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V Castle, G Coates, JG Kelton and M Andrew
Thrombocytopenia is a common occurrence (20%) in sick neonates, but the
causes have not been well studied. In this report we demonstrate that
thrombocytopenia in the neonate is characterized by increased platelet
destruction as shown by shortened homologous 111In-oxine-labeled platelet
life spans. Thirty-one prospectively studied thrombocytopenic neonates were
investigated by measuring the 111In-labeled platelet life span,
platelet-associated IgG (PAIgG), and coagulation screening tests. In every
infant, the thrombocytopenia was shown to have a destructive component
since the mean platelet life span was significantly shortened to 65 +/- 6
(mean +/- SEM) hours with a range of one to 128 hours compared with adult
values (212 +/- 8; range, 140 to 260; gamma function analysis). The
platelet survival was directly related to the lowest platelet count and
inversely related to both the highest mean platelet volume and duration of
the thrombocytopenia. In 22 infants the percent recovery of the
radiolabeled platelets was less than 50%, which suggested that increased
sequestration also contributed to the thrombocytopenia. Infants with
laboratory evidence of disseminated intravascular coagulation (n = 8) or
immune platelet destruction evidenced by elevated levels of PAIgG (n = 13)
had even shorter platelet survivals and a more severe thrombocytopenia
compared with the ten infants in whom an underlying cause for the
thrombocytopenia was not apparent. Full-body scintigraphic images obtained
in 11 infants showed an increased uptake in the spleen and liver, with a
spleen-to- liver ratio of 3:1. This study indicates that thrombocytopenia
in sick neonates is primarily destructive, with a subgroup having evidence
of increased platelet sequestration.
This article has been cited by other articles:
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| Copyright © 1987 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
