银屑病
医学
阿达木单抗
乌斯特基努马
银屑病面积及严重程度指数
英夫利昔单抗
血管内皮生长因子
内科学
胃肠病学
白细胞介素
发病机制
不利影响
免疫学
血管内皮生长因子受体
肿瘤坏死因子α
细胞因子
作者
Takatoshi Shimauchi,Satoshi Hirakawa,Takahiro Suzuki,Ayako Yasuma,Yuta Majima,Kazuki Tatsuno,Hiroaki Yagi,Taisuke Ito,Y. Tokura
标识
DOI:10.1111/1346-8138.12248
摘要
Abstract The T‐helper (Th)17 cell plays a crucial role in the pathogenesis of psoriasis, and several biological therapies have shown to be highly efficient in the treatment. However, some patients respond poorly to these therapies and may even develop paradoxical adverse effects. To evaluate the significance of serum immunological factors or circulating competent cells for biomarkers or predictors to biological therapies, we retrospectively analyzed 28 patients with psoriasis (19 psoriasis vulgaris, three pustular psoriasis and six psoriasis arthropathica). The numbers of patients treated with each agents were 16 for ustekinumab, six for adalimumab and six for infliximab. Patients were classified into three types according to the responsiveness: 13 patients were high‐responders showing a 75% or more reduction of Psoriasis Area and Severity Index ( PASI ); 10 patients were moderate‐responders showing PASI reduction of less than 75%; and five patients were non‐responders showing PASI elevation. During the treatments, serum levels of interleukin ( IL )‐22 and vascular endothelial growth factor ( VEGF ) were monitored. At baseline, serum IL ‐22 levels were significantly higher in the psoriatic patients than the normal controls. Both serum IL ‐22 and VEGF levels significantly correlated with PASI . After the treatment, the high‐responders showed significant decreases in serum IL ‐22 and VEGF . On the other hand, serum IL ‐22 levels in the non‐responders were elevated. However, the baseline levels of serum IL ‐22 and VEGF were not significantly different between the three groups. These results suggest that serum IL ‐22 and VEGF levels serve as sensitive biomarkers but not as predictors of therapeutic response to biologics in patients with psoriasis.
科研通智能强力驱动
Strongly Powered by AbleSci AI