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Dysfunctional antithrombin III in sick premature infants.

作者信息

Andrew M, Massicotte-Nolan P, Mitchell L, Cassidy K

出版信息

Pediatr Res. 1985 Feb;19(2):237-9. doi: 10.1203/00006450-198502000-00020.

DOI:10.1203/00006450-198502000-00020
PMID:3982886
Abstract

Antithrombin III, a major inhibitor of activated coagulation factors has low immunologic levels in the human infant. The objective of this study was to determine if the antithrombin III molecule is fully functional in sick premature infants. The populations studied included: adult controls (n = 20), full term healthy infants (n = 18), sick premature infants on day 1 (n = 16) and at greater than 7 days of age (n = 10), and infants with disseminated intravascular coagulation (n = 11). This was diagnosed in the presence of prolonged screening tests, decreased levels of fibrinogen, and platelets along with elevated fibrin degradation products. Plasma antithrombin III levels were measured biologically (chromogenic substrate S2238) and immunologically (radialimmunodiffusion), and expressed as a percent of adult pooled plasma. Crossed immunoelectrophoresis were performed in the presence and absence of heparin. The antithrombin III biologic/immunologic ratios for adults, healthy full term infants, and sick premature infants on day 1 of life were all near unity. In contrast sick premature infants beyond the 1st wk of life and infants with disseminated intravascular coagulation had lower biologic activity compared to immunologic (B/I = 0.77 +/- 0.28, 0.78 +/- 0.17, p less than 0.01), respectively. In all groups, the antithrombin III molecule was normal on crossed immunoelectrophoresis except for one infant with disseminated intravascular coagulation. Sick premature infants may acquire a dysfunctional antithrombin III molecule in the postnatal period.

摘要

相似文献

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引用本文的文献

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Antithrombin III Supplementation in a Premature Infant: Is There a Target Antithrombin Level?对一名早产儿补充抗凝血酶III:是否存在目标抗凝血酶水平?
J Pediatr Pharmacol Ther. 2021;26(8):850-856. doi: 10.5863/1551-6776-26.8.850. Epub 2021 Nov 10.
2
Ligand-dependent enhancement of human antithrombin gene expression by retinoid X receptor alpha and thyroid hormone receptor beta.视黄酸X受体α和甲状腺激素受体β对人抗凝血酶基因表达的配体依赖性增强作用。
Biochem J. 1996 Aug 15;318 ( Pt 1)(Pt 1):263-70. doi: 10.1042/bj3180263.