Effect of vitamin E supplementation with standard treatment on oxidant-antioxidant status in chronic obstructive pulmonary disease.

ABSTRACT

BACKGROUND & OBJECTIVES: Chronic oxidant burden and depletion of endogenous antioxidants have been proposed to play a key role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Exogenous antioxidants have potential therapeutic implications and their role has not been explored in COPD. The objective of this study was to investigate the effect of supplementation of standard treatment (inhaled long-acting beta(2) agonists, anticholinergics and corticosteroids) with vitamin E on oxidant-antioxidant balance in patients with COPD. METHODS: The study was carried out in the outpatient setting. Patients were divided into two groups group A- placebo group (n=14), receiving only standard therapy, and group B- vitamin E-supplemented group (n=10), receiving 400 IU of vitamin E capsules twice daily in addition to standard therapy. Spirometry and clinical assessment were carried out at the start and completion of 8 wk treatment along with measurements of several biochemical parameters of oxidant-antioxidant status in plasma, leukocytes and red cells separated from venous blood. RESULTS: Leukocyte superoxide generation was decreased in both the groups. Vitamin E-supplemented group had significantly increased levels of plasma sulphydryls and red cell catalase while the placebo group had decreased levels of plasma nitrates and nitrites. No significant differences were observed in red cell superoxide dismutase and glutathione peroxidase activities, total blood glutathione, and plasma total antioxidant capacity, lipid peroxides and glutathione peroxidase activity in either group. There was a similar degree of lung function and clinical improvement in both the groups. INTERPRETATION & CONCLUSION: Our findings showed that an 8 wk supplementation of standard treatment with 400 IU twice daily of vitamin E did not provide any additional clinical benefit although it augmented certain endogenous antioxidants in patients with COPD.