Aspirin Therapy in Cardiovascular Disease with Glucose‑6‑Phosphate Dehydrogenase Deficiency, Safe or Not?
Aspirin Therapy in Cardiovascular Disease with Glucose‑6‑Phosphate Dehydrogenase Deficiency, Safe or Not?
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DOI：
10.1007/s40256-020-00460-8
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发表时间：
2020
影响因子：
3
通讯作者：
Jinsheng Zeng
中科院分区：
文献类型：
--
作者：
Jianle Li;Yicong Chen;Zilin Ou;Fubing Ouyang;Jiahui Liang;Zimu Jiang;Chunyong Chen;Pingping Li;Jiaxin Chen;Jiating Wei;Jinsheng Zeng
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzyme defect, which may present as acute hemolysis, neonatal jaundice, or chronic hemolysis. Ingestion of fava beans, as well as infection and certain drugs, are the most typical causes of acute hemolysis in people with G6PD deficiency. Aspirin, the cornerstone in current therapies for the prevention of cardiovascular disease (CVD), is occasionally reported to induce acute hemolysis in G6PD-deficient individuals. G6PD deficiency is typically asymptomatic and many CVD patients with this enzyme defect start to take long-term aspirin therapy without G6PD activity examination; however, no consensus on the safety of aspirin in this population has been reached. A few studies have reported on this issue and produced contradictory results. In this review, we discuss the possible mechanisms of aspirin-induced hemolysis, and summarize clinical evidence regarding the safety of aspirin in subjects with G6PD deficiency.
