and psychiatric symptomatology. Objective: Since psychiatric symptomatology is a growing concern in post-menopausal women, hence we tried to examine whether a comorbidity of metabolic and psychiatric disorders occurs in this patient population or whether these disorders occur independently. The study was planned to examine comorbidity of recurrent depressive disorder with thyroid dysfunction and altered lipid metabolism in post-menopausal women (PMW). Method: To conduct this study a cross sectional, case-control study was planned. The experimental group consisted of PMW with recurrent depressive disorder (ICD-10 criteria) (n=100), and was compared with a control group (n=100) of PMW without recurrent depressive disorder. Subjects were assessed through Beck’s depressive self-rating inventory and their blood level of Thyroid Stimulating Hormone (TSH) and lipid profile was assessed. Group comparison was done with chi square test and z test. Correlation analysis was undertaken using Pearson correlation coefficients (r). Result: Results obtained depicted that serum total cholesterol, triglyceride, TSH levels were significantly higher and HDL levels were significantly lower in the depressed group.Highly significant positive correlation was found between Beck’s score and TSH levels in depressed PMW. Conclusion: Taken together, these data demonstrated that comorbidity of recurrent depressive disorder with Thyroid dysfunction and lipid metabolism abnormality in post-menopausal women is common and needs clinical attention.
1. Alexopoulas G S, Kalz I R, Reynolds C F III, Carpenter D, Doherthy J P. The expert consensus guideline series: Pharmacotherapy of depressive disorders in older patients. Post graduate medicine special report.2001 2. Anderson E, Hamburger S, Liu J H, Rebar R W. Characteristics of menopausal women seeking assistance. Am J ObstetGynecol 1987; 156: 428-33. 3. Archer J S. Relationship between estrogen, serotonin and recurrent depressive disorder. Menopause .1999; 6: 71-8. 4. Artt W.Androgen therapy in women .Eur J Endocrinol. 2006; 154:1-11. 5. Beck AT, Rial WY, Rickets K. Short form of recurrent depressive disorder inventory: cross validation. Psychol Rep.1974; 34(3):1184-6. 6. Beck, AT, Steer RA. Internal consistencies of the original and revised Beck Recurrent depressive disorder Inventory. J ClinPsychol 1984; 40(6):1365-7. 7. Beck, Ward, Mendelson, Mock and Erbaugh. An inventory for necologic care.1961; 4th ed., St. Louis:Mosby. 8. Beck, Ward, Mendelson, Mock, Erbaugh .An inventory for measuring recurrent depressive disorder. Arch Gen Psychiat 1961; 4: 561-571. 9. Bobak, IM, Jensen MD, Zalar MK. Maternity and gynecologic care 1990; 4th ed., St Louis: Mosby. 10. Bromberger, JT, Matthes KA, Schott LL. Depressive symptoms during the menopausal transition: the study of women’s health across the nation (SWAN). J Affect Disord 2007; 103: 267-72. 11. Brown, ES, Varghese, FP and McEwen, BS. Association of depression with medical illness: does cortisol play a role? Biological Psychiatry. 2004; Vol 55: 1; 1-9. 12. BuccoloG .Quantitative determination of serum triglyceride by use of enzymes. ClinChem 1973; 19(5):476-482. 13. Burger HG, Dudley EC, Robertson DM and Dennerstein L. Hormonal changes in the menopause transition. Recent Prog Horm Res. 2002; 57:257–75. 14. Burt VK and Stein K. Epidemiology of depression throughout the female life cycle. J Clin Psychiatry.2002; 63 (Suppl 7) : 9-15 15. Canaris G J, Manowitz N R and Major G. The Colorado thyroid disease prevalence study. Arch Intern Med. 2000; 160: 526 -34. 16. Chang ER. A study on factors that affect ego-identity and recurrent depressive disorder of middle-aged women. Masters thesis. 2000: Seoul Theological University, Seoul. 17. Chedraui P, Hidalgo L, Chanez D, Morocho N, Alvarado M and Huc A. Menopausal symptoms and associated risk factors among PMW screened for the metabolic syndrome. Arch Gynecol Obstet.2007;275:161-168 18. ChienChih C, Tiao Lai H. Association of serum Lipid Profiles with Depressive and Anxiety Disorders in Menopausal Women. Chang Gung Med J 2006; 29: 325-30. 19. Chowta N K, Sabastian J and Chowta M N. Comparative study of menopausal symptoms in postmenopausal and Perimenopausal women. Journal of Clinical and Diagnostic Research. 2008 Aug; (2): 959-962. 20. Das P P, Malhotra S, Chakrabarti S and Sharma S. Elevated total cholesterol in severly depressed patients: Role in cardiovascular risk? World J Biol Psychiatry. 2009. 21. De Kleijn MJ, VanderSchouw YT, Banga JD, Vander GY. The effect of menopause on risk factors for ischemic diseases. Ned TijdschrGeneeskd 1996; 140: 478–482. 22. Dennerstein L, Lehert P, Burger H G and Guthrie J R. New findings from non- linear longitudinal modelling of menopausal hormone changes. Hum Reprod Update. 2007. 23. Ellen WF, Mary DS, HuiL, Deborah BN. Association of hormones and menopausal status with depressed mood in women with no history of recurrent depressive disorder. Arch Gen Psychiatry 2006; 63 (4): 375-382. 24. Engelberg H. Low serum cholesterol and suicide. Lancet 1992; 339: 727-9. 25. Freedman M A.Quality of life and menopause: The role of estrogen. J Women Health .2002; 11:703-18. 26. Gibbs Z, Lee S, Kulkarni, J. Factors associated with depression during menopausal transition. Women’s Health Issues. 2013 Sep-Oct; 23(5):e301-7. doi: 10.1016/j.whi.2013.07.001 27. Gupta S, Saha P K and Mukhopadhyay A. Prevalance of hypothyroidism and importance of cholesterol estimation in patients suffering from major depressive disorder. J Indian Med Assoc. 2008; 106 : 240-2 28. Hadine J, Claudio NS, Lee SC. Assessment and treatment of hot flushes and menopausal mood disturbance. PsychiatrClin N Am 2003; 26: 563-580. 29. Holland WW, Detels R, Knox G, Fitxsimons B, Gardner L. Oxford textbook of public health. 1991; 2nded, Oxford university press, 170-172. 30. Huang TL. Serum Lipid profiles in major recurrent depressive disorder with clinical subtypes, suicide attempts and episodes. J Affect Disord 2005; 86: 75-9. 31. Karen AM, Elaine M, Lewis HK, Sheryl FK, Arlene WC, Rne RW. Menopause and Risk Factors for Coronary Heart Disease. N Engl J Med 1989; 321(7): 641-646. 32. Kessler RC, McGonagle KA, Zhao S, Nelson CB, Hughes M, Eshleman S, Wittchen HU, Kendler KS. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States. Results from the National Comorbidity Survey. Arch Gen Psychiatry 1994; 51: 8-19. 33. Kim SS. The associated factors with the recurrent depressive disorder of middle-aged women living in a city. Unpublished doctoral dissertation.2000; Chosun University, Kwangju. 34. Kwon SH, Kim YJ, Moon KN, Kim IS, Park KJ, Park CW, Bae JE, Song AR, Yeo JH, Jung ES, Jung HM. The climacteric symptoms and recurrent depressive disorder in middle-aged women. Korean J Women Health Nurs 1995; 2(2): 235-243. 35. Lee Y W. Recurrent depressive disorder in postmenopausal women. TaihanKanhoHakhoe Chi 2003; 33(4):471-477. 36. Lepine JP, Bouchez S. Epidemiology of recurrent depressive disorder in the elderly. IntClinPsychopharmacol 1998; 13: S7 – S12. 37. Lindberg G, Larsson G, Setterlind S, Rastam L. Serum lipids and mood in working men and women in Sweden. J EpidemiolCommun Health 1994; 48: 360-3. 38. Maes M, Smith R, Christophe A, Vandoolarghe E, Vangastle A, Neels H, Demendts P, Wauters A, Meltz HY. Lower serum high density lipoprotein cholesterol (HDL-C) in major recurrent depressive disorder and in depressed men with serious suicidal attempts: relationship with immune inflammatory markers. ActaPsychiatrica Scandinavia 1997; 95(3): 212-221. 39. Markovitz J H, Smith D, Raczynski J M, Oberman A, Williams O D, Knox S, Jacobs DR . Lack of relations of hostility, negative affect, and high-risk behavior with low plasma lipid levels in the Coronary Artery Risk Development in Young Adults Study. Arch Intern Med. 1997; 157: 1953-9. 40. McCallum J, Simons L, Simons J, Friedlander Y. Low serum cholesterol is not associated with recurrent depressive disorder in the elderly: data from an Australian community study. Aust NZ J Med. 1994; 26:561-4. 41. Milan M T, Jelena D, Sanja M, Tihomir M and Bratislava T. Influence of red clover-derived isoflavones on serum lipid profile in postmenopausal women. JObstetGynaecolRes.Dec 2009; 35(6):1091-1095. 42. Mudali S, Dobs AS, Ding J, Jingzhong D, Cauley JA, Moyses S and Golden SH. Endogenous postmenopausal hormones and serum lipids: the Atherosclerosis Risk in Communities Study. Journal of Clinical Endocrinology and Metabolism. 2005; 90: 1202–1209. 43. Naito H K: Cholestrol. Clin Chem.1984; 1194-11206. 44. Naito H K: HDL Cholestrol.Clin Chem.1984; 1207-1213. 45. Olusi S O, Fido A A. Serum Lipid Concentration in patients with major depressive disorder. Biol Psychiatry. 1996; 40:1128-31. 46. Ossewaarde ME, Bots ML, van der Schouw YT, Thijssen JHH, Westerveld T, de Jong FH and Grobbee DE. Plasma and urinary sex hormones are differently related to lipids in healthy postmenopausal women. Maturitas. 2003; 44: 181–187 47. Papakostas GI, Petersen T, Sonawalla SB, Merens W, Iosifescu DV, Alpert JE, Fawa M and Nerenberg AA. Serum cholesterol in treatment – resistant depression. Neuropsychobiology. 2003; 47(3): 146 – 51. 48. Parry B L, Meliska C J, Martinez L F, Basavaraj N and Zirpoli G G. Menopause: neuroendocrine changes and hormone replacement therapy. J Am Med Womens Assoc. 2004 Spring; 59(2): 135-45. 49. Paterson ME, Sturdee DW, Moore B and Whitehead TP. The effect of menopausal status and sequential mestranol and norethisterone on serum cholesterol, triglyceride and electrophoretic lipoprotein patterns. Br J Obstet Gynaecol. 1979 Oct; 86(10): 810-5. 50. Schindler TH, Campisi R, Dorsey D, Prior JO, Olschewski M, Sayre J, Schelbert HR. Effect of hormone replacement therapy on vasomotor function of the coronary microcirculation in post-menopausal women with medically treated cardiovascular risk factors. Eur Heart J. 2009 Apr; 30(8):978-86. Doi: 10.1093/eurheartj/ehp013. Epub 2009 Feb 26 51. Shin M H. A study on the relationship between the climacteric symptoms and recurrent depressive disorder in menopausal women who have received hormonal replacement therapy. Master thesis.2001; Soonchunhyang University, Onyang. 52. Stevenson J C, Crook D, Godsland I F. Influence of age and menopause on serum lipids and lipoproteins in healthy women. Atherosclerosis. 1993; 98:83-90. 53. Stevenson J C, David C and Ian F G. Influence of age and menopause on serum lipids and lipoproteins in healthy women. Atherosclerosis.1993; 98(1): 83-90. 54. Sung, M H. An analysis of the relationship between climacteric symptoms and recurrent depressive disorder of middle-aged women. Korean J Women Health Nurs.2000; 6(4): 465-476. 55. Soares C N. Newyork, Arlington, V A: American Phycriatic Publishing; 2004. Perimenopause related mood disturbance: An update on risk factors and novel treatment strategies available. In: meeting programs and abstracts. Psychopharmacology and reproductive transitions symposium. American psychiatric association 157th annual meeting; May 1-6, 2004; pp51-61 56. Wood N F and Mitchell E S. Patterns of depressed mood in midlife women: Observation from the Seattle midlife women’s health study. Res Nurs Health. 1996; 19: 111-123.
Incidence, risk factors and microbiological profile of Surgical Site Infections in cardiac surgery patients
A K Baburajan, T S Shailaja, C K Shibu
Objective: To find out the incidence of surgical site infections(SSI) in cardiac surgery patients, the organisms responsible and the risk factors associated with such infections. Materials and methods: The study is conducted in 1000 consecutive adult patients who underwent cardiac surgeries between January 2011 and August 2015 in a cardiac surgical department attached to a teaching hospital in Central Kerala, India. Results: SSIs were diagnosed in 1.8% of the patients (18 of 1,000). Of these, 15 were superficial wound infections and three were mediastinitis and all got cured with conservative management without any mortality. Culture was positive in 13 cases and the most commonly isolated pathogen was Staphylococcus spp. Though age > 60 years and male sex predisposed to SSIs, these were not statistically significant. 13 of our 18 SSI patients were diabetics. Conclusion: The incidence of surgical site infections in this centre is comparable with other studies from India as well as abroad which range from 0.53% to 18.7% [1, 2, 3, 4].
1. Jonathan T Tan, Kristina Coleman, Sarah Norris, Jayashree Mapari, Satyanand Shastri, Laurent Metz. Surgical-site infection in India: A systematic review of the incidence and economic burden .htanalysts, www. htanalysts.com 2. Sanjeev Singh, Murali Chakravarthy, Victor Daniel Rosenthal, Sheila N. Myatrad, Arpita Dwivedy et al. Surgical site infection rates in 6 cities of India: findings of the International Nosocomial Infection Control Consortium (INICC). International Health : doi:10.1093/inthealth/ihu089 3. Lepelletier D, Perron S, Bizouarn P, Caillon J, Drugeon H, Michaud JL, Duveau D. Surgical-site infection after cardiac surgery: incidence, microbiology, and risk factors. Infect Control Hosp Epidemiol. 2005 May; 26(5):466-72. 4. Manoj Kumar Sahu, Bharat Siddharth, Arin Choudhury, Sreenivas Vishnubhatla, Sarvesh Pal Singh, Ramesh Menon, Poonam Malhotra Kapoor, Sachin Talwar, Shiv Choudhary, Balram Airan. Incidence, microbiological profile of nosocomial infections, and their antibiotic resistance patterns in a high volume Cardiac Surgical Intensive Care Unit Year: Annals of Cardiac Anaesthesia .2016 ; 19 (2): 281-287 5. Ahmed Abdulaziz Abuzaid1, Mahmood Zaki2, Habib Al Tarief Potential risk factors for surgical site infection after isolated coronary artery bypass grafting in a Bahrain Cardiac Centre: A retrospective, case-controlled study . Heart Views. 2015; 16 ( 3) : 79-84. 6. Heilmann C, Stahl R, Schneider C, Sukhodolya T, Siepe M, Olschewski M, et al. Wound complications after median sternotomy: A single-centre study. Interact Cardiovasc Thorac Surg 2013;16: 643-8. 7. Itagaki S, Cavallaro P, Adams DH, Chikwe J. Bilateral internal mammary artery grafts, mortality and morbidity: An analysis of 1 526 360 coronary bypass operations. Heart 2013;99:849-53 8. Parissis H, Al-Alao B, Soo A, Orr D, Young V. Risk analysis and outcome of mediastinal wound and deep mediastinal wound infections with specific emphasis to omental transposition. J Cardiothorac Surg 2011;6:111 9. Jonkers D, Elenbaas T, Terporten P, Nieman F, Stobberingh E. Prevalence of 90-days postoperative wound infections after cardiac surgery. Eur J Cardiothorac Surg 2003;23: 97–102.CrossRef,PubMed,Web of Science® Times Cited: 10. Sharma M, Berriel-Cass D, Baran J Jr. Sternal surgical-site infection following coronary artery bypass graft: prevalence, microbiology, and complications during a 42-month period. Infect Control Hosp Epidemiol 2004;25: 468–71.CrossRef,PubMed,Web of Science® Times Cited: 20 11. Tegnell A, Aren C, Ohman L. Coagulase-negative staphylococci and sternal infections after cardiac operation. Ann Thorac Surg 2000;69: 1104–9. 12. Gårdlund B, Bitkover CY, Vaage J. Postoperative mediastinitis in cardiac surgery – microbiology and pathogenesis. Eur J Cardiothorac Surg 2002;21: 825–30. 13. Quenia Cristina Gonçalves da Silva; Maria Helena Barbosa .Risk factors for surgical site infection in cardiac surgery. Acta Paulista de Enfermagem On-line version ISSN 1982-0194 Acta paul. enferm.vol.25 no.spe2 São Paulo 2012 http://dx.doi.org/10.1590/S0103 21002012000900014 14. Filsoufi F, Castillo JG, Rahmanian PB, Broumand SR, Silvay G, Carpentier A, et al Epidemiology of deep sternal wound infection in cardiac surgery. J Cardiothoracic Vasc Anesth. 2009; 23(4):488-94. 15. Ennker IC, Malkoc A, Pietrowski D, Vogt PM, Ennker J, Albert A. The concept of negative pressure wound therapy (NPWT) after poststernotomy mediastinitis – a single center experience with 54 patients. J Cardiothorac Surg. 2009; 4:5. 16. Risnes I, Abdelnoor M, Almdahl SM, Svennevig JL. Mediastinitis after coronary artery bypass grafting risk factors and long-term survival. Ann Thorac Surg. 2010; 89(5):1502-9 17. Ahmed D, Cheema FH, Ahmed YI, Schaefle KJ, Azam SI, Sami SA, et al Incidence and predictors of infection in patients undergoing primary isolated coronary artery bypass grafting: a report from a tertiary care hospital in a developing country. J Cardiovasc Surg (Torino). 2011; 52 (1):99-104. 18. Talbot TR. Diabetes mellitus and cardiothoracic surgical site infections. Am J Infect Control 2005;33:353 19. Robinson PJ, Billah B, Leder K, Reid CM, ASCTS Database Committee. Factors associated with deep sternal wound infection and haemorrhage following cardiac surgery in Victoria. Interact Cardiovasc Thorac Surg 2007;6:167-71. 20. Filsoufi F, Castillo JG, Rahmanian PB, Broumand SR, Silvay G, Carpentier A, et al. Epidemiology of deep sternal wound infection in cardiac surgery. J Cardiothorac Vasc Anesth 2009;23:488-94. 21. Mangram AJ, Horan TC, Pearson ML, Silver LC, Jarvis WR. Guideline for prevention of surgical site infection, 1999. Hospital Infection Control Practices Advisory Committee. Infect Control Hosp Epidemiol. 1999; 20(4):247-78.