背景:与生物药物(BD)和Janus激酶抑制剂(JAKi)相关的感染风险已在文献中得到广泛探讨。然而,有一个缺乏的研究,评估两个药物组一起,此外,比较它们。这里,我们回顾了与皮肤病学使用的BD和JAKI相关的感染风险。
方法:进行叙述性回顾。选择2010年1月至2024年2月期间评估BD和JAKI感染和机会性感染风险的所有相关文章。
结果:总体而言,感染的发生率,严重感染,与BD和JAKI相关的机会性感染较低,但高于普通人群。JAKI批准用于皮肤病(abrocitinib,baricitinib,deucravitinib,upadacitinib,利替尼,和局部鲁索利替尼)已被证明是安全的,并呈现低感染率。我们发现风险升高,特别是抗肿瘤坏死因子(抗TNF)药物,利妥昔单抗,和JAKI(特别是高剂量的托法替尼)。与感染的特定关联包括抗TNF药物和托珠单抗的结核病和结核病再激活;抗白介素(IL)17药物的念珠菌病;利妥昔单抗的乙型肝炎病毒再激活,抗TNF,和JAKI;JAKI引起的单纯疱疹和带状疱疹感染(尤其是高剂量的托法替尼和upadacitinib)。ustekinumab和抗IL-23感染的发生率非常低。抗IL-1,奈莫珠单抗,tralokinumab,和奥马珠单抗与感染风险增加无关.Dupilumab可以降低皮肤感染的发生率。
结论:抗TNF药,利妥昔单抗,和JAKI(特别是托法替尼)可增加感染风险。建议密切监测接受这些治疗的患者。需要进行长期随访的前瞻性研究,以比较评估BD和JAKi治疗引起的感染风险。
BACKGROUND: The risk of infections associated with biological drugs (BD) and Janus kinase inhibitors (JAKi) has been extensively explored in the literature. However, there is a dearth of studies that evaluate both pharmacological groups together and, furthermore, compare them. Here, we review the risk of infections associated with BD and JAKi used in dermatology.
METHODS: A narrative review was performed. All relevant articles evaluating the risk of infection and opportunistic infections with BD and JAKi between January 2010 and February 2024 were selected.
RESULTS: Overall, the incidence of infections, serious infections, and opportunistic infections associated with BD and JAKi is low, but higher than in the general population. JAKi approved for dermatological disorders (abrocitinib, baricitinib, deucravacitinib, upadacitinib, ritlecitinib, and topical ruxolitinib) have been shown to be safe, and present a low rate of infections. We found an elevated risk, especially with anti-tumor necrosis factor (anti-TNF) agents, rituximab, and JAKi (particularly tofacitinib at high doses). Specific associations with infections include tuberculosis and tuberculosis reactivation with anti-TNF agents and tocilizumab; candidiasis with anti-interleukin (IL) 17 agents; hepatitis B virus reactivation with rituximab, anti-TNF, and JAKi; and herpes simplex and herpes zoster infections with JAKi (especially tofacitinib and upadacitinib at high doses). The incidence of infections with ustekinumab and anti-IL-23 was very low. Anti-IL-1, nemolizumab, tralokinumab, and omalizumab were not associated with an increased risk of infections. Dupilumab could decrease the incidence of cutaneous infections.
CONCLUSIONS: Anti-TNF agents, rituximab, and JAKi (particularly tofacitinib) can increase the risk of infections. Close monitoring of patients undergoing these therapies is recommended. Prospective studies with long-term follow-up are needed to comparatively evaluate the risks of infection deriving from treatment with BD and JAKi.