Oxidative stress in gastric mucosa in Helicobacter pylori infection.

BACKGROUND: Infection with Helicobacter pylori is believed to be associated with generation of reactive oxygen molecules which leads to oxidative stress in the gastric mucosa; but the relation between oxidative stress and gastrointestinal mucosal damage has not been documented. AIM: To look for evidence of oxidative stress and lipid peroxidation in the gastric mucosa in H. pylori-associated peptic ulcer. METHODS: 34 duodenal ulcer (DU) patients with H. pylori infection, 14 DU patients without H. pylori infection and 10 healthy subjects without H. pylori infection were studied. H. pylori infection was diagnosed by histology and rapid urease test on endoscopic biopsies from the gastric body and antrum. Reduced glutathione (GSH) and malondialdehyde (MDA) content were measured in biopsies taken from the gastric antrum. Statistical analysis was done using Student's t test. RESULTS: Tissue levels of GSH were significantly lower (91.7 [35.4] nmole/100 mg versus 147.3 [41.2] nmole/100 mg; p < 0.001) and MDA higher (163.0 [83.4] nmole/100 mg versus 109.2 [51.3] nmole/100 mg; p < 0.01) in patients with DU associated with H. pylori infection as compared to those without H. pylori infection. GSH levels were significantly lower and MDA levels higher in DU patients with or without H. pylori infection as compared to control subjects. Serum MDA levels in DU patients with H. pylori infection were also significantly higher than in patients without H. pylori infection. CONCLUSION: Depletion of gastric mucosal glutathione in H. pylori-infected DU patients may be due to failure of the antioxidant defense system. Failure of the glutathione-dependent defense system results in accumulation of free radicals which can initiate membrane damage by lipid peroxidation.

Hepatic manifestations in chronic arsenic toxicity.

OBJECTIVE: The hepatotoxic action of arsenic, when used as a therapeutic agent, has long been recognized. Data on liver involvement following chronic exposure to arsenic-contaminated water are scanty. We report the nature and degree of liver involvement on the basis of hospital-based and cohort follow-up studies in patients who consumed arsenic-contaminated drinking water for 1 to 15 years. METHODS: 248 patients with evidence of chronic arsenic toxicity underwent clinical and laboratory examinations including liver function tests and HBsAg status. Liver biopsy was done in 69 cases; in 29 patients, liver arsenic content was estimated by neutron activation analysis. A cohort follow up of 23 patients who took arsenic-free water for 2-12 years was also carried out. RESULTS: Hepatomegaly was present in 190 of 248 patients (76.6%). Noncirrhotic portal fibrosis (91.3%) was the predominant lesion in liver histology. The maximum arsenic content in liver was 6 mg/Kg (mean 1.46 [0.42], control value 0.16 [0.04]; p < 0.001); it was undetected in 6 of 29 samples studied. Cohort follow-up studies showed elevation of globulin in four cases and development of esophageal varices in one case. CONCLUSION: We report the largest number of patients with liver disease due to chronic arsenicosis from drinking arsenic-contaminated water. Noncirrhotic portal fibrosis is the predominant lesion in this population.

Isolated myoepithelial duodenal hamartoma presenting with upper gastrointestinal bleed.

Myoepithelial duodenal hamartoma, a rare lesion, usually occurs as a part of diffuse gastrointestinal tract polyposis in Peutz-Jegher's and Gardner's syndromes. Solitary duodenal hamartoma in the absence of other manifestations of polyposis syndrome is rare. We report one such patient presenting with massive gastrointestinal bleeding.

Chronic arsenic toxicity in west Bengal--the worst calamity in the world.

Since 1983 large number of people are being encountered with arsenic toxicity due to drinking of arsenic contaminated water (0.05-3.2 mg/l) in 6 districts of West Bengal. Clinical and various laboratory investigations were carried out on 156 patients to ascertain the nature and degree of morbidity and mortality that occurred due to chronic arsenic toxicity. All the patients studied had typical rain drop like skin pigmentation (being inclusion criteria) while thickening of palm and sole were found in 65.5% patients. Other features included weakness (70%), gastro-intestinal symptoms (58.6%), involvement of respiratory system (57.08%) and nervous system (50.6%). Lung function tests showed restrictive lung disease in 53% (9/17) and combined obstructive and restrictive lung disease in 41% (7/17) of patients. Abnormal electromyography was found in 34.8% (10/29) and altered nerve conduction velocity in 34.8% (10/29) of cases. Enlargement of liver was found in 120 cases (76.9%) while splenomegaly in 31.4% cases. Liver function test showed elevated globulin level in 15.8% and alkaline phosphatase in 51.3%, alanine amino transferase (ALT) in 11.8% and aspartate amino transferase (AST) in 27.6% of cases. Evidence of portal hypertension was found in 33.3% patients. Liver biopsy reports of 45 patients showed non-cirrhotic portal fibrosis in 41, cirrhosis in 2 and normal histology in 2 cases. There was no correlation between the quantity of arsenic taken through water and the level of arsenic in hair, nail, liver tissues and the degree of fibrosis. There were 5 deaths of which one had skin cancer. The various non-cancer manifestations which were observed in these patients were much severe than those reported in similar cases in other parts of the world.