Abstract

Increased reactive oxygen species (ROS) and oxidative stress (OS) has been reported in many allergic and inflammatory skin diseases, including urticaria, psoriasis, and atopic dermatitis (AD). Melatonin is a hormone secreted from the pineal gland and is a potent antioxidant. The aim of the study was to measure serum antioxidant melatonin, oxidants of nitric oxide (NO), and malondialdehyde levels to calculate the serum oxidant-antioxidant balance based on the NO/melatonin and malondialdehyde/melatonin ratios and to determine the correlation with the disease severity in children with AD. Seventy-three children with AD and 67 healthy controls were included in the study. The clinical diagnosis of AD was based on the diagnostic criteria of Hanifin-Rajka. The severity of AD was evaluated by the scoring AD (SCORAD) index, and atopy was determined by skin prick tests (SPTs) with commercial extracts. The OS-related parameters of serum melatonin, NO, malondialdehyde, and the NO/melatonin and malondialdehyde/melatonin ratios were calculated and compared with the results of healthy controls. Serum melatonin levels were higher (p<0.0001) and serum NO levels and the NO/melatonin and malondialdehyde/melatonin ratios were lower in children with AD than in healthy controls (p=0.045, p<0.0001, p<0.0001, respectively). There was no difference between children with AD and healthy controls in terms of serum malondialdehyde levels (p=0.119). Serum melatonin levels were significantly lower in severe AD than in mild AD (p=0.012). However, in terms of serum melatonin levels, there was no difference between mild and moderate AD (p=0.742) and moderate to severe AD (p=0.301). There was no significant difference in serum NO and malondialdehyde levels and NO/melatonin and malondialdehyde/melatonin ratios among children with mild, moderate, and severe AD (p>0.05). A negative correlation was found between serum melatonin levels and the SCORAD index (r=-0.252, p=0.031), and a positive correlation was found between NO/melatonin and malondialdehyde/melatonin ratios (r=0.511, p<0.0001). There was no statistically significant relationship between age (≤24 or >24months), disease duration (≤6 or >6months), and sex for the OS-related parameters (p>0.05). The serum oxidant-antioxidant balance was impaired in children with AD. Serum melatonin levels were higher in children with AD; however, this was negatively correlated with disease severity. Serum NO levels and NO/melatonin and malondialdehyde/melatonin ratios were lower in children with AD than in healthy controls. Melatonin might be used as a promising antioxidant to evaluate disease severity in children with AD. Thus, further studies are needed to clarify the role of melatonin in AD pathogenesis.

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