Oxidative stress in alopecia areata and its association with disease severity, treatment and autoimmunity

Alopecia areata (AA) is a hair follicle disease characterized by non scarring hair loss that affects any site of the body. Etiopathogenesis is unknown, but the focus is particularly on the role of autoimmune reactions, genetic predisposition, atopic status, emotional stress, lack of trace elements, infection and neurological factors. In recent years, in order to evaluate oxidative stress parameters in tissue or blood of patients with AA, malondialdehyde (MDA) and nitric oxide (NO) as the oxidant system components as well as superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzymes as the antioxidant system components had been researched. The data indicates impaired balance of oxidant/antioxidant functioning. The aim of our study is to understand the role of oxidative stress in the pathogenesis of AA by looking at plasma levels of MDA, NO, SOD and GPx, assess the effect of topical and systemic treatment on oxidative stress and to investigate its relationship with severity of disease and other autoimmune diseases. The study included two groups consisted of 15 patients with AA who have indicated topical or systemic corticosteroids (CS) for their treatment, and a control group of 26 healthy subjects. Fasting peripheral venous blood was collected for detecting pre and posttreatment MDA, NO, SOD and GPx levels. The results were compared with each others and the healthy controls. The level of NO was significantly increased (p<0.05) and the levels of MDA and SOD were significantly decreased in the patient group (p<0.05) compared to healthy controls. Serum level of GPx was statistically insignificant from healthy subjects. No correlation was found between the disease severity, autoimmunity and the oxidtive stress parameters. Despite signifanct decrease in the Severity of Alopecia Tool (SALT) in both topical and systemic CS treatment groups (p<0.05) there was no significant difference between pre and posttreatment levels of MDA, NO and SOD. The level of GPx was indifferent in topical CS group too while it was significantly increased in systemic CS recieving group (p<0.05). These data suggest that despite clinical improvement in AA with CS treatment, their regulatory effects on markers of oxidant and antioxidant systems are inadequate or abscent. Without making a definite comment, beacause of the follow-up of our patients have not been done, this may be the reason of recurrence seen in the patients with AA after successful treatment with CS.