Background: Antituberculosis treatment (ATT) induced hepato-toxicity is common, but risk factors predicting its development are poorly understood. The present study evaluates the clinical risk factors predicting the development of hepatotoxicity in Indian patients with tuberculosis on antituberculosis treatment. Methods: Three groups of patients were studied at three service hospitals over a 3 year period from 2000-2002. Patients given ATT were followed up with monthly LFTs. Consecutive patients who developed Liver dysfunction (rise in SGPT > 5 times upper limit of normal) were studied, along with matched controls who did not. Markers for hepatitis B were also noted in these patients once in 6 months. A third group of patients who did not receive ATT but were HBsAg positive, were also similarly followed up. The possible association of age and sex of the patient, alcoholism, unrecognized chronic liver disease, hepatitis B virus carrier status and nutritional status with ATT-induced hepatitis was assessed. Statistical analysis was carried out by Chi square test/Fisher's exact test using WHO provided software Epi Info 6. Sixty-nine patients with ATT-induced hepatotoxicity were prospectively studied. In addition 128 patients on anti-tuberculosis drugs without hepatotoxicity and 39 HBsAg carriers not on ATT were followed up for 1 year. Results: Age, Sex, history of alcohol intake and BMI were not found to be related to development of hepatotoxicity. Presence of HBV infection or an underlying silent chronic liver disease were found to significantly increase the risk of development of ATTinduced hepatotoxicity. Continuation of ATT after development of jaundice was associated with a high fatality rate. It was possible to re-introduce isoniazid in 96% and rifampicin in 88% of patients with ATT induced hepatotoxicity. Conclusion: ATT-induced hepatitis is common and is potentially fatal. It is likely to occur in those with underlying silent chronic liver disease, HBV infection and have been given ATT without a definite evidence of tuberculosis. Discontinuation of ATT leads to rapid recovery in most cases and drugs can safely be introduced after recovery in a majority of cases. MJAFI 2006; 62 : 45-49

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There are reports of migration of Helicobacter pylori from the gastric antrum to the proximal stomach following acid suppression therapy. The diagnosis of H pylori infection is usually based on rapid urease test and histology of gastric antral biopsies. 50 consecutive patients of peptic ulcer, 22 on proton pump inhibitors and 28 on histamine-2 receptor antagonists for at least 4 weeks were subjected to biopsies from the gastric corpus in addition to the antrum at the time of upper gastrointestinal endoscopy. H pylori infection was detected in 42 (84%) patients. The diagnosis was established from both antral and corpus biopsies in 34 (68%) and only antrum in 4 (8%). In 4 patients, 3 on proton pump inhibitors and one on H-2 receptor antagonists, H pylori was isolated only from the corpus. The rapid urease test was positive at a mean time of 67.6 minutes from the antrum as compared to 234.6 minutes from the corpus. Testing for H pylori from the antrum alone and not the corpus would have resulted in a false negative result in 8% patients. Biopsy from the gastric antrum should always be combined with biopsy from gastric corpus for the diagnosis of H pylori infection in patients with dyspepsia on acid suppression therapy. were placed in separate commercially available RUT, Helikochek, which were considered positive if colour change occurred within 24 hours. The time taken for positivity of the RUT from both sites was noted. If the RUT was negative from any of the two sites, the remaining biopsy bits were subjected to histology for HP stained with haematoxylin and eosin. Patients who received antibiotics over the preceding 4 weeks were excluded.

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