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Clinical and Experimental Dermatology 2015-Aug

Investigation of oxidative stress in patients with alopecia areata and its relationship with disease severity, duration, recurrence and pattern.

Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
Odkaz je uložen do schránky
J Z Yenin
G Serarslan
Z Yönden
K T Ulutaş

Klíčová slova

Abstraktní

BACKGROUND

Alopecia areata (AA) is an inflammatory autoimmune disease that causes hair loss on the scalp or trunk without scarring. Although the precise aetiopathogenesis of alopecia areata remains unknown, oxidative stress is thought to play a role.

OBJECTIVE

To investigate the relationship between severity and the role of oxidative stress in AA, by measuring plasma oxidant levels and antioxidant enzyme activities in erythrocytes.

METHODS

In total, 62 patients with AA (24 males and 38 females), and 62 sex- and age-matched healthy controls (HCs) were enrolled in the study. We investigated the levels of plasma malondialdehyde (MDA) and the activities of erythrocyte catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). The relationship between oxidative stress and AA was also investigated with regard to disease pattern, severity, duration and recurrence.

RESULTS

The mean erythrocyte GSH-Px and SOD activities were significantly reduced (P < 0.001 and P < 0.001 respectively) compared with the control group. Plasma MDA levels were increased but statistically insignificant (P = 0.08) in patients with AA compared with controls. No significant difference between erythrocyte CAT activities was observed between patients and controls (P = 0.2). In addition, we observed no statistically significant difference in patient plasma MDA levels or erythrocyte CAT, GSH-Px or SOD activities with regard to AA severity, duration, recurrence or pattern (P > 0.05).

CONCLUSIONS

Patients with AA displayed reduced erythrocyte SOD and GSH-Px activities and enhanced plasma MDA levels. These findings support the possible role of oxidative stress in the pathogenesis of AA.

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