Solak Yalcin, Demircioglu Sinan, Polat Ilker, Biyik Zeynep, Gaipov Abduzhappar, Acar Kadir, Turk Suleyman
Division of Nephrology, Department of Internal Medicine, Meram School of Medicine, Konya University, Konya, Turkey.
Hemodial Int. 2013 Apr;17(2):320-3. doi: 10.1111/j.1542-4758.2012.00710.x. Epub 2012 May 28.
Heparin-induced thrombocytopenia (HIT) is caused by heparin exposure and presents with reduced platelet count. Patients undergoing hemodialysis (HD) treatment have increased risk of developing HIT due to prolonged exposure to unfractionated heparin or low-molecular weight heparin. We report a 79-year-old male patient with end-stage renal disease who developed type-II HIT during maintenance HD. Platelet count of the patient decreased gradually and antiplatelet factor IV antibody was found to be positive. The patient was treated with fondaparinux and continued heparin-free HD. Unfortunately, despite favorable initial response without any thrombotic episodes, the patient died due to severe sepsis complicated by gastrointestinal hemorrhage.
肝素诱导的血小板减少症(HIT)由肝素暴露引起,表现为血小板计数降低。接受血液透析(HD)治疗的患者因长期接触普通肝素或低分子量肝素,发生HIT的风险增加。我们报告一例79岁终末期肾病男性患者,在维持性血液透析期间发生II型HIT。患者血小板计数逐渐下降,抗血小板因子IV抗体检测呈阳性。患者接受磺达肝癸钠治疗,并继续进行无肝素血液透析。不幸的是,尽管最初反应良好,未发生任何血栓形成事件,但患者因严重脓毒症并发胃肠道出血死亡。