摘要本文旨在探討係統性紅斑狼瘡血栓並發症中血栓收縮可能的作用。使用一種新型的自動化方法，我們調查了51名SLE患者和60名健康獻血者的血液凝塊收縮的動力學。使用流式細胞術通過P-選擇素和纖維蛋白原結合能力的表達來評估SLE患者中血小板的功能。 SLE患者的血栓收縮率和程度明顯低於正常人，特別是血液中抗dsDNA抗體水平較高的患者。血小板收縮力降低與從SLE患者血液中分離的血小板對由凝血酶受體激活肽誘導的刺激的部分不應性相關。為了測試抗dsDNA自身抗體是否引起血小板的持續活化，以及細胞的衰竭和功能障礙，我們在凝血之前將來自SLE患者的純化的外源抗dsDNA自身抗體加入到正常血液中。為了支持這一假設，抗體首先增強血塊收縮，然後以時間依賴性的方式抑製它。重要的是，血塊收縮參數與疾病嚴重程度的直接相關性表明，血管內凝塊和血栓的致密性降低可能是SLE中的致病因素，其可能誇大血栓形成部位處的受損血流。綜上所述，SLE自身抗體可影響血小板收縮能力，導致凝塊和血栓體積縮小的能力下降，增加血管阻塞，加重SLE血栓並發症的發生，發展。

附原文：The aim of this work was to examine a possible role ofclot contraction/retraction in thrombotic complications of systemic lupuserythematosus (SLE). Using a novel automated method, we investigated kineticsof clot contraction in the blood of 51 SLE patients and 60 healthy donors. Thefunctionality of platelets in the SLE patients was assessed using flowcytometry by expression of P-selectin and fibrinogen-binding capacity. The rateand degree of clot contraction were significantly reduced in SLE patientscompared to healthy subjects, especially in the patients with higher bloodlevels of anti-dsDNA antibodies. The reduced platelet contractility correlatedwith partial refractoriness of platelets isolated from the blood of SLEpatients to stimulation induced by the thrombin receptor activating peptide. Totest if the anti-dsDNA autoantibodies cause continuous platelet activation,followed by exhaustion and dysfunction of the cells, we added purifiedexogenous anti-dsDNA autoantibodies from SLE patients to normal blood beforeclotting. In support of this hypothesis, the antibodies first enhanced clotcontraction and then suppressed it in a time-dependent manner. Importantly, adirect correlation of clot contraction parameters with the disease severitysuggests that the reduced compactness of intravascular clots and thrombi couldbe a pathogenic factor in SLE that may exaggerate the impaired blood flow atthe site of thrombosis. In conclusion, autoantibodies in SLE can affectplatelet contractility, resulting in reduced ability of clots and thrombi to shrinkin volume, which increases vessel obstruction and may aggravate the course andoutcomes of thrombotic complications in SLE.

引自：Le Minh G,Peshkova AD,Andrianova IA,et al.Impaired contraction of bloodclots as a novel prothrombotic mechanism in systemic lupus erythematosus. ClinSci (Lond), 2018 Jan 19;132(2):243-254. doi: 10.1042/CS20171510. Print 2018 Jan31.