4.4 Article

A case of neonatal thrombocytopenia due to maternal Helicobacter pylori-associated immune thrombocytopenia

Journal

HELICOBACTER
Volume 28, Issue 3, Pages -

Publisher

WILEY
DOI: 10.1111/hel.12976

Keywords

Helicobacter pylori; intravenous immunoglobulin; maternal immune thrombocytopenia; neonatal thrombocytopenia; neonate; pediatrics

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The association between Helicobacter pylori (H. pylori) infection and chronic immune thrombocytopenia (ITP) is well-established in adults but remains controversial in children. We report a case of neonatal passive ITP due to maternal H. pylori-associated ITP, suggesting that maternal H. pylori infection can lead to the production of platelet autoantibodies that destroy antibody-sensitized platelets in both the mother and neonate. Pregnant women diagnosed with H. pylori-associated ITP should receive eradication therapy to prevent their neonates from developing passive ITP.
Many studies in adults have suggested an association between Helicobacter pylori (H. pylori) infection and chronic immune thrombocytopenia (ITP). In adults with ITP and H. pylori infection, eradicating H. pylori is recommended as the first-line therapy. However, the association between ITP and H. pylori in children remains controversial. Diagnosing thrombocytopenia in pregnant women is challenging but crucial because maternal ITP causes neonatal ITP through transplacental transfer of immunoglobulin G, also known as passive ITP. Herein, we report a case of neonatal passive ITP due to maternal H. pylori-associated ITP. A boy was born at term with neonatal thrombocytopenia to a mother tentatively diagnosed with gestational thrombocytopenia. However, further examination suggested that maternal thrombocytopenia was associated with H. pylori, and neonatal thrombocytopenia was diagnosed as ITP due to maternal ITP. The newborn received intravenous immunoglobulin treatment, and the thrombocytopenia did not recur. The mother was examined using esophagogastroduodenoscopy, and her rapid urease test using gastric mucosa tissue samples was positive. Subsequently, she was diagnosed with H. pylori infection and received H. pylori eradication therapy, after which her platelet count remained normal. To our knowledge, this is the first reported case of neonatal passive ITP secondary to maternal H. pylori-associated ITP. This case suggests that maternal H. pylori infection can lead to the production of platelet autoantibodies, which can destroy antibody-sensitized platelets in the mother and neonate. To summarize, H. pylori infection can also cause ITP in children. Therefore, pregnant women diagnosed with H. pylori-associated ITP should receive H. pylori eradication therapy to prevent their neonates from developing passive ITP.

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