ArticleFrontiers in oncology2025
Case Report: Zolbetuximab-induced gastritis with protein-losing gastroenteropathy and hypogammaglobulinemia: a case implicating IgA vasculitis.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Clinical implications of zolbetuximab-associated hypoalbuminemia in CLDN18.2-positive gastric or gastroesophageal junction cancer.ESMO gastrointestinal oncology · 2026Article
- Claudin-18.2 in Gastric and Gastroesophageal Junction Adenocarcinoma: From Biology to Therapeutic Targeting: A Narrative Review.Targeted oncology · 2026Review
- Zolbetuximab-induced gastric mucosal injury and hypoalbuminemia: a mechanism-informed clinical analysis.Cancer chemotherapy and pharmacology · 2026Article
- Safety signals of zolbetuximab in gastric or gastroesophageal junction adenocarcinoma: a comprehensive analysis of the FDA adverse event reporting system (FAERS) data.Frontiers in oncology · 2026Article
- Zolbetuximab-associated adverse event reporting signals in gastric cancer: a FAERS disproportionality analysis.Frontiers in pharmacology · 2026Article
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13 authors.
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Abstract
Zolbetuximab (ZOL), a monoclonal antibody targeting Claudin-18.2, is a promising therapeutic agent for the treatment of advanced gastric cancer. We report the first case of ZOL-induced acute gastritis leading to protein-losing gastroenteropathy, characterized by severe hypogammaglobulinemia and hypoalbuminemia, possibly mediated by IgA vasculitis. A 41-year-old woman with metastatic Claudin-18.2-positive gastric cancer was treated with ZOL in combination with chemotherapy. On day 8 of the second treatment cycle, she developed severe gastrointestinal symptoms and immunologic abnormalities. Laboratory tests revealed marked hypogammaglobulinemia (IgG 193 mg/dL) and hypoalbuminemia (albumin 1.9 g/dL). Esophagogastroduodenoscopy showed severe acute gastritis, and biopsy specimens demonstrated infiltration of CD4
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