Résumé
Objective:To evaluate the efficacy of Liangxue-Xiaofeng Decoction combined with acitretin A capsule in the treatment of psoriasis vulgaris. Methods:A total of 80 patients with psoriasis vulgaris from March 2015 to June 2019 in our hospital, who met the inclusion criteria, were divided into two groups according to the random number table method, 40 patients in each group. The control group was given acitretin A capsules on the basis of conventional western medicine treatment, and the study group was given Liangxue-Xiaofeng Decoction on the basis of the control group. Both groups were treated for 2 months and followed up for 6 months. The skin lesion area and Psoriasis Area and Severity Index (PASI) scores were performed before and after treatment. The levels of IL-8, IL-6 and TNF-α were detected by real time PCR amplification, and the levels of histone acetyltransferase (HATs) and histone deacetylase (HDACs) by ELISA. The adverse reactions and recurrence during the follow-up period were recorded and the clinical efficacywas evaluated. Results:The total effective rate of the study group was 82.5% (33/40) and that of the control group was 62.5% (25/40). The difference between the two groups was statistically significant ( χ2=4.012, P=0.045). After treatment, the PASI score of the study group was significantly lower than that of the control group ( t=7.921, P<0.01), and the serum levels of IL-8, IL-6 and TNF-α were significantly lower than those in the control group ( t=12.749, 13.933, 10.856, all Ps<0.01); the activity of HATs [(35.03 ± 3.79) g/L vs. (29.26 ± 2.41) g/L, t=8.125] of the study group was significantly higher than that of the control group ( P<0.01), and HDACs activity [(31.00 ± 2.71) g/L vs. (37.55 ± 3.08) g/L, t=10.098] of the study group was significantly lower than that of the control group ( P<0.01). Conclusions:Acitretin A capsule combined with Liangxue-Xiaofeng Decoction can reduce the level of inflammatory cytokines in patients with psoriasis vulgaris, and prevent the disease progression. The mechanism may be related to the regulation of homeostasis balance in acetylation.