Neonatal Alloimmune Thrombocytopenia: A Concise Review.

Journal Article (Review;Journal Article)

Background

Neonatal alloimmune thrombocytopenia (NAIT) is defined as an uncommon platelet disorder caused by maternal alloimmunization to human-specific antigens (HPAs) that are paternally inherited, resulting in low fetal/neonatal platelet levels and debilitating effects on the newborn. The incidence of NAIT is 1 in every 1000 live births within the United States; it is the most common cause of severe thrombocytopenia (<30 × 109/L) and intracranial hemorrhage in term newborns.

Purpose

The purpose of this article is to discuss the pathophysiology, clinical manifestations, diagnosis, and treatment of NAIT and its implications upon the lifespan of the neonate.

Methods

A literature review was conducted using PubMed, CINAHL, and Google Scholar (2014-2019). Search terms included NAIT, neonatal/fetal alloimmune thrombocytopenia, newborn platelets, and intracranial bleeding and NAIT.

Results

NAIT can affect first pregnancies and often goes undiagnosed until delivery. Universal screening tools with a focus on HPA-1a typing via noninvasive testing have been successfully trialed and have yielded promising results indicating a 75% reduction in risks associated with NAIT; however, none have been incorporated into practice and prophylactic treatment remains unavailable.

Implications for research

Adopting a universal screening tool and prophylaxis for NAIT would allow for early diagnosis and treatment in utero.

Implications for practice

Many healthcare providers are not familiar with NAIT often focusing on other causes of thrombocytopenia as a potential diagnosis.

Full Text

Duke Authors

Cited Authors

  • Norton, T; Newberry, D; Jnah, A

Published Date

  • April 2021

Published In

Volume / Issue

  • 21 / 2

Start / End Page

  • 115 - 121

PubMed ID

  • 32657948

Electronic International Standard Serial Number (EISSN)

  • 1536-0911

International Standard Serial Number (ISSN)

  • 1536-0903

Digital Object Identifier (DOI)

  • 10.1097/anc.0000000000000775

Language

  • eng