Metoni Adriana, Mambet Cristina, Necula Laura G, Aldea Ioana M, Neagu Ana I, Matei Lilia, Dragu Denisa, Bleotu Coralia, Ion Daniela A, Diaconu Carmen C
Roum Arch Microbiol Immunol. 2014 Jul-Dec;73(3-4):92-8.
Thrombotic events are highly prevalent in systemic lupus erythematosus (SLE). Antiphospholipid antibodies play an essential role in promoting thrombosis by activating several intracellular signaling pathways (TLR4, p38MAPK, NFkB) in platelets, monocytes and endothelial cells. New therapeutic opportunities might be offered by addressing these molecular targets. Chronic inflammatory status, the degree of disease activity and accelerated atherosclerosis are also responsible for the thrombotic phenotype in patients with SLE. The aim of this review is to highlight thrombosis mechanisms and to look for possible connection between SLE, antiphospholipid antibodies and cancer, especially myeloproliferative neoplasms.
血栓形成事件在系统性红斑狼疮(SLE)中非常普遍。抗磷脂抗体通过激活血小板、单核细胞和内皮细胞中的几种细胞内信号通路(TLR4、p38MAPK、NFκB)在促进血栓形成中起重要作用。针对这些分子靶点可能会带来新的治疗机会。慢性炎症状态、疾病活动程度和加速的动脉粥样硬化也与SLE患者的血栓形成表型有关。本综述的目的是强调血栓形成机制,并寻找SLE、抗磷脂抗体与癌症,尤其是骨髓增殖性肿瘤之间的可能联系。