Late‐onset aspirin‐related hemolysis and subsequent subdural hemorrhage in patient with glucose‐6‐phosphate dehydrogenase deficiency

Abstract

Key Clinical Message Aspirin‐related hemolysis in G6PD deficiency could be late‐onset during long‐term administration. Hemolytic anemia could continue for a relatively long time in elder patient with G6PD deficiency, which might be related to other adverse events. Abstract Aspirin‐related hemolysis in G6PD‐deficient individuals was generally reported among patients who received high‐dose supplements within several days after ingestion. The safety of long‐term and low‐dose (50–325 mg/day) aspirin in patients coexist G6PD deficiency and cardiovascular disease is neglected in clinical practice. In this case, we observed a late‐onset hemolysis and subsequent fatal subdural hemorrhage in one G6PD‐deficient individual who had received long‐term and low‐dose aspirin. An 83‐year‐old male was diagnosed with acute ischemic stroke and treated with 100 mg/day aspirin at the emergency room. After admission, the patient was diagnosed with severe G6PD deficiency based on enzyme activity, but no hemolysis occurred within 10‐day aspirin therapy in the hospital. Hence, 100 mg/day aspirin was continued on discharge. Two months later, the patient presented acute hemolysis manifested as fatigue, dark urine, and moderate jaundice. Although hemolysis was self‐limit in a few days, hemoglobin decline continued for 20 days until a fatal subdural hemorrhage occurred. Our study indicated aspirin‐related hemolysis could be late‐onset in G6PD‐deficient individual even receiving low‐dose treatment and is probably linked to subsequent major bleeding events.

Keywords

• aspirin
• glucose‐6‐phosphate dehydrogenase deficiency
• hemolysis
• ischemic stroke
• subdural hemorrhage