Browsing by Author "Desai, H G"
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Item Acid output in control subjects and patients with duodenal ulcer using fixed doses of histamine.(1970-01-01) Desai, H G; Zaveri, M P; Mohalla, D J; Antia, F PItem Acquired apolipoprotein B deficiency with chronic hepatitis C virus infection.(2006-11-01) Gupte, P; Dudhade, A; Desai, H GChronic hepatitis C virus (HCV) infection is often associated with fatty liver. Apolipoprotein B (ApoB) deficiency is one of the known causes of fatty liver and acquired ApoB deficiency has recently been reported with HCV infection. We report two patients (47-year-old lady and 48-year-old man) who had asymptomatic transaminase elevation, fatty liver, anti-HCV positive with high viral load (genotype 3). Their lipid profile showed low total cholesterol, low-density lipoprotein, triglycerides and ApoB. One of the patients who received treatment for HCV infection showed improvement in lipid profile and ApoB levels.Item Acute gastroenteritis or tropical sprue?(1974-05-01) Antia, F P; Desai, H GItem Acute viral E hepatitis with chronic liver disease (autoimmune hepatitis).(2005-03-05) Desai, H G; Naik, A SA 36 years old male presented with anorexia, jaundice and ascites. He was suffering from acute viral E hepatitis. In view of ascites, he was investigated for associated asymptomatic chronic liver disease (CLD). The CLD was diagnosed as cirrhosis with autoimmune hepatitis and was treated with steroid with good response. He is maintaining good health with low dose steroid, on follow up for 1 year.Item Acute viral hepatitis in Bombay.(1988-11-01) Choksi, A P; Desai, H GItem Aetiology of Indian childhood cirrhosis: a new hypothesis.(1976-06-01) Kumar, A; Desai, H GItem Age-related prevalence of Helicobacter pylori antibodies in Indian subjects.(1994-07-01) Gill, H H; Majmudar, P; Shankaran, K; Desai, H GOBJECTIVE: To determine the age-related prevalence of Helicobacter pylori antibodies in Indian subjects without upper gastrointestinal symptoms. MATERIAL AND METHODS: Sera of 340 subjects without any upper gastrointestinal complaints were screened for IgG and IgA Helicobacter pylori antibodies by the ELISA technique. RESULTS: The prevalence of IgG and IgA antibodies was 22%, 56% and 87% and 48%, 58% and 83% in 0-4, 5-9 and 10-19 year age groups respectively; thereafter it remained almost constant upto fifth decade. A significant fall in IgG and IgA prevalence was observed from fifth to seventh decades. CONCLUSION: Our data indicate that in India exposure to Helicobacter pylori occurs early in life and is widespread; about 83% of the population is exposed to Helicobacter pylori during the first two decades of life. The comparable prevalence rates of IgG antibodies to Helicobacter pylori and hepatitis A virus, in different age groups, in India and in the West, suggest a feco-oral mode of transmission for Helicobacter pylori.Item Apolipoprotein deficiency and chronic liver disease.(2001-02-28) Shah, S S; Desai, H GDeficiency of apolipoprotein can be of genetic origin or due to diseases like advanced chronic liver disease. Deficiency of apolipoprotein A causes Tangier disease without any major hepatic involvement being reported. Deficiency of apolipoprotein B causes abetalipoproteinemia or familial hypobetalipoproteinemia; with hepatic involvement in the form of raised transaminases, fatty liver and cirrhosis. Advanced chronic liver disease itself can cause reduction of apolipoprotein A and apolipoprotein B levels and acanthocytosis. In patients with chronic liver disease of undetermined etiology, lipid profile and apolipoprotein levels should be obtained routinely. If it suggests apolipoprotein B deficiency, then liver biopsy can be avoided, as the etiology of chronic liver disease is established. Isolated deficiency of either apolipoprotein A or apolipoprotein B suggests etiology of chronic liver disease, while deficiency of both apolipoprotein A and apolipoprotein B is a manifestation of advanced chronic liver disease.Item Ascitic fluid protein and cellular changes during diuretic therapy in cirrhosis of liver.(1991-03-01) Parikh, S S; Amarapurkar, D N; Viswanath, N; Desai, H G; Kalro, R HThirty four patients with peritoneoscopy and/or biopsy proven uncomplicated cirrhosis of liver with ascites were studied for the effect of diuretic therapy on ascitic fluid protein and cell count. Renal function tests, liver function tests, ascitic fluid protein concentration and cell count were estimated prior to diuretic therapy and once every week till the end of therapy. There was no change in mean total serum protein (5.71 +/- 0.58 g/dl to 5.72 +/- 0.63 g/dl). The rise in mean ascitic fluid protein from 1.55 +/- 0.77 g/dl to 1.76 +/- 0.79 g/dl was not significant (P greater than 0.05). Twenty one patients (Group I) showed a rise in ascitic fluid protein concentration while 13 patients (Group II) did not show a rise or showed a fall in protein concentration during diuretic therapy. The rise in ascitic fluid protein concentration in Group I from 1.62 +/- 0.69 g/dl to 2.05 +/- 0.67 g/dl was statistically significant (P less than 0.05). Group I patients had a mean weight loss of 6.21 +/- 3.66 kg as compared to 3.15 +/- 2.00 kg in Group II patients (p less than 0.05). There was no other difference between Group I and Group II patients. Only 5 patients showed a rise in ascitic fluid cell count (more than 50 cell/mm3). It is concluded that diuretic therapy alters ascitic fluid protein concentration in a majority of patients but has no significant effect on cell count.Item Bacteriological study of small intestinal fluid in tropical sprue.(1966-04-01) Desai, H G; Parekh, D V; Jeejeebhoy, K NItem Bile salt metabolism in intestinal tuberculosis increased glycine: taurine ratio of conjugated bile salts.(1975-12-01) Desai, H G; Zaveri, M P; Antia, F PItem Bile salt metabolism in tropical sprue.(1972-08-01) Desai, H G; Zaveri, M P; Antia, F PItem Biliary ascariasis.(1984-07-01) Kalro, R H; Esmail, J H; Contractor, Q Q; Desai, H GItem Blind loop syndrome with tropical sprue.(1968-03-01) Desai, H G; Patel, C T; Jeejeebhoy, K NItem Calculated maximal response and ED50 for acid secretion in control subjects and patients with duodenal ulcer.(1974-12-01) Desai, H G; Zaveri, M P; Antia, F PItem Campylobacter pylori. A new era in gastroduodenal disorders?(1990-02-01) Gill, H H; Kalro, R H; Desai, H GItem Can ascitic fluid transmit hepatitis B virus?(1988-10-01) Choksi, A P; Desai, H GItem Carcinoma in an oesophageal diverticulum.(1992-02-01) Shah, S M; Desai, H GA young male who had minimal dysphagia since childhood complained of increasing difficulty in swallowing for a few months. Upper Gastrointestinal endoscopy was normal on two occasions done by two gastroenterologists. Barium swallow showed minimal extrinsic pressure on the oesophageal wall. X-ray chest was normal. CT scan showed a large growth close to the oesophagus. Resection of the growth showed a carcinoma completely filling an oesophageal diverticulum with a normal oesophageal lumen.Item Cholate concentration in duodenal contents in non-cirrhotic portal fibrosis.(1973-12-01) Desai, H G; Zaveri, M P; Antia, F PItem Cholate concentration in the duodenum in protein malnutrition.(1978-07-01) Desai, H G; Zaveri, M P; Antia, F P