Poonam Khairnar, S. K. Nagle, Kartik Parelkar, Shubhangi Kedar, Bandu Nagarale
Introduction: Lipoid proteinosis is a rare autosomal recessive disorder, characterized histologically by infiltration of periodic acid Schiff-positive hyaline material into the skin, upper aerodigestive tract, and internal organs. Classical clinical features include skin scarring, beaded eyelid papules, and laryngeal infiltration leading to hoarseness. Usually, the hoarse voice is present at birth or in early infancy, as the first manifestation. In more severe cases, diffuse infiltration of the pharynx and larynx might cause respiratory distress, at times requiring tracheostomy. This paper reports a classical case of lipoid proteinosis with laryngeal and oral manifestations.
1. Heyl T. Geological study of lipoid proteinosis in South Africa. Br J Dermatol 1970; 83:338-40. [PubMed] 2. Hofer PA. Urbach-Wiethe disease (lipoglycoproteinosis; lipoid proteinosis; hyalinosis cutis et mucosae): a review. Acta Dermatol Venereol 1973; 53(Suppl 71):1-52. [PubMed] 3. van Hougenhouck-Tulleken W, Chan I, Hamada T, Thornton H, Jenkins T, McLean WHI, et al. Clinical and molecular characterization of lipoid proteinosis in Namaqualand, South Africa. Br J Dermatol 2004; 151:413-23. [PubMed] 4. Savage MM, Crockett DM, McCabe BF. Lipoid proteinosis of the larynx: a cause of voice change in the infant and young child. Int J Pediatric Otol 1988; 15:33-8. [PubMed] 5. Friedman L, Mathews RD, Swanepoel PD. Radiographic and computed tomographic findings in lipid proteinosis. A case report. S Afr Med J 1984; 65:734-5. [PubMed] 6. Kleinert R, Cervos-Navarro J, Kleinert G, Walter GF, Steiner H. Predominantly cerebral manifestation in Urbach-Wiethe’s syndrome (lipoid proteinosis cutis et mucosae): a clinical and pathomorphological study. Clin Neuropathol 1987; 6:43-5. [PubMed] 7. Hamada T, McLean WHI, Ramsay M, Ashton GHS, Nanda A, Jenkins T, et al. Lipoid proteinosis maps to 1q21 and is caused by mutations in the extracellular matrix protein 1 gene (ECM1). Hum Mol Genet 2002; 11:833-40. [PubMed] 8. Chan I. The role of extracellular matrix protein 1 in human skin. Clin Exp Dermatol 2004; 29:52-6. [PubMed] 9. Smits P, Ni J, Feng P, Wauters J, Van Hul W, Boutaibi ME, et al. The human extracellular matrix gene 1 (ECM1): genomic structure, cDNA cloning, expression pattern, and chromosomal localization. Genomics 1997; 45:487-95. [PubMed] 10. Mongiat M, Fu J, Oldershaw R, Oldershaw R, Greenhalgh R, Gown AM, et al. Perlecan protein core interacts with extracellular matrix protein 1 (ECM1), a glycoprotein involved in bone formation and angiogenesis. J Biol Chem 2003; 278:17491-9. [PubMed] 11. Grevers G. Manifestation of Urbach-Wiethe syndrome in ENT area. Laryngorhinootologie 1994; 73:543-4. [PubMed] 12. Hamada T, Wessagowit V, South AP, South AP, Ashton GHS, Chan I, et al. Extracellular matrix protein 1 gene (ECM1) mutations in lipoid proteinosis and genotype-phenotype correlation. J Invest Dermatol 2003; 120:345-50. [PubMed] 13. Aziz MT, Mandaur MA, El-Ghazzawi, Belal AEA, Tallant AM. Urbach-Wiethe disease in ORL practice. J Laryngol Otol 1980; 94:1309-19. [PubMed] 14. Hamada T. Lipoid Proteinosis. Clin Exp Dermatol 2002; 27:624-9. [PubMed] 15. François J, Bacskulin J. Manifestations oculaires du syndrome d’Urbach Wiethe. Opthalmologica 1968; 155:433-8. [PubMed] 16. Arnold HL, Odom RB, James WD. Andrews’ disease of the skin. 8th Edn. Philadelphia: WB Saunders 1990. 17. Black MM. Lipoid proteinosis. In: Textbook of Dermatology. 5 th Edn. Oxford: Blackwell Scientific Publications; 1993. p. 2347-8. 18. Muda AO, Paradisi M, Angelo C, Mostaccioli S, Atzori F, Puddu P, et al. Lipoid proteinosis: clinical, histologic and ultrastructural investigations. Cutis 1995; 56:220-4. [PubMed] 19. Deckers MM, Smits P, Karperien M, Ni J, Tylzanowski P, Feng P, et al. Recombinant extracellular matrix protein 1 inhibits alkaline phosphatase activity and mineralization of mouse embryonic metatarsals in vitro. Bone 2001; 28:14-20. [PubMed] 20. Han Z, Ni J, Smits P, Underhill CB, Xie B, Chen Y, et al. Extracellular matrix protein 1 (ECM1) has angiogenic properties and is expressed by breast tumour cells. FASEB J 2001; 15:988-94. [PubMed] 21. Smits P, Poumay Y, Karperien M, Tylzanowski P, Wauters J, Huylebroeck D, et al. Differentation-dependent alternative splicing and expression of the extracellular matrix protein 1 gene in human keratinocytes. J Invest Dermatol 2000; 114:718-24. [PubMed] 22. Dunlevy JR, Hassell JR. Heparan sulphate proteoglycans in basement membranes: Perlecan, agrin and collagen XVIII. In: Iozzo RV, editor. Proteoglycans: Structure, Biology and Molecular Interactions. New York: Marcel Dekker Inc.; 2000. p. 275-336.
J B Leena, Mrudula, Sumanth Devaraju, Crysle Saldhana, Veronica
Introduction: Reliable platelet count is crucial for minimizing errors in coagulation studies. Platelet poor plasma is routinely used for coagulation studies as platelets interfere with coagulation. In this study randomly collected 30 samples of platelet poor plasma for routine coagulation studies received in haematology laboratory of Father Muller Medical College Hospital, Mangalore for a period of 3 months were analysed and counts were done by both manual method and automated methods. Platelets were analyzed by using Neubauer chamber and were compared with automated method. The study analysis showed that there was no significant difference between manual and automated platelet counts in platelet poor plasma. The intraclass correlation between automated and manual method showed significance with p value 0.00, and also showed an excellent agreement (ICC: 0.868) with a positive correlation between the two methods. Hence this study shows that both methods can be used to asses platelets in platelet poor plasma as a part of quality control procedure. Manual method is thus recommended even at places where automation is unavailable to improve quality of coagulation studies.
1. Cornbleet PJ, Myrick D, Judkins S, Levy R. Evaluation the cell DYN 3000 differential.AM J Clin Pathol.1992;98(6):603-14 2. Sultan A. Five minute preparation of platelet poor plasmafor routine coagulation testing. Eastern Mediterraneane Health journal. 2010;16(2):233-6 3. Latten M and RA Manning: Investigation of haemostasis in: Dacie and Lewis Practical haematology.10th edition, London, Churchill Livingston.2006;391-392 4. Dickerhoff R, Von Ruecker A. Enumeration of platelets by multiparameters flow cytometry using platelet specific antibody and flurescent reference particles. Clin Lab Haematol 1995;17(2):163-75 5. Ault KA. Plaetelet counting : Is there room for improvement?.Lab Hematol.1996;2:139-43 6. Hansler E, Fehr J, Keller H. Estimation of the lower limits of manual and automated platelet counting. Am J Clin Pathol.1996;105(6):782-7 7. Kim SY et al. Accuracy of platelet counting by Automated Hematologic Analyzer in Acute Leukemia and Disseminated intravascular coagulation. Am J Clin Pathol.2010;134:634-647 8. Brecher G, Cronkite EP. Morphology and enumeration of human blood platelets. J Appl Physiol.1950;3:365-77 9. Oliveira RA, Takadachi MM, Nonoyama K, Barretto CO.Is automated platelet counting still a problem in thrombocytopenic blood.Sao Paulo Medical Journal.2003;121:1-3 10. Brecher G, Schnciderman MA, Cronkite EP. The reproducibility and consistency of the platelet count. Am J Clin Pathol. 1953;23:15-26 11. Olivera RA, Takadchi MM, Nonoyama K, Barretto CO. The absolute recommendation of Neubauer methods for platelet counting instead of indirect method in sever thrombocytopenic patients. J Bras Pathol.Med.Lab.2003;39(2):139-141 12. Plebani M, Favaloro EJ, Lippi G. Patient safty and quality in laboratory and hemostasis testing:a renewed loop?Semin Thromb Hemost.2012;38:553-8 13. Bonar R, Emmanuel JFavaloro, Dorothy M, Adocock.quality in coagulation in haemostasis testing,Biomedica2010;20(2):184-99 14. Lippi G, Salvagno G, Montagna M, Franchini M, Guidi GC. Phlebotomyissues and quality improvement in results of laboratory testing. Clin Lab2006;52:217-230 15. Kalra J. Medical error: Impact on clinical laboratories and other critical area. Clin Biochem. 2004;37:1052-62 16. SA Anjali and S Amy. platelet function disorder. In DrSam Schulman Editor. Tretment of haemophilia.Sec Editon. World federation of Hemophilia.2008;1-3 17. Charie LA, Harrison P, Smith CU, Cobb JRC, et al. accuracy in the low platelet count range: A comparison of Automated platelet count on Beckman Coulter high volume Haematology analyzers with the ISLH/ICSH platelet reference method. Lab Hematol.2001;7:236-244.
H C Savitha, Sanjay Kumar C2, Deepthi H R
Background: Teenage pregnancy is a social problem worldwide with a serious implication on maternal and child health. The objective of this study is to compare the maternal and perinatal outcomes between teenage girls (age between 13 to 19 years) and pregnant adults (age between 20-29 years). Methods: We performed a retrospective analysis of case records on teenage pregnancies from January 2013 to June 2013 in the department of Obstetrics and Gynaecology, Mandya Institute Of Medical Sciences, Mandya, Karnataka, India, a referral tertiary care centre and teaching hospital with over 6000 deliveries annually. Pregnancy outcomes in girls aged 13-19 years were compared with those in women aged 20-29years. Results: The incidence of teenage pregnancy was 6.56%, majority of teenagers were primigarvida. The study showed that teenage mothers are at increased risk of having abortions, preeclampsia, low birth weight babies and perinatal mortality. Conclusion: Our study showed that risk of obstetric complication was no higher in adolescents than in adult women, but adolescent tended to have higher incidence of abortion, pre-eclampsia, low birth weight babies and perinatal mortality. Early booking and good antenatal care should improve the obstetric and perinatal outcome in teenage pregnancies
1. WHO. Adolescent pregnancy: issues in adolescent health and development. Geneva: WHO, 2004. 2. Cibula Dwomen’s contraceptive practices and sexual behavior in Europe. Eur J Contracept Reprod Health Care. 2008 Dec;13(4):362-75 3. Prianka Mukhopadhyay, R.N. Chaudhuri, Bhaskar Paul. Hospital-based Perinatal Outcomes and Complications in Teenage Pregnancy in India.J Health PopulNutr2010 Oct; 28(5):494-500. 4. KD, Chauhan M. Outcomes of Adolescent Pregnancy at Kathmandu University Hospital, Dhulikhel Hospital. Kathmandu Univ Med J 2011; 33(1):50-3. 5. Supanan Chairaj, KasornTosang, SuvannaAsavapiriyanont, Uraiwan Chotigeat. Outcome of Teenage Pregnancy in Rajavithi Hospital. J Med Assoc Thai 2010; 93(1):1-8. 6. Suwal A. Obstetric and Perinatal Outcome of Teenage Pregnancy. J Nepal Health Res Counc 2012 Jan; 10(20):52-6. 7. Vorapong Phupong, KengSuebnukarn. Obstetric Outcome in Nulliparous Young Adolescents. Southeast Asian J Trop Med Public Health 2007 Jan; 38(1):141-145. 8. M.C. Jolly, N. Sebire, J. Harris, S. Robinson, L. Regan. Obstetric Risks of Pregnancy in Women Less Than 18 Years Old. ObstetricGynecol 2000; 96(6):962-6. 9. Sabry M. Hammad, RedaQ. Al-Enazi. Does teenage pregnancy affect obstetric outcomes.The Egyptian Journal of Community Medicine.2010 July; 26(3):25-35. 10. ChutatipTantayakom, JaparathPrechapanich. Risk of Low Birth Weight Infants from Adolescent Mothers: Review Case Study in SirirajHospital. Thai Journal of Obstetrics and Gynecology April 2008; 16(2):103-106. 11. Nusrat Shah, Dileep Kumar Rohra, SamiaShuja, Nagina Fatima Liaqat, Nazir Ahmad Solangi, Kelash Kumar et al. Comparison of obstetric outcome among teenage and non-teenage mothers from three tertiary care hospitals of Sindh, Pakistan. J Pak Med Assococt2011; 61(10):963-967. 12. Nathalie A, Fleming, XiaowenTu, Amanda Y. Black. Improved Obstetrical Outcomes for Adolescents in a Community- Based Outreach Program: A Matched Cohort Study. J ObstetGynaecol Can 2012; 34(12):1134-1140. 13. CandanIltemir DUVAN, NilgunOzturk TURHAN, IlknurInegol GUMUS, Hilal YUVACI, Elif GOZDEMIR. Adolescent Pregnancies: Maternal and Fetal Outcomes. The New Journal of Medicine 2010; 27:113-116. 14. Bhalerao AR, Desai SV, Dastur NA, Daftary SN. Outcome of teenage pregnancy.J Postgrad Med 1990; 36:136-9. 15. Siddhartha Yadav, DilipChoudhary, Narayan K.C.,Rajesh Kumar Mandal, Achyut Sharma, Siddharth Singh Chauhan et al. Adverse Reproductive Outcomes Associated With Teenage Pregnancy. McGill journal of medicine 2008;11(2):141-1 16. Dutta I, et al Maternal and perinatal outcome in teenage vs. vicenarianpimigravidae- a cinical study. J ClinDiagn Res. 2013 Dec; 7(12): 2881-4.
J B Leena, M B Sandeep, Crysle Saldanha, Megha, Krishnaprasad H V
Background: Lesions of the scalp are rare comprise a heterogeneous assemblage varying from benign to malignant. The clinical experience regarding these rare lesions is limited .Hence there is corresponding paucity of data in the medical literature regarding the incidence and prevalence of scalp lesions with an extremely wide range of pathology appearances. This study is intended to determine the distribution of both benign and malignant lesions. Materials and Methods: This is a 2 year (2010 2012) retrospective study of all scalp lesions received at our referral teaching hospital, Father Muller medical college, Mangalore, India. All the histopathologically proven cases of scalp lesions were reviewed and clinical details were obtained from the archives. Age, gender, and histology of all the specimens were evaluated Results: Among the 45 cases, 39 (87%)) cases were benign lesions and remaining 6 (13%) were malignant lesions. Most common clinical presentation was a scalp swelling or a nodule. The male to female ratio among the benign tumors was 1.5:1. Age distribution in benign lesions was 20-40 years whereas malignant lesions were seen in the elderly. Trichelemmal cyst was the most common benign lesion and basal cell carcinoma was the most common malignant lesion. Conclusion: Scalp lesions are rare, benign tumors are more common and malignant tumors are not uncommon. In each case of a scalp lesion a broad differential diagnosis has to be considered. Improved clinical experience and hospital attendance with more comprehensive reporting would yield more representative data.
1. Dawber RPR. Nevi, tumors and cysts of the scalp. In Diseases of the hair and scalp, 3rd ed., eds R. Dawber. Oxford: Blackwell Scientific Publications; 1997. P.528-63. 2. Phieffer LS, Jones EC, Tonneson MG, Kriegel DA. Melanoma of the scalp: an underdiagnosed malignancy?Cutis 2002; 69:362-64. 3. Manchanda Y, Khalawany El, Al-Mutairi N. A clinicopathologico-epidemiological study of non-Melanoma malignant skin tumors of the scalp. The Gulf Journal of Dermatology and Venereology. 2012; 19:22-27. 4. Saikia B, Dey P, Saikia U N, Das. A Fine Needle aspiration cytology of metastatic scalp nodules. Acta cytol.2001; 45:537-541. 5. Carson H J, Gattuso P, Castelli MJ, Reddy V. Scalp lesions. A review of histopathologic and fine-needle aspiration biopsy findings. Am J Dermatopathol.1995; 17:256-9. 6. Fong PH, Lee ST, Lim Tan SK. Primary scalp cancer in Singapore. Ann Acad Med Singapore 1986; 15:67-70. 7. Minor LB, Panje WR. Malignant neoplasms of the scalp: etiology, resection, and reconstruction. Otolaryngol Clin North Am 1993; 26:279-93. 8. Prasoon D. Follicular carcinoma of thyroid gland presenting as scalp metastasis. Acta Cytol 1998; 42:451-52. 9. Siddha, Buddrukar and Shet T et al., Malignant pilar tumours of the scalp: A case report and review of literature, J Can Res Ther 3 (2007) 240–243. 10. Adu E J. K. Tumours of the Scalp: A Review of Ten Cases. Journal of US-China Medical Science. 2013; 10: 57–62. 11. Chang S J , Sims J, Murtagh F R,Mc Caffrey J C, Messina J L . Proliferating Trichilemmal Cysts of the Scalp on CT. Am J Neuroradiol . 2006; 27:712–14. 12. Conley JJ. Malignant tumors of the scalp. I. Analysis of 92 cases of malignant epithelial and somatic tumors of the scalp. Plast Reconstr Surg 1964; 33:1-15. 13. Katz TM, Silapunt S, Goldberg LH, Jih MH, Kimyai-Asadi A. Analysis of 197 female scalp tumors treated with Mohs micrographic surgery. J Am Acad Dermatol 2005; 52:291-94. 14. Connor and Cohen. Cutaneous metastases of breast carcinoma presenting as neoplastic alopecia, South Med J 102: 2009; 385–389.
Khetre R R, Bansude M E, Dode C R, Umbare R B, Chormale D
Hanging is very common mode of suicide particularly in young adults. Its incidence in India is approximately 25% of total cases of suicide. It is a painless method of committing suicide and death is instantaneous. However, a few cases have been reported in literature in which death has occurred after certain period of time or patient has survived after prolonged resuscitative measures. Here we present two cases of delayed deaths in hanging with the victims eventually succumbing to one or more of the fatal complications after surviving for different time duration.
1. Aggarwal NK, Kishore U, Agarwal BB. Hanging-delayed death (a rare Phenomenon). Med Sci Law. 2000 Jul; 40:270-2. 2. Kumar M, Mandhyan R, Shukla U, Kumar A, Rautela RS. Delayed pulmonary oedema following attempted suicidal hanging- a case report. Indian J Anaesth. 2009 Jun; 53(3): 355-7. 3. Kumar V. Delayed hanging death: a case report. J Pak Med Assoc. 2007 Jan; 57(1): 39-41. 4. Guharaj PV. Forensic Medicine. 2nd ed, Hyderabad: Hyderabad University Press; 2009, p. 177. 5. Nithin MD, Manjulatha B, Pramod Kumar GN, Sameer S (2011) Delayed Death in Hanging. J Forensic Res S1:001. doi:10.4172/2157-7145. 6. Vander KL, Wolfe R. The emergency department management of near hanging victims. J Emerg Med. 1994; 12: 285-92. 7. Kumar RR, Punitha R. Delayed causes of death in hanging: an autopsy study. J Punjab Acad Forensic Med Toxicol. 2014, 14(1):32-35. 8. Maxeiner H. Delayed death following strangulation (hanging). Arch Kriminol 1987; 180:161-71. 9. Bhoi SB, Tumram NK, Shinde DK, Chandekar KS. Delayed death after attempted suicide by hanging. J Punjab Acad Forensic Med Toxicol. 2013, 13(2):86-87. 10. Hausmann R, Betz P. Delayed death after attempted suicide by hanging. Int J Legal Med. 1997; 110(3): 164-6. 11. Vaghela DR, Patel PR. Late death in case of hanging- a case report. Anil Aggrawal’s Internet Journal of Forensic Medicine and Toxicology. 2009; Vol. 10, No.1 (January- June 2009). 12. Verma SK, Agarwal BB. Accidental hanging with delayed death in a lift. Med Sci Law. 1999; 39(4): 342-4. 13. Fremingston K. Marak & R. Balaraman. Delayed death in hanging. J Indian Acad Forensic Med. 2008; 30(3): 149-150. 14. Venkatesaprasanna J, Parmar P, Balaraman R. Delayed death after survival period of 28 days in case of hanging- a rare case report. IJMPS. 2012; 3(4): 23-6. 15. Fremont RD, Kallet RH, Matthay MA, Ware LB. Post obstructive pulmonary oedema: a case for hydrostatic mechanisms. Chest 2007; 131:1742-6. 16. Oswalt CE, Gates GA, Holmstrom MG. Pulmonary oedema as complication of acute airway obstruction. JAMA. 1997; 238: 1833-5.
Rajeshwari K., Ashok Kumar Behera
Introduction: Anaemia is the commonest medical disorder in pregnancy and has a varied prevalence, aetiology and degree of severity in different populations. Anaemia during pregnancy has been shown to be associated with a two-fold risk for preterm delivery and a three-fold risk for low birth-weight as well as maternal mortality. The World Health Organization (WHO) estimates that anaemia contributed to approximately 20% of the 515,000 maternal deaths worldwide in 1995. Keeping these facts in view, the present study embodies the observation of 250 cases among 400 cases attending labour room of S. C. B. Medical College, Cuttack (Orissa), giving an incidence of 62.5%, which is quite high in comparison to developed countries.
1. Schwartz WJ, Thurnau GR.Iron Deficiency Anaemia In Pregnancy. Clin Obstet Gynecol 1995; 38: 443- 454 2. WHO/UNICEF/UNU. Indicators for assessing iron deficiency and strategies for its prevention: WHO draft, Geneva. WHO , 1996 3. WHO, Report of WHO group of experts on Nutritional Anaemias. Technical report series no 503. Geneva WHO1972. 4. World Health Organization.United Nations Children's Fund UNU. Iron deficiency anemia; Assessment, Prevention and Control; A guide for programme managers. World Health Organization, Geneva, 2001. 5. Geneva WHO1DWNM922. The Prevalence of Anaemia in Women. WHO 1992; 1-99. 6. WHO. Revised 1990. Estimates of Maternal Mortality. WHO/FRH/MSM/96.1. Geneva: WHO, 1996 7. Turmen T, Abou Zahr C. Safe Motherhood. Int. J Gynecol Obstet 1994; 46: 145 – 153. 8. Bhatt R. Maternal mortality in India, FOGSI-WHO study. J.Obstet Gynecol India 1997; 47: 207-214. 9. Viteri FE. The consequences of iron deficiency and anaemia in pregnancy. Adv Exp Med Biol 1994; 352 : 127 – 139 10. Prema K, Neela KS, Ramalakshmi BA. Anaemia and adverse obstetric outcome. Nutri Rep Int 1981; 23: 637 – 643 11. Lozoff B, Jimenez E, Wolf AW. Long term developmental outcome of infants with iron deficiency. N Endl J Med 1992 ; 325: 687 – 694 12. Monika Malhotra, J B Sharma, S Batra, S. Sharma, N.S. Murthy, R.Arora, International Journal Of Gynecology and Obstetrics, Volume 79, Issue 2, Nov. 2002, pages 93-100 13. CO Aimakhu, O Olayemi. West African Journal of Medicine > Vol 22, No 1 (2003) 14. J I Brian-D Adinma, Joseph I Ikechebelu, UN Onyejimbe, G Amilo, Echendu Adinma. Tropical journal of Obstetrics and Gynecology,Vol 19, No 2 (2002) 15. Jai Bhagwan Sharma, Dimple Soni, Nandagudi Srinivasa Murthy, Monika Malhotra. Department of Obstetrics and Gynecology, Department of Biostatistics, Maulana Azad Medical College, New Delhi, India .Journal of Obstetrics and Gynaecology Research, Volume 29, Issue 2, pages 73–78, April 2003 16. Dairo MD, Lawoyin TO, Afr J Med Med Sci. 2004 Sep; 33(3):213-7. 17. U. Rusia, C. Flowers, N. Madan, N. Agarwal, S. K. Sood and M. Sikka. Annals of Hematology . 2005, Volume 78, Number 8, 358-363, DOI: 10.1007/s002770050529 18. Mary Glover-Amengor, W B Owusu, and BD Akanmori, Ghana Med J. 2005 September; 39(3):102–107.PMCID:PMC1790823. 19. Toteja GS, Singh P, Dhillon BS, Saxena BN, Ahmed FU, Singh RP, Prakash B, Vijayaraghavan K, Singh Y, Rauf A, Sarma UC, Gandhi S, Behl L, Mukherjee K, Swami SS, Meru V, Chandra P, Chandrawati, Mohan U. Food Nutr Bull. 2006 Dec; 27(4):311-5. 20. Anorlu RI, Oluwole AA, Abudu OO. J Obstet Gynaecol. 2006 Nov; 26(8):773-6. 21. Marahatta, R, Nepal Medical College Journal. 2007 Dec; 9(4): 270-4. 22. Riffat Jaleel, Ayesha Khan, Journal Of Surgery Pakisthan (International) 13(4) Oct- Dec 2008 23. M. Bukar , B. M. Audu, U. R. Yahaya and G. S. Melah. Anaemia in pregnancy at booking in Gombe, North-eastern Nigeria 2008, Vol. 28, No. 8 , Pages 775-778 (doi:10.1080/01443610802463835) 24. Parveen Rasheed, Manal R Koura, Badria K Al-Dabal, Suhair M Makki Department of Family and Community Medicine, College of Medicine, King Faisal University, Dammam, Saudi Arabia, date of web publication 24-Aug-2009 Ann Saudi Med [serial online] 2008 [cited 2011 Jun 28];28:449-52. 25. Maternal risk factors and anaemia in pregnancy: A prospective retrospective cohort study. J. A. Noronha, A. Bhaduri, H. Vinod Bhat, A. Kamath. February 2010, Vol. 30, No. 2, Pages 132-136. 26. Zuguo Mei, Mary E Cogswell, Anne C Looker, Christine M Pfeiffer, Sarah E Cusick, David A Lacher, and Laurence M Grummer-Strawn. 2011 American Society for Nutrition 27. Abel R, Rajarathnam J, Sampathkumar V. Anaemia in pregnancy. Impact of iron, deworming and IEC, RUSHA Dept. Tamilnadu: CMC Vellore 1999 28. Indian Council of Medical Research. Evaluation of the National Nutritional Anaemia Prophylaxis Programme. Task Force Study. New Delhi: ICMR, 1989 29. Sarin AR. Severe anaemia of pregnancy, recent experience. Int J Gynecol Obstet 1995; 50 (Suppl. 2): S45 – S49. 30. Brabin L, Nicholas S, Gogate A, Karande A. High prevalence of anaemia among women in Mumbai, India. Food Nutr Bull 1998; 19: 205 – 209.
Vaishali P. Ahire, Lakshmi Rajgopal
Introduction: The radial nerve anterior to the lateral epicondyle divides into superficial and deep terminal branches. Entrapment or compression neuropathy of the deep branch of radial nerve (DBRN) or posterior interosseous nerve (PIN) leads to radial tunnel syndrome or PIN syndrome. It may also be one of the differential diagnoses of lateral epicondylitis. This study was performed on 38 upper limbs of 19 formalin-fixed cadavers. In most of the instances it was found that the radial nerve divided 1.4 cm above the interepicondylar line (IEL). The nerve to extensor carpi radialis brevis (ECRB) arose at 1.2 cm from the IEL. We also observed the nature of some of the important structures which may compress deep branch of radial nerve. This knowledge is important for exploring elbow region during surgical decompression of DBRN.
1. Soubhagya RN, Lakshmi R et al: Extensor carpi radialis brevis origin, nerve supply and its role in lateral epicondylitis: Surg Radiol Anat. 2010; 32:207-211. 2. Eversmann WW: Operative hand surgery. 1988; 2nd Ed. Vol.2. Edinburgh: Churchill Livingstone. P 1454-1460. 3. Debouck C, Rooze M: The arcade of Frohse: an anatomical study: Surg Radiol Anat. 1995; 17:245 -248. 4. Fuss FK, Wurzl GH: Radial nerve entrapment at the elbow: surgical anatomy: J Hand Surg [Am]. 1991; 16:742-747. 5. Konjengbam M, Elangbam J: Radial nerve in the radial tunnel: anatomic sites of entrapment neuropathy: Clin Anat. 2004; 17:21-25. 6. Papadopoulos N, Paraschos A, Pelekis P: Anatomical observation on the arcade of Frohse and other structures related to the deep radial nerve: anatomical interpretation of deep radial nerve entrapment neuropathy: Folia Morphol (Praha). 1989; 37:319-327. 7. Prasartritha T, Liupolvanish P, Rojanakit A: A study of the posterior interosseous nerve (PIN) and the radial tunnel in 30 Thai cadavers: J Hand Surg [Am]. 1993; 18:107-112. 8. Riffaud L, Morandi X, Godey B, Brassier G, Guegan Y, Darnault P, Scarabin JM: Anatomic bases for the compression and neurolysis of the deep branch of the radial nerve in the radial tunnel: Surg Radiol Anat. 1999; 21:229-233.
Khetre R R, Batra A K, Shrigiriwar M B, Kuchewar S V, Jambure M P
Introduction: Sudden natural death, especially when it occurs in an apparently healthy person, can have a great impact on society. Sudden natural deaths undoubtedly constitute a significant portion of deaths which undergo autopsy for investigation of death. Therefore, a prospective autopsy based study of sudden natural non-traumatic deaths (SNND) was decided to determine age, sex and system wise involvement. Aims and Objectives: The study was aimed to find out the burden (percentage) of sudden natural non-traumatic deaths and also to determine age, sex and body system wise involvement. Material and Methods: This prospective autopsy based study was conducted in the Department of Forensic Medicine and Toxicology, Shri V. N. Government Medical College, Yavatmal, Maharashtra, India. During study period from 1st October, 2010 to 31st August, 2012, total 1711 medico-legal autopsies were conducted in the department, of which those cases which were turned out to be sudden natural non-traumatic deaths (SNND) were studied. Observations and Results: The burden (percentage) of SNND cases was 7.3% (125/1711). Total SNND cases were 125, out of which maximum number of cases i.e. 72 (57.6%) were seen in the age group of 21 to 50 years. The average age of SNND was 37.5 ± 18.5 years for both sexes. Amongst 125 cases, maximum i.e. 92 (73.6%) were males and 33 (26.4%) were females. The male to female ratio was 2.8:1. Out of total 125 cases of SNND, maximum i.e. 41 (32.8%) cases were of cardiovascular causes followed by 32 (25.6%) due to respiratory causes. 17 (13.6%) cases were of central nervous causes, 20 (16%) were of gastrointestinal causes, 05 (04%) due to genitourinary causes and 10 (08%) were of miscellaneous causes. System wise differences in male and female cases was found to be statistically significant (χ2=17.22, p= 0.004105). An age group wise difference in male and female cases was found to be statistically significant (χ2= 21.38, p= 0.003246) Conclusion: Sudden death was the most common indication in natural deaths for medico-legal autopsy. Burden of sudden natural non-traumatic death (SNND) cases was 7.3%. So, it is the need of time to implement necessary steps to reduce this burden. SNND cases had male preponderance and target age group for maximum SNND cases was 21 to 50 years. Cardiovascular system was most vulnerable. Survival period, rapidity of death and their frequent occurrence must be considered in planning emergency referral, transport and emergency and super speciality medical services to cope with immediate events prior to death.
1. Saukko P, Knight B. Knight’s Forensic Pathology. 3rd ed. London: Hodder Arnold; 2004. Chapter 25, The pathology of sudden death; p. 492-526. 2. Reddy KSN. The Essentials of Forensic Medicine and Toxicology. 29th ed. Hyderabad: K. Suguna Devi; 2010. 3. Nandy A. Principles of Forensic Medicine including Toxicology. 3rd ed. Kolkata: New Central Book Agency (P) Ltd; 2010. Chapter 6, Death and post mortem changes; p.221-86. 4. Udnoon J, Chirachariyavej T, Peonim V. Sudden Unexpected Deaths In Different Age Groups At Ramathibodi Hospital, Bangkok, Thailand: A Retrospective Autopsy Study During 2003-2007. Southeast Asian J Trop Med Public Health 2009; 40(1): 162-68. 5. Park K. Park’s Textbook of Preventive and Social Medicine. 20th ed. Jabalpur: M/s Banarsidas Bhanot Publishers; 2009. 6. Sarkioja T, Hirvonen J. Causes of sudden unexpected deaths in young and middle aged persons. Forensic Sci. Int. 1984; 24(4):247-61. 7. Siboni A, Simonsen J. Sudden unexpected natural death in young persons. Forensic Sci. Int. 1986; 31(3):159-66. 8. Zanjad NP, Nanadkar SD. Study of sudden unexpected deaths in medico-legal autopsies. Journal of Indian Academy of Forensic Medicine 2006; 28(1) ISSN: 0971-0973. 9. Rao DS, Yadhukul. Sudden and unexpected natural deaths- A four-year autopsy review. Journal of Punjab Academy of Forensic Medicine & Toxicology 2008; 8(2):21-3. 10. Chaturvedi M, Satoskar M, Khare MS, Kaigutkar AD. Sudden, unexpected and natural death in young adults of age between 18 and 35 years: A clinicopathological study. Indian Journal of Pathology and Microbiology 2011; 54(1):47-50. 11. Kuller L, Lilienfeld A, Fisher R. Sudden and unexpected deaths in young adults. JAMA 1966; 198(3):248-52. 12. Escoffery CT, Shirley SE. Causes of sudden natural death in Jamaica: A medico-legal (coroner’s) autopsy study from University Hospital of West Indies. Forensic Sci Int 2002; 129(2):116-21. 13. Meina Singh A, Subadani Devi S, Nabachandra H, Fimate L. Sudden deaths in Manipur – A preliminary study. JFMT 2002; 19(2):26-28. 14. Azmak AD. Sudden natural deaths in Edirne, Turkey, from 1984 to 2005. Med Sci Law 2007; 47(2):147-55. 15. Kumar V, San KP, Idwan A, Shah N, Hajar S, Norkahfi M. A study of sudden natural deaths in medico legal autopsies in University Malaya Medical Centre (UMMC), Kuala Lumpur. J Forensic Leg Med 2007; 14(3):151-4. 16. Kagne RN, Kamble SR, Godbole HV, Borde BS. Study of sudden natural deaths. JFMT 1999; 16 (1):31-3. 17. Thomas AC, Knapman PA, Krikler DM, Davis MJ. Community study of the causes of “natural” sudden death. BMJ 1988; 297:1453-56. 18. Anderson RE, Hill RB, Broudy DW, Key CR, Pathak D. A population-based autopsy study of sudden, unexpected deaths from natural causes among persons 5 to 39 years old during a 12-year period. Human pathology 1994; 25(12):1332-40. 19. Puranik R, Chow CK, Duflou JA, Kilborn MJ, Mcguire MA. Sudden death in young children. Heart Rhythm 2005; 2(12):1277-82. 20. Dikshit PC. Textbook of Forensic Medicine and Toxicology. 1st ed. New Delhi: Peepee Publishers and Distributors (P) Ltd; 2010. Chapter 11, Sudden and unexpected deaths; p.147-54. 21. Pillay VV. Textbook of Forensic Medicine and Toxicology. 15th ed. Hyderabad: Paras Medical Publisher; 2010. 22. Luke JL, Helpern M. Sudden unexpected death from natural causes in young adults. Arch Pathol 1968; 85(1):10-17. 23. Wentworth P, Jentz LA, Croal AE. Analysis of sudden unexpected death in southern Ontario, with emphasis on myocarditis. CMA Journal 1979; 120: 676-706. 24. Penttila antti. Sudden and unexpected natural deaths of adult male. An analysis of 799 forensic autopsies in 1976. Forensic Science International 1980; 16(3):249-59. 25. Fornes P, Lecomte D, Nicolas G. Sudden out-of-hospital coronary death in patients with no previous cardiac history. An analysis of 221 patients studied at autopsy. J Forensic Sci 1993; 38(5):1084-91. 26. De la Grandmaison GL, Durigon M. Sudden adult death: a medico-legal series of 77 cases between 1995 and 2000. Med Sci Law 2002; 42(3):225-32.
Shilpashree Y D, Suma M N, Devaki R N, Prashant V
Introduction: Oxidative stress resulting from enhanced free-radical generation and/or a decrease in antioxidant defenses has been implicated in the pathogenesis of diabetic retinopathy. This study was conducted to evaluate oxidative stress and antioxidant balance in diabeticretinopathy and to correlate this with glycemic control Method: Thirty patients with diabetic retinopathy and thirty age matched healthy controls were included in the study. Fasting blood glucose and glycosylated hemoglobin (HbA1C) were estimated to assess the severity of diabetes and the glycemic control respectively. Serum malondialdehyde (MDA) levels were assessed as a marker of lipid peroxidation and hence oxidative stress. Erythrocyte glutathione peroxidase (GPx) levels were assessed for antioxidant status. Results: HbA1c in patients with diabetic retinopathy compared to healthy control was statistically highly significant (p<0.000). Significant positive correlation was found between serum MDA levels and HbA1c (r = 0.387, p < 0.0001) in patients with diabetic retinopathy. There was statistically significant reduction in the Glutathione peroxidase levels. Further, MDA levels were inversely correlated with GPx (r = - 0.90, p < 0.0001) levels. Conclusion and summary: oxidative stress is greatly increased in patients suffering from diabetic retinopathy and is inversely related to glycemic control. This may be due to depressed antioxidant enzyme levels and may also be responsible for further depletion of antioxidant enzyme GPx. This worsens the oxidative stress and creates a vicious cycle of imbalance of free radical generation and deficit of antioxidant status in these patients which may lead to nervous system damage causing diabetic retinopathy. A good glycemic control is essential for prevention of diabetic retinopathy.
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M. S. Bhonde, A. H. Bagade, A. D. Dhanavijay
Introduction: Yoga helps in improvement of physical strength and neuromuscular co-ordination. Suryanamaskar (Sun Salutation) is an integral part of Yogic exercises. It involves exercising almost all the muscles and joints of the body. Hand grip strength (HGS) is not only a measure of the strength of muscles of the upper limb but also neuromuscular co-ordination. The objective of the study was to evaluate the effect of suryanamaskar on HGS in healthy adult subjects. 120 newly enrolled healthy volunteers (62 females) in the age group of 20 to 40 years were selected from a reputed Yoga canters in Mumbai. HGS was measured using hand grip dynamometer set at second handle position at 0º and 90º elbow flexion before the start of study. The subjects were then instructed to practice suryanamaskar for 30 minutes daily for 12 weeks. HGS was measured after completion of study period. Paired t test was used for analysis of data. It was observed that the mean HGS before study was 27.73 which increased significantly to 30.28 after the practice of suryanamaskar (p< 0.001). We conclude that the increase in hand grip strength is probably due to strengthening of the muscular system of the body also involving upper limb muscles due to stimulation of muscles during the isometric contraction maintained during the steady state of yogic postures and improved co-ordination as a result of practice of suryanamaskar.
1. Bal B.S, Kaur P.J: Effects of selected Asanas in hatha Yoga on agility and flexibility level: J Sport Health Res, 2009; 1(2):75-87 2. Rantanen T, Guralnik JM, Foley D, et al: Midlife hand grip strength as a predictor of old age disability: JAMA 281 (6): 558–60 3. Raghuraj P, Nagarathna R, Nagendra HR, Telles S: Pranayama increases grip strength without lateralized effects: Indian J Physiol Pharmacol. 1997 Apr; 41(2):129-33. 4. Dash M, Telles S: Improvement in hand grip strength in normal volunteers and rheumatoid arthritis patients following Yoga training: Indian J Physiol Pharmacol. 2001 Jul; 45(3):355-60. 5. Mandanmohan, Jatiya L, Udupa K, Bhavanani AB: Effect of Yoga training on handgrip, respiratory pressures and pulmonary function: Indian J Physiol Pharmacol. 2003 Oct; 47(4):387-92. 6. Udupa KN, Singh RH, Settiwar RM: Physiological and biochemical studies on the effect of yogic and certain other exercises: Indian J Med Res. 1975 Apr; 63(4):620-4. 7. Selvamurthy W, Ray US, Hegde KS, Sharma RP: Physiological responses to cold (10 degrees C) in men after six months' practice of Yoga exercises: Int J Biometeorol. 1988 Sep; 32(3):188-93. 8. Ray US, Mukhopadhyaya S, Purkayastha SS, Asnani V, Tomer OS, Prashad R, Thakur L, Selvamurthy W: Effect of yogic exercises on physical and mental health of young fellowship course trainees: Indian J Physiol Pharmacol. 2001 Jan; 45(1):37-53.
Shekhar P Shiradhonkar, Aradhana Arvind Deshmukh, S M Handergulle
Introduction: The present study was conducted at S. R. T. R. Medical College, Ambajogai. Fifty hypertension cases and 50 controls were taken according to different age groups. Platelet aggregation, plasma fibrinogen level and euglobulin clot lysis time were compared with age matched control and also cases were compared amongst themselves depending upon the duration of hypertension. Analysis of results showed a statistically significant increase in platelet aggregation and plasma fibrinogen level in all the hypertensive cases when compared with age matched control. Euglobulin clot lysis time showed a statistically significant decrease (increase in fibrinolysis) in all the hypertensive cases when compared with age matched control. When the increase in Euglobulin clot lysis time (decrease in fibrinolysis) was correlated with duration of hypertension, it was found that the decrease in fibrinolysis varies directly with increase in duration of exposure.
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Nisha J Marla, Ramesh Naik, Hilda Fernandes, Jayaprakash C S, Kirana Pailoor
Aims and Objectives: 1)To evaluate histopathological findings in Lupus Nephritis and to classify it according to the International Society of Nephrology/Renal Pathology Society (ISN/RPS 2003) classification system for Lupus Nephritis. 2) To correlate the histological findings with the disease process. Materials and Methods: Renal biopsy performed at a tertiary care centre and Hospital in South India, for duration of 2 years was collected along with relevant clinical data. Ultrasound guided renal biopsy was performed and tissue were processed routinely and the slides were stained with Hematoxylin and Eosin. Special stains that is per iodic acid Schiff (PAS) and Methanamine silver (PASM) were performed for all cases. All the cases were correlated with Immunofluroscence (IF) study. 30 Renal biopsies were performed, 21 cases were of Primary Glomerulonephritis and 9 cases were Secondary Glomerulonephritis out of which 6 were cases of Systemic Lupus Erythematosus. Renal Biopsy of all the cases of SLE was classified according to ISN/RPS classification system. Results: Out of 30 cases (n=30), Primary glomerulonephritis (GN) accounted for 70% and secondary GN accounted for 30%. Among secondary glomerulonephritis predominant lesion were systemic lupus nephritis (66.7%) followed by diabetes mellitus (22.2%) and Amyloidosis (11.1%). In secondary GN the predominant lesion was Systemic Lupus Nephritis, Out of 6 (100%) cases of Lupus Nephritis, 4 (66.7%) cases were class IV, 1(16.7%) case was class II and 1(16.7%) case was class V. Conclusion: Management goals in patients with Lupus Nephritis include early diagnosis and appropriate therapy whilst preserving overall Kidney function without undue side effects and prevent irreversible damage. ISN/RPS 2003 classification tends to correlate with clinical syndrome and provide valuable information regarding prognosis and guideline for treatment. ISN/RPS classification system also intends to facilitate a higher degree of reproducibility, resulting in a better patient care. A renal biopsy examined by routine light microscopy, Immunofluroscence and electron microscopy contributes toward diagnosis, prognostic information, and appropriate management.
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Shetty PN, Ray B, D’Souza AS, Sushma RK, Nayak D, Rao ACK, Chakraborti S
Phthalate esters are plasticizers widely used in the manufacture of plastics. Di iso butyl phthalate (DIBP) is used as a plasticizers, ranging from the plasticization of PVC to the production of paints, printing inks and adhesives. Therefore, DIBP exposure in people in adhesive industries and pharmaceutical industries are higher in comparison to general population where it is low. Major route of excretion of DIBP is through urine, with some excretion in the faeces, presumably due to biliary excretion. Aim of this study was to determine the effect of single dose of DIBP on developing liver of Wistar rat. One hundred and eight adult pregnant Wistar rats were divided into control and experimental groups. Rats in experimental group were given DIBP on10, 12and 14day of gestation at 0.375, 0.75 and 1.25ml/kg body weight doseintraperitoneally in a single dose.Sections of liver collected on day 21of gestation were stained with haematoxyline and eosin and examined histologically.The remarkable histo-pathological changes were not observed, when exposed to above dose of DIBP.But, there was a significant reduction in the weight of foetalrat liver, when mother rat exposed to DIBP on 10thday of gestation compared to 12th and 14th days. As pregnant women are constantly exposed, effect of DIBP on the liver of a developing fetus would denote the consequence in future generation.
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Bhushan Mahajan, S. K. B. Patil, Vaishali Mahajan
Introduction: Prolonged hyperglycemia is known to cause an increase in levels of non enzymatically glycosylated proteins which is thought to contribute to long term complications of disease by enzyme inactivation, inhibition of binding of regulatory molecules, decreased proteolysis and cross-linking of glycated proteins. In present study, fructosamine and albumin levels were measured in normal healthy controls and Diabetic patients before and after supplementation of Multi-vitamin multi-mineral tablets. Serum fructosamine level was decreased significantly in diabetic patients after multi-vitamin multi-mineral supplementation.
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