Smiyan Svitlana, Kuzmina Ganna, Garmish Olena, Komorovsky Roman
Department of Internal Medicine II, Ivan Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.
Department of Therapy, Cardiology and Family Medicine, Faculty of Postgraduate Education, Dnipro State Medical University, Dnipro, Ukraine.
Open Access Rheumatol. 2025 Aug 24;17:173-183. doi: 10.2147/OARRR.S541224. eCollection 2025.
Antiphospholipid syndrome (APS) is a complex multisystem disorder traditionally classified into primary forms and those associated with autoimmune diseases. However, is gaining attention as a distinct subset due to the increasing recognition of thrombotic complications occurring in the context of viral or bacterial infections. Despite its clinical relevance, this phenomenon remains poorly characterized. This narrative review synthesizes current knowledge on the pathogenesis, clinical manifestations, and diagnostic challenges of infection-induced APS. A literature search was conducted in the Medline and PubMed databases for English-language articles published between 2014 and May 2025. Of the identified publications, 35 were selected for detailed analysis. Evidence supports a multifaceted relationship between infections and APS, with proposed mechanisms including molecular mimicry, Toll-like receptor activation, generation of non-pathogenic antiphospholipid antibodies (aPL), impaired immune complex clearance, neutrophil extracellular trap formation, direct endothelial damage, and the "second hit" hypothesis. Clinical presentations are diverse, ranging from mild, transient symptoms to severe thrombotic events, and often complicate the distinction between true APS and transient aPL positivity secondary to infection. Diagnostic difficulties are compounded by the fluctuating presence of aPL and the overlap of infection-related symptoms with APS criteria. Currently, there are no standardised criteria for infection-induced APS, underscoring the need for definitions that reflect its temporal dynamics and immunological heterogeneity.
抗磷脂综合征(APS)是一种复杂的多系统疾病,传统上分为原发性形式和与自身免疫性疾病相关的形式。然而,由于越来越多地认识到在病毒或细菌感染情况下发生的血栓形成并发症,它作为一个独特的亚组正受到关注。尽管其具有临床相关性,但这一现象的特征仍不明确。本叙述性综述综合了目前关于感染诱发的APS的发病机制、临床表现和诊断挑战的知识。在Medline和PubMed数据库中检索了2014年至2025年5月发表的英文文章。在已识别的出版物中,选择了35篇进行详细分析。有证据支持感染与APS之间存在多方面的关系,提出的机制包括分子模拟、Toll样受体激活、非致病性抗磷脂抗体(aPL)的产生、免疫复合物清除受损、中性粒细胞胞外陷阱形成、直接内皮损伤以及“二次打击”假说。临床表现多种多样,从轻微的短暂症状到严重的血栓形成事件,并且常常使真正的APS与继发于感染的短暂aPL阳性之间的区分变得复杂。aPL的波动存在以及感染相关症状与APS标准的重叠加剧了诊断困难。目前,对于感染诱发的APS没有标准化的标准,这突出了需要反映其时间动态和免疫异质性的定义。