Biomedical subjects
Publications and source records attributed to D Amarapurkar.
Gastric lipoma is one of the rare benign gastric tumors. Its preoperative diagnosis obviates the need of an extended gastrectomy. We report a case of gastric lipoma who presented with symptoms of dyspepsia and was treated by surgical gastrectomy and tumour enucleation.
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AIM: To study the significance of hepatitis C genotypes in relation to severity of liver disease, progression of liver disease and response to treatment. METHODS: Sixty one consecutive patients with hepatitis C infection were evaluated with detailed history, clinical examination, biochemical, imaging and virological profile, liver histology whenever feasible. Hepatitis C infection was confirmed with AntiHCV third generation ELISA assay. HCVRNA by PCR and HCV genotyping by direct sequencing. RESULTS: Demographic profile of patients was as M:F 36:25, mean age 46.3 +/- 13.6 years (range 10 to 70 years). Clinical presentations of these patients were as cirrhosis 23, cirrhosis with HCC 3, chronic hepatitis 22, acute hepatitis 4, asymptomatic with normal enzymes nine. Distribution of genotypes was as follows; 13/61 (21%) genotype I, 15/61 (25%) genotypes II and 33/61 (54%) genotype III. Cirrhosis was significantly common in genotype I (77%) when compared to genotype II and III (33%); p < 0.001. Mean time of presenting as cirrhosis was much faster in genotype I (8.7 +/- 6.7 years) as compared to other genotypes (type II 12.8 +/- 4.2 years and genotype III 15.8 +/- 6.9 years). Genotype distribution in CRF and renal transplant patient was genotype I 8/23 (35%), genotype II 5/23 (22%) and genotype III 10/23 (43%). Fourteen patients were treated with interferon and ribavarine combination for one year. Sustained response seen in 8/14 (57%). All these patients had genotype non 1. All the four patients with Genotype I were non-responders. CONCLUSION: Hepatitis C genotype III is common in India, Genotype I runs a more severe course, faster progression and non responders to interferon as compared with genotype II and III.
Hepatitis C is a heterogeneous disease whose natural history is controversial and perplexing. However, it can be a pernicious disease and is responsible for considerable mortality and morbidity. More than 80% individuals infected with the hepatitis C virus (HCV) develop chronic infection; the remaining 10-20% develop spontaneous clearance with natural immunity. The majority of patients who develop chronic HCV infection are asymptomatic; but 60-80% develop chronic hepatitis as indicated by elevated ALT; around 30% maintain normal ALT. One-third of chronically infected patients develop progressive liver injury, fibrosis and cirrhosis over a period of 20-30 years, and 15% develop hepatocellular carcinoma. Acquiring infection after the age of 40 years, male sex, excessive alcohol-consumption, HBV or HIV co-infection and the immunosuppressive state have been identified as factors associated with progression of fibrosis and development of cirrhosis. The relationship between virus load, HCV genotype I and quasispecies variability and progression of live disease is controversial. In the present study on 141 patients with chronic HCV infection and established chronic liver disease, the median time to develop cirrhosis was 20 years. Progression to cirrhosis was faster (16 vs 20 years) in those who acquired infection after the age of 35 years, and in immunosuppressed patients (8 vs 21 years), whereas diabetes, sex and HBV co-infection were not associated with faster progression.
Cavernous hemangioma of the rectum are uncommon benign vascular lesions. Misdiagnosis often occurs because of lack of awareness of classic clinical features. Endoscopy, plain x-ray abdomen, barium enema, and selective angiography are useful means of investigation for accurate diagnosis. Three cases of rectal haemangioma are presented that were earlier misdiagnosed as ulcerative colitis.
AIMS: To study mucin histochemistry of the normal esophagus, esophageal adenocarcinoma, and carcinoma exhibiting glandular and squamous elements, to ascertain the origin of these tumors. METHODS: Mucin histochemistry was studied in sections of the normal cardioesophageal junction obtained from 25 post-mortem specimens and in 12 mucin-secreting esophageal carcinomas. RESULTS: The normal submucosal esophageal glands and three adenocarcinomas secreted predominantly sulfomucins; a mixture of neutral and sialomucins was seen in the nine carcinomas with squamous and glandular traits. Barrett's metaplasia was not encountered. CONCLUSIONS: In the absence of Barrett's metaplasia, esophageal adenocarcinoma probably arises from the submucosal glands, whereas squamous carcinomas with mucin-secreting component could arise from metaplastic change in squamous epithelium, cardiac glands, or multipotent stem cells in the epithelium.
Hereditary pancreatitis is an idiopathic form of chronic pancreatitis which affects multiple members of a family in an autosomal dominant mode of inheritance. Most of the case reports are in caucasians of European descent. In this report, we present our data on four affected members spanning three generations in a family from India. Current data on hereditary pancreatitis are summarized, to revive an interest in this rare form of chronic pancreatitis.
We report a patient with hepatocellular carcinoma (HCC) with membranous obstruction of the inferior vena cava (IVC). He underwent balloon dilatation of the IVC with good results. The HCC was managed by chemoembolization followed by resection. At follow up of eleven months the patient is asymptomatic.
BACKGROUND: The association of diabetes with liver disease is well known. AIM: To study the spectrum of liver disease in patients of chronic liver disease (CLD) with diabetics and compare it with age and sex matched patients of CLD without diabetes. METHODS: We studied the patients of chronic liver disease presenting over a period of one year and their diagnosis were established by biochemical studies, imaging, endoscopic examination and liver biopsy when required. They were evaluated for the aetiological causes of liver diseases. RESULTS: A total of 53 patients of CLD with diabetes, M:F 43:8, with an age range of 35-70 years, median age of 51 years were taken as study group. Demographic picture of control group was n = 115, with M:F = 100: 15, age range of 37-68 years, with a median age of 52 years. Spectrum of liver disease in diabetic group were as follows: 56.6% cirrhosis, 15.1% chronic hepatitis, 22.6% fatty liver, 5.7% cirrhosis + hepatocellular carcinoma (HCC). The spectrum in control group was as follows, cirrhosis 46.1%, chronic hepatitis 36.5%, fatty liver 14.8%, cirrhosis and HCC 2.6%. Aetiology of chronic liver disease in diabetic group was as follows: Non-alcoholic steatohepatitis (NASH) with cirrhosis 11.3%, NASH 18.9%, cryptogenic cirrhosis 22.6%, hepatitis B virus (HBV) 17%, hepatitis C virus (HCV) 13.2%, alcohol 17%. Aetiology of chronic liver disease in nondiabetic group was as follows: NASH with cirrhosis 1.7%, NASH 13.0%, cryptogenic cirrhosis 7.8%, HBV 30.43%, HCV 13%, alcohol 29.6% and autoimmune in 4.3%. Incidence of NASH with cirrhosis and cryptogenic cirrhosis were found to be statistically significantly high in diabetic group. Incidence of diabetes in cryptogenic cirrhosis was found to be 57% versus 30% in noncryptogenic cirrhosis. CONCLUSION: NASH, NASH with cirrhosis and cryptogenic cirrhosis are the major causes of chronic liver disease in patients with diabetes mellitus. Alcohol and viral causes are found to be important aetiologies in nondiabetic control group. Diabetes mellitus is an important risk factor for chronic liver disease and progression of NASH to cirrhosis, which may present as cryptogenic cirrhosis.
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