Sezer E, Ozugurlu F, Ozyurt H, Sahin S, Etikan I
Department of Dermatology, Gaziosmanpasa University School of Medicine, Tokat, Turkey.
Clin Exp Dermatol. 2007 Jul;32(4):430-4. doi: 10.1111/j.1365-2230.2007.02436.x. Epub 2007 Apr 24.
Lichen planus (LP) is an inflammatory skin disease of unknown aetiology. Recently, increased oxidative stress has been implicated in the pathogenesis of various skin diseases such as atopic dermatitis, psoriasis vulgaris and vitiligo.
To evaluate the status of the oxidative stress and antioxidant defence system in patients with LP.
In total, 40 patients with LP (23 men, 17 women; mean +/- SD age 43.27 +/- 1.96 years) and 40 control subjects, matched for age and gender, were enrolled in this prospective study. The exclusion criteria included medication with immunosuppressive agents, history of trauma and surgery, and history of alcohol ingestion for at least 1 month prior to the study. The serum nitric oxide (NO), malondialdehyde (MDA) and superoxide dismutase (SOD) levels and the erythrocyte catalase (CAT) levels were investigated in both groups.
Mean +/- SD levels of serum NO (74.60 +/- 17.96 micromol/L) and MDA (18.24 +/- 5.21 micromol/L) in patients with LP were higher than those of the control group (P = 0.007 and P = 0.031, respectively). Serum SOD levels (18.19 +/- 3.71 U/mL) in patients with LP were also higher than in healthy controls (P = 0.002). In contrast, erythrocyte CAT levels (13 557.80 +/- 4134.42 U/kg haemoglobin) were significantly lower in the patient group than in the control group (P = 0.009).
The findings of this study suggest that increased oxidative stress, increased lipid peroxidation and an imbalance in the antioxidant defence system may be involved in the pathogenesis of LP.
扁平苔藓(LP)是一种病因不明的炎症性皮肤病。最近,氧化应激增加与多种皮肤病如特应性皮炎、寻常型银屑病和白癜风的发病机制有关。
评估LP患者氧化应激和抗氧化防御系统的状态。
本前瞻性研究共纳入40例LP患者(23例男性,17例女性;平均±标准差年龄43.27±1.96岁)和40例年龄及性别匹配的对照者。排除标准包括使用免疫抑制剂、有创伤和手术史以及在研究前至少1个月有饮酒史。两组均检测血清一氧化氮(NO)、丙二醛(MDA)和超氧化物歧化酶(SOD)水平以及红细胞过氧化氢酶(CAT)水平。
LP患者血清NO(74.60±17.96微摩尔/升)和MDA(18.24±5.21微摩尔/升)的平均±标准差水平高于对照组(分别为P = 0.007和P = 0.031)。LP患者血清SOD水平(18.19±3.71单位/毫升)也高于健康对照组(P = 0.002)。相反,患者组红细胞CAT水平(13557.80±4134.42单位/千克血红蛋白)显著低于对照组(P = 0.009)。
本研究结果表明,氧化应激增加、脂质过氧化增加以及抗氧化防御系统失衡可能参与LP的发病机制。