Dose antioxidant ascorbic acid supplementation delay lung function deterioration in stable patients with chronic obstructive pulmonary disease

ABSTRACT Objective To determine whether antioxidant ascorbic acid supplementation holdup the lung function deterioration in stable chronic obstructive pulmonary disease patients. Patients and Methods The single blind uncontrolled comparative clinical study was carried out at Basic Medical Sciences Research Laboratory, LUMHS, Jamshoro. Forty five enrolled patients were indiscriminately divided into two groups, group-I (n=22), getting standard treatment which included salbutamol 100µg and beclomethasone 50µg in metered-dose aerosol two times a day and group-II (n=23) receiving 500 mg of ascorbic acid twice daily along with standard treatment. Pre-treatment and post-treatment spirometry was carried out as per protocol. Results In group-I patients an average FEV1/FVC ratio 65.79+2.6% was obtained at baseline which significantly dropped to 58.86+1.47% (P=0.026) at the end of study. While in group-II patients mean FEV1/FVC ratio 65.99+0.943% was at baseline, which non-significantly decreased to 63.59+2.1% (P=0.328) at the end of study. Conclusion The response of vitamin C in delaying lung function deterioration may point out that oxidative stress is a major component in COPD pathology. So ascorbic acid could be considered as a component of recovery program. (Rawal Med J 2010;35: ). Key Words Antioxidant, ascorbic acid, chronic obstructive pulmonary disease. INTRODUCTION In recent years chronic obstructive pulmonary disease (COPD) is coupled with a towering frequency of morbidity, mortality and a significant cause of declined quality of life and increased number of hospitalizations.1-4 There is escalating confirmation for a close association among cigarette smoking and COPD that progresses gradually.5,6 Contemporary confirmation incriminates augmented oxidative stress as an imperative mechanism of the pulmonary inflammation7 which crop up in cigarette smokers.1 Cigarette smoke restrains and creates a hefty quantity of reactive oxygen species (ROS) which facilitate pulmonary inflammation.8 The symmetry among the free radicals creation and exhaustion of endogenous antioxidants in the body has been postulated to play critical role in pathogenesis of COPD.9 Overstated free radicals congregation and exceptionally squat antioxidants accessibility put up a state of oxidative stress,10 which causes failure to repair DNA damage leading to structural alterations, deteriorations in pulmonary function and amplify pulmonary inflammatory response.11-13 Access of leukocytes to site of inflammation further leads to a rise in the confined synthesis of inflammatory mediators, and ROS, ending with enhanced oxidative stress which adds to oxidative spoil14 and plays a foremost role in pathogenesis of COPD, described by low lung function15 and escalating mortality.16,17 A number of management approaches which successfully attenuate and seize the oxidative load coupled with fewer adverse effects have been considered.18 Ascorbic acid, with influential sca