Lood Christian, Tydén Helena, Gullstrand Birgitta, Nielsen Christoffer T, Heegaard Niels H H, Linge Petrus, Jönsen Andreas, Hesselstrand Roger, Kahn Robin, Bengtsson Anders A
Department of Clinical Sciences Lund, Section of Rheumatology, Lund, Sweden.
Department of Autoimmunology and Biomarkers, Statens Serum Institut, Copenhagen, Denmark.
Rheumatology (Oxford). 2017 Mar 1;56(3):408-416. doi: 10.1093/rheumatology/kew437.
. SLE is an autoimmune disease with increased cardiovascular morbidity and platelet activation. In the general population, increased platelet size predicts platelet reactivity and cardiovascular disease. The aim of this study was to investigate whether platelet size related to platelet activation and cardiovascular disease in SLE.
. Fresh blood samples from SLE patients ( n = 148), healthy volunteers ( n = 79) and disease controls ( n = 40) were analysed for platelet size and activation by flow cytometry, ELISA and cell count. Associations to manifest cardiovascular disease, venous thrombosis and APS were adjusted for traditional cardiovascular risk factors using logistic regression analysis.
. SLE patients had decreased platelet size as compared with healthy controls ( P = 0.003). In SLE, decreased platelet size was related to increased platelet activation, in particular microparticle formation ( P < 0.0001, r = -0.46) and release of serotonin from dense granules ( P < 0.001, r = 0.57). SLE patients with aCL had decreased platelet size ( P = 0.02) and aCL decreased platelet size in vitro ( P = 0.007). In contrast to the general population, increased platelet size was not associated with cardiovascular disease. Instead, decreased platelet size was associated with secondary APS, even after adjusting for traditional cardiovascular risk factors ( P = 0.01, odds ratio 3.58).
. Platelet size is decreased in SLE patients and associated with microparticle formation and APS. Future studies are needed to determine the underlying mechanism(s) as well as the potential predictive value of small platelets for disease complications in SLE.
系统性红斑狼疮（SLE）是一种自身免疫性疾病，心血管发病率和血小板活化增加。在一般人群中，血小板体积增大预示着血小板反应性和心血管疾病。本研究旨在探讨SLE患者血小板大小是否与血小板活化及心血管疾病相关。
采用流式细胞术、酶联免疫吸附测定（ELISA）和细胞计数法，对SLE患者（n = 148）、健康志愿者（n = 79）和疾病对照者（n = 40）的新鲜血样进行血小板大小和活化分析。使用逻辑回归分析，针对传统心血管危险因素对与显性心血管疾病、静脉血栓形成和抗磷脂综合征（APS）的相关性进行校正。
与健康对照相比，SLE患者的血小板体积减小（P = 0.003）。在SLE中，血小板体积减小与血小板活化增加相关，尤其是微粒形成（P < 0.0001，r = -0.46）和致密颗粒中5-羟色胺的释放（P < 0.001，r = 0.57）。抗心磷脂抗体（aCL）阳性的SLE患者血小板体积减小（P = 0.02），且aCL在体外可使血小板体积减小（P = 0.007）。与一般人群不同，血小板体积增大与心血管疾病无关。相反，即使校正了传统心血管危险因素后，血小板体积减小仍与继发性APS相关（P = 0.01，比值比3.58）。
SLE患者血小板体积减小，且与微粒形成和APS相关。未来需要开展研究以确定其潜在机制以及小血小板对SLE疾病并发症的潜在预测价值。
