Hyman P E, Abrams C E, Zipser R D
Am J Dis Child. 1987 Jun;141(6):686-9. doi: 10.1001/archpedi.1987.04460060102046.
Urinary thromboxane B2 levels increased threefold to 20-fold in infants with neonatal necrotizing enterocolitis compared with healthy infants and infants with benign causes of heme-positive stools. Increased urinary thromboxane B2 levels were detected coincidently with the initial signs of necrotizing enterocolitis, and values paralleled the course of the illness. Infants with serious illnesses other than necrotizing enterocolitis had increased urinary thromboxane B2 levels but with lower values than those of infants with necrotizing enterocolitis. Indomethacin therapy appeared to reduce urinary thromboxane B2 levels and reduce their usefulness as a marker of illness. Another product of platelet activation, beta-thromboglobulin, was increased in the urine of infants with necrotizing enterocolitis. Decreased platelet counts in infants with necrotizing enterocolitis correlated inversely with urinary thromboxane. Results of beta-thromboglobulin and platelet studies are consistent with the concept that platelet consumption due to ischemic thrombosis was the source of enhanced thromboxane excretion.
与健康婴儿以及粪便潜血阳性的良性病因婴儿相比，新生儿坏死性小肠结肠炎婴儿的尿血栓素B2水平升高了3倍至20倍。尿血栓素B2水平升高与坏死性小肠结肠炎的初始体征同时出现，且数值与疾病进程平行。患有除坏死性小肠结肠炎之外严重疾病的婴儿尿血栓素B2水平也升高，但低于坏死性小肠结肠炎婴儿。吲哚美辛治疗似乎可降低尿血栓素B2水平，并降低其作为疾病标志物的效用。血小板活化的另一种产物β-血小板球蛋白，在坏死性小肠结肠炎婴儿的尿液中升高。坏死性小肠结肠炎婴儿血小板计数降低与尿血栓素呈负相关。β-血小板球蛋白和血小板研究结果与以下概念一致，即缺血性血栓形成导致的血小板消耗是血栓素排泄增加的来源。
