# Severe Persistent Neonatal Immune Thrombocytopenia Despite Optimized Maternal Chronic Immune Thrombocytopenia (ITP) Management

**Authors:** Nick Trevino, Gabriella Kuffour, Adora Okogbule-Wonodi, Shannon Wentworth, Ahmed Ali, Mekdem Bisrat, Miriam Michael, Inez Reeves

PMC · DOI: 10.7759/cureus.102833 · Cureus · 2026-02-02

## TL;DR

A newborn developed severe immune thrombocytopenia despite optimal maternal treatment, highlighting the ongoing risks and management challenges.

## Contribution

This case highlights the persistent risk of neonatal immune thrombocytopenia despite optimal maternal ITP management.

## Key findings

- A term neonate presented with severe thrombocytopenia requiring multiple interventions despite maternal antenatal therapy.
- The infant required 29 days of hospitalization but eventually recovered platelet counts.
- The case emphasizes the importance of early recognition and multidisciplinary management to reduce morbidity.

## Abstract

Immune thrombocytopenia (ITP) is the most common cause of thrombocytopenia in pregnancy, with maternal autoantibodies crossing the placenta and predisposing neonates to severe thrombocytopenia. Neonatal immune thrombocytopenia (NIT) can result in significant morbidity, including intracranial hemorrhage. We report a term neonate born to a mother with chronic severe ITP. Despite antenatal therapy with corticosteroids, intravenous immunoglobulin (IVIG), and elective cesarean delivery at a safe maternal platelet threshold, the neonate presented with severe thrombocytopenia requiring multiple platelet transfusions, repeated courses of IVIG, and adjunctive steroids. The infant’s course was prolonged, requiring 29 days of hospitalization, though ultimately discharged with recovery of platelet counts. This case underscores the persistent risk of NIT despite optimal maternal management, highlights maternal predictors such as prior affected offspring and history of splenectomy, and illustrates the therapeutic dilemmas in neonatal care. Early recognition and coordinated multidisciplinary management remain critical to reducing morbidity in mother-infant dyads affected by ITP.

## Linked entities

- **Chemicals:** steroids (PubChem CID 139082353)

## Full-text entities

- **Genes:** POU2F3 (POU class 2 homeobox 3) [NCBI Gene 25833] {aka Epoc-1, OCT-11, OCT11, OTF-11, PLA-1, PLA1}
- **Diseases:** neonatal thrombocytopenic purpura (MESH:D011696), Thrombocytopenia (MESH:D013921), blood loss (MESH:D016063), ecchymoses (MESH:D004438), disease (MESH:D004194), platelet (MESH:D001791), maternal disease (MESH:D000079262), upper extremity hemangioma (MESH:D006391), petechiae (MESH:D011693), NIT (MESH:D054098), intracranial hemorrhage (MESH:D020300), bruising (MESH:D003288), bleeding (MESH:D006470), neonatal disease (MESH:D007232), autoimmune disorder (MESH:D001327), ITP (MESH:D016553)
- **Chemicals:** dexamethasone (MESH:D003907), prednisone (MESH:D011241), Steroids (MESH:D013256)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12959383/full.md

## References

19 references — full list in the complete paper: https://tomesphere.com/paper/PMC12959383/full.md

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Source: https://tomesphere.com/paper/PMC12959383