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.

Ascitic fluid protein and cellular changes during diuretic therapy in cirrhosis of liver.

Thirty 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.