Castle V, Andrew M, Kelton J, Giron D, Johnston M, Carter C
J Pediatr. 1986 May;108(5 Pt 1):749-55. doi: 10.1016/s0022-3476(86)81059-9.
We performed a 1-year prospective study of 807 consecutive infants admitted to a regional neonatal intensive care unit to determine the frequency, natural history, mechanism(s), and cause of thrombocytopenia. Thrombocytopenia developed in 22% of the infants. The platelet count nadir usually occurred by day 4 and resolved by day 10. Possible mechanisms responsible for the thrombocytopenia were assessed by comparing mean platelet volume, platelet-associated IgG (PAIgG), and coagulation test results in those infants whose platelet count fell below 100 X 10(9)/L (n = 97) with values in age-, weight-, and disease-matched control infants without thrombocytopenia (n = 80). In some thrombocytopenic infants, 111In-labeled-platelet survival, an estimate of megakaryocyte number in bone marrow biopsy specimens obtained at autopsy, and response to platelet infusions were also assessed. The thrombocytopenia was caused by increased platelet destruction, as shown by short 111In-labeled-platelet survival (12 to 128 hours), a rising mean platelet volume during the first week of life, normal numbers of megakaryocytes, and a poorer than predicted response to platelet infusions. A potential cause for the thrombocytopenia could be found in the majority of infants: 52% had elevated levels of PAIgG, 21% had laboratory evidence of disseminated intravascular coagulation, and 12% had had exchange transfusions. In contrast, the control infants had normal coagulation assay results, and only 15% had elevated levels of PAIgG. Birth asphyxia was identified as an associated risk factor for thrombocytopenia. This study demonstrates that transient, destructive thrombocytopenia develops in a large proportion (22%) of infants admitted to a neonatal intensive care unit, and that birth asphyxia is an important risk factor.
我们对一家地区新生儿重症监护病房连续收治的807例婴儿进行了为期1年的前瞻性研究，以确定血小板减少症的发生率、自然病程、机制及病因。22%的婴儿出现了血小板减少症。血小板计数最低点通常出现在第4天，并在第10天恢复。通过比较血小板计数低于100×10⁹/L的婴儿（n = 97）与年龄、体重和疾病匹配的无血小板减少症对照婴儿（n = 80）的平均血小板体积、血小板相关IgG（PAIgG）和凝血试验结果，评估了导致血小板减少症的可能机制。对于一些血小板减少症婴儿，还评估了¹¹¹In标记血小板存活时间、尸检时获得的骨髓活检标本中巨核细胞数量的估计值以及对血小板输注的反应。血小板减少症是由血小板破坏增加引起的，表现为¹¹¹In标记血小板存活时间短（12至128小时）、出生后第一周平均血小板体积上升、巨核细胞数量正常以及对血小板输注的反应比预期差。大多数婴儿血小板减少症都能找到潜在病因：52%的婴儿PAIgG水平升高，21%的婴儿有弥散性血管内凝血的实验室证据，12%的婴儿接受过换血治疗。相比之下，对照婴儿凝血试验结果正常，只有15%的婴儿PAIgG水平升高。出生窒息被确定为血小板减少症的一个相关危险因素。这项研究表明，在新生儿重症监护病房收治的很大一部分（22%）婴儿中会发生短暂性、破坏性血小板减少症，且出生窒息是一个重要的危险因素。
