Prevalence of anti-HCV antibodies in western India.

Nearly 2000 serum samples collected from different risk groups from Pune and Bombay metropolitan areas were tested for antibodies to hepatitis C virus (anti-HCV) by Recombinant Immunoblot Assay-3 (RIBA-3). Patients undergoing haemodialysis showed 24.5 per cent seropositivity whereas 5.7 and 5.3 per cent of multiply transfused patients (>2 units) and chronic liver disease patients respectively were anti-HCV positive. Leprosy patients had almost 0.7 per cent seropositivity. In other risk groups the positivity rate was nil. In normal population only one out of 830 persons had anti-HCV antibodies. It is therefore apparent that the prevalence of hepatitis C virus (HCV) in western India is not high. However, special care needs to be taken for dialysis patients. As none of the 430 pregnant women and 86 children below the age of 5 yr were anti-HCV positive, vertical mode of HCV transmission seems to be negligible.

Role of Helicobacter pylori in gastric carcinoma.

BACKGROUND. Helicobacter pylori infection has recently been incriminated in the pathogenesis of gastric carcinoma and chronic atrophic gastritis and intestinal metaplasia are considered to be precursors of this condition. Although the incidence of Helicobacter pylori infection in India is high that of gastric carcinoma is low. We, therefore, decided to examine the association between Helicobacter pylori, intestinal metaplasia and gastric carcinoma in a prospective study. METHODS. Fifty patients with carcinoma of the stomach and 50 with non-ulcer dyspepsia underwent upper gastro-intestinal endoscopy and had biopsies from the antrum, body and carcinomatous tissue. In 12 cases of gastric carcinoma, tissue was obtained from resected specimens at operation. The types of gastritis, intestinal metaplasia and presence of Helicobacter pylori were assessed by staining with haematoxylin and eosin, periodic acid-Schiff reagent with alcian blue and Warthin-Starry stains. RESULTS. The incidence of chronic atrophic gastritis, intestinal metaplasia and Helicobacter pylori were 82%, 36% and 38% in patients with carcinoma and 86%, 4% and 68% in those with non-ulcer dyspepsia. Helicobacter pylori positivity was significantly higher (p < 0.05) and intestinal metaplasia significantly lower (p < 0.001) in patients with non-ulcer dyspepsia than in those with carcinoma. Of the 50 cases with carcinoma, 28 were of the intestinal and 22 of the diffuse type. The incidence of chronic atrophic gastritis, intestinal metaplasia and Helicobacter pylori in the intestinal type of carcinoma was 71%, 46% and 39% while in the diffuse type it was 32%, 23% and 36%. The incidence of Helicobacter pylori infection did not differ significantly in the two types of carcinoma. CONCLUSIONS. We have found that although Helicobacter pylori infection and chronic atrophic gastritis are common in Indians, the incidence of intestinal metaplasia is low. Helicobacter pylori infection was equally common in both the intestinal and diffuse type of gastric carcinomas. Our findings, therefore, cast doubt on the role of Helicobacter pylori infection in gastric carcinogenesis.

Effect of acute ingestion of tobacco on gastric mucosa. An endoscopic study.

One hundred patients with non ulcer dyspepsia with history of chronic tobacco chewing were examined endoscopically to assess the effect of tobacco ingestion on the gastric mucosa. Gastric erosions were seen in 20 patients in the fasting state. The remaining 80 patients in whom gastroscopy did not reveal erosions were subjected to repeat gastroscopy after tobacco ingestion. In 40 patients, endoscopy was repeated 30 minutes after 200 mg of tobacco ingestion (Group I) and in another 40 patients endoscopy was repeated 1 hour after 400 mg of tobacco ingestion (Group II). Eleven patients (27.5%) in Group I and 19 (47.5%) in Group II developed gastric erosions. Erosions were observed mainly along the lesser curvature, and in the fundus and the body of stomach. Gastric pH, determined after tobacco ingestion, was 2.4 +/- 0.43 in patients with erosions and 3.0 +/- 0.67 in patients without erosions. It is concluded that tobacco ingestion produces dose-dependent damage to the gastric mucosa as seen on endoscopy. Hence, history of tobacco ingestion should always be asked for in patients with gastric erosions.