Indian Journal of Public Health Research & Development

Tuberculosis is an infectious disease caused by mycobacterium tuberculosis which primarily affects the lungs to cause pulmonary tuberculosis. One of the major adverse effects of anti-tubercular treatment is hepatoxicity. The anti – tubercular drugs known to cause hepatoxicity are isoniazid, rifampicin and pyrazinamide. The frequency of hepatoxicity is increased when these drugs are used in combination as they are used now-a – days in DOTS regimen (directly observed treatment short course). VIT-E and VIT-C have hepatoprotective effect due to their anti- oxidant property.

To study the level of markers of oxidative stress in patients of TB suffering from ATT induced hepatotoxicity & to observe the role of exogenously administered antioxidants like VIT – E and VIT-C in such patients

This is an open label, randomized comparative study.

Five groups of 8 patients each were taken.

Group 1- Normal healthy volunteer.

Group2-Newly diagnosed patients of pulmonary tuberculosis

Group 3 –[HT] Patients with diagnosis of ATT induced hepatotoxicity. No intervention.

Group4-[HTE] Patients with diagnosis of ATT induced hepatotoxicity. VIT-E given.

Group5- [HTEC] Patients with diagnosis of ATT induced hepatotoxicity. VIT-E + VIT-C given.

Estimation of liver function tests of all patients (Serum bilirubin, SGOT, SGPT, Alkaline phosphatase [ALP])

Estimation of markers of oxidative stress glutathione peroxidase (GPx), Super Oxidedismutase (SOD), Glutathione (GLT), Malonaldehyde (MDA), catalase (CAT).

All patients were reviewed weekly. Their LFTs were performed at weekly interval. The markers of oxidative stress were assessed on diagnosis of hepatotoxicity and upon resolution of hepatotoxicity. In the end, all the patients in each group completed the study and results were analysed statistically for these patients.

There has been a significant change when oxidative stress markers and liver function tests were repeatedly measured post intervention positively.

Vit E & Vit C administration induces reduction in oxidative stress in patients of hepatotoxicity indicated by increased level of anti-oxidant enzymes.