Psoriatic arthritis (PsA) is a heterogeneous chronic musculoskeletal disease, affecting up to 30% of people with psoriasis. Research into PsA pathogenesis has led to the development of targeted therapies, including Tumor Necrosis Factor inhibitors (TNF-i). Good response is only achieved by ~60% of patients leading to ‘trial and error’ drug management approaches, adverse reactions and increasing healthcare costs. Robust and well-validated biomarker identification, and subsequent development of sensitive and specific assays, would facilitate the implementation of a stratified approach into clinical care. This review will summarise potential genetic biomarkers for TNF-i (adalimumab, etanercept and infliximab) response that have been reported to date. It will also comment upon the importance of managing clinical confounders when understanding drug response prediction. Variants in multiple gene regions including TNF-A, FCGR2A, TNFAIP3, TNFR1/TNFR1A/TNFRSF1A, TRAIL-R1/TNFRSF10A, FCGR3A have been reported to correlate with TNF-i response at various levels of statistical significance in patients with PsA. However, results were often from heterogenous and underpowered cohorts and none are currently implemented into clinical practice. External validation of genetic biomarkers in large, well-documented cohorts is required, and assessment of the predictive value of combining multiple genetic biomarkers with clinical measures is essential to clinically embed pharmacogenomics into PsA drug management.

银屑病关节炎 (PsA) 是一种异质性慢性肌肉骨骼疾病，影响多达 30% 的银屑病患者。对 PsA 发病机制的研究导致了靶向治疗的发展，包括肿瘤坏死因子抑制剂 (TNF-i)。只有约 60% 的患者会导致“试错”药物管理方法、不良反应和增加医疗保健成本，才能获得良好的反应。稳健且经过充分验证的生物标志物鉴定，以及随后开发的敏感和特异性检测，将有助于在临床护理中实施分层方法。本综述将总结迄今为止已报道的 TNF-i（阿达木单抗、依那西普和英夫利昔单抗）反应的潜在遗传生物标志物。它还将评论在理解药物反应预测时管理临床混杂因素的重要性。多个基因区域的变异，包括据报道，TNF-A、FCGR2A、TNFAIP3、TNFR1/TNFR1A/TNFRSF1A、TRAIL-R1/TNFRSF10A、FCGR3A与 PsA 患者的 TNF-i 反应在不同的统计显着水平上相关。然而，结果通常来自异质和动力不足的队列，目前没有一个应用于临床实践。需要在大量、有据可查的队列中对遗传生物标志物进行外部验证，并且评估将多种遗传生物标志物与临床措施相结合的预测价值对于在临床上将药物基因组学纳入 PsA 药物管理至关重要。