Knot E A, ten Cate J W, Bruin T, Iburg A H, Tytgat G N
Gastroenterology. 1985 Aug;89(2):421-5. doi: 10.1016/0016-5085(85)90346-4.
125I-Antithrombin III metabolism studies were performed in 2 patients with ischemic and ulcerative colitis, respectively. Both patients had acquired antithrombin III deficiency and objectively diagnosed deep venous thrombosis. A decreased 125I-antithrombin III plasma disappearance halflife and an increased fractional catabolic rate was found in both patients. The transcapillary flux ratio was elevated in the patient with ischemic colitis. A follow-up study of the first patient during a period when no signs of an ischemic colitis were present and no medication was taken showed completely normal tracer data. The data are consistent with both gastrointestinal loss and intravascular consumption of antithrombin III. The antithrombin III deficiency could not be explained by other causes such as proteinuria, liver dysfunction, or obvious disseminated intravascular coagulation. Reduced antithrombin III plasma levels were considered to have contributed to the development of deep venous thrombosis in both patients.
分别对2例缺血性结肠炎和溃疡性结肠炎患者进行了125I-抗凝血酶III代谢研究。两名患者均患有获得性抗凝血酶III缺乏症，并经客观诊断患有深静脉血栓形成。两名患者均出现125I-抗凝血酶III血浆清除半衰期缩短和分数分解代谢率增加。缺血性结肠炎患者的跨毛细血管通量比升高。对第一名患者在无缺血性结肠炎迹象且未服用药物期间进行的随访研究显示示踪剂数据完全正常。这些数据与抗凝血酶III的胃肠道丢失和血管内消耗均一致。抗凝血酶III缺乏症无法用蛋白尿、肝功能障碍或明显的弥散性血管内凝血等其他原因解释。抗凝血酶III血浆水平降低被认为是两名患者深静脉血栓形成的原因。
