Lee Nuri, Kim Ji-Eun, Yoo Hyun Ju, Gu JaYoon, Kim Hyori, Chung Junho, Koh Youngil, Kim Hyun Kyung
Department of Laboratory Medicine, Seoul National University Hospital, Seoul, Korea.
Cancer Research Institute, Seoul National University Hospital, Seoul, Korea.
Ann Clin Lab Sci. 2016 Dec;46(6):696-700.
We present a case of acquired dysfibrinogenemia caused by an autoantibody that inhibited fibrin polymerization in a patient previously diagnosed with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, stroke-like episodes). The patient showed prolonged PT, aPTT, and thrombin time. There was no factor deficiency but fibrinogen antigen and activity were decreased. ELISA for detection of fibrinogen antibodies were performed and IgG purified from the patient's plasma bound to fibrinogen more strongly than did control IgG, indicating the presence of a fibrinogen-specific antibody. Thrombin-mediated fibrin polymerization was severely impaired in the patient, although thrombin-induced fibrinopeptide A release was normal. Scanning electron microscopy was used to investigate the structure of fibrin clots and revealed many pores on the surface of patient's fibrin clots. Since MELAS is often associated with autoimmune disorders, a work-up for the presence of anti-fibrinogen antibody is necessary when bleeding tendency occurs in MELAS patients along with prolonged thrombin time.
我们报告了一例由自身抗体引起的获得性异常纤维蛋白原血症病例,该自身抗体抑制了一名先前被诊断为MELAS(线粒体肌病、脑病、乳酸酸中毒、卒中样发作)患者的纤维蛋白聚合。患者的凝血酶原时间(PT)、活化部分凝血活酶时间(aPTT)和凝血酶时间延长。无凝血因子缺乏,但纤维蛋白原抗原和活性降低。进行了检测纤维蛋白原抗体的酶联免疫吸附测定(ELISA),从患者血浆中纯化的IgG与纤维蛋白原的结合比对照IgG更强,表明存在纤维蛋白原特异性抗体。尽管凝血酶诱导的纤维蛋白肽A释放正常,但患者的凝血酶介导的纤维蛋白聚合严重受损。采用扫描电子显微镜研究纤维蛋白凝块的结构,发现患者纤维蛋白凝块表面有许多孔隙。由于MELAS常与自身免疫性疾病相关,当MELAS患者出现出血倾向且凝血酶时间延长时,有必要检查是否存在抗纤维蛋白原抗体。