Acute Hemolytic Anemia Due to Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency Triggered by Helicobacter pylori Quadruple Therapy in a Jehovah’s Witness: A Case Report

Glucose-6-phosphate dehydrogenase (G6PD) deficiency, the most common erythrocyte enzymatic disorder, predisposes patients to oxidative stress-induced acute hemolysis. Affected patients are at risk of developing hemolysis in the setting of triggers such as certain drugs, infections, or foods (fava beans). Although some drugs like antimalarials (primaquine, tafenoquine), sulfonamides, and dapsone are well-known triggers of hemolysis, reports of this adverse effect are rare with standard bismuth-based quadruple therapy for <i>Helicobacter pylori</i>. In this report, we present a 65-year-old male who developed profound anemia (hemoglobin 5.8 g/dL, drop of 4.4 points from baseline) within hours of initiating metronidazole- and tetracycline-containing quadruple therapy. Laboratory evaluation revealed reduced G6PD enzyme activity (3.8 U/g; normal 9.9-16.6 U/g), confirming acute hemolytic anemia secondary to G6PD deficiency. Notably, the patient was a Jehovah's Witness and declined all blood products, requiring atypical management. Quadruple therapy was discontinued, and the patient was managed with intravenous fluids, iron supplementation, and erythropoietin (EPO) therapy, resulting in gradual hematologic recovery. Regarding <i>H. pylori </i>treatment, the patient was initiated on triple therapy (clarithromycin, amoxicillin, proton pump inhibitor), without recurrence of hemolysis. This case highlights the rarity of G6PD deficiency as an etiology of unexplained hemolysis during initiation of <i>H. pylori</i> eradication therapy and underscores the importance of unique management strategies in the setting of blood transfusion refusal. Clinicians should maintain a high suspicion for G6PD deficiency in high-risk populations and exercise caution when prescribing oxidative regimens for <i>H. pylori</i> in these patients.