Paika Sulaiman, Machini Matthew, Parmar Mayur S
Dr. Kiran C. Patel College of Osteopathic Medicine, Nova Southeastern University, Clearwater, Florida, USA.
Oxid Med Cell Longev. 2025 Aug 5;2025:7041213. doi: 10.1155/omcl/7041213. eCollection 2025.
Glucose-6-phosphate dehydrogenase (G6PD) deficiency, a prevalent enzymopathy, predisposes individuals to hemolytic anemia upon exposure to various medications. This literature review explores the molecular underpinnings of drug-induced hemolytic anemia (DIHA) in G6PD-deficient patients, focusing on dapsone, amoxicillin, and primaquine. These drugs are essential for treating infections such as leprosy and malaria. However, they can damage red blood cell (RBC) membranes through complex mechanisms distinct from traditional immune-mediated pathways. Evidence suggests that drug metabolites, such as dapsone hydroxylamine and 5-hydroxyprimaquine, induce oxidative stress and disrupt RBC membrane integrity. The band 3 protein, a critical component of the RBC cytoskeleton, emerges as a key player in this process, undergoing tyrosine phosphorylation and aggregation, leading to membrane remodeling and instability. This review underscores the need for further research to elucidate the precise molecular interactions involved in drug-induced hemolysis in G6PD deficiency. Understanding these mechanisms may pave the way for developing targeted therapies, including adjuvant treatments and novel drug formulations, to mitigate the risk of hemolytic anemia in this vulnerable population.
葡萄糖-6-磷酸脱氢酶（G6PD）缺乏症是一种常见的酶病，会使个体在接触各种药物后易患溶血性贫血。这篇文献综述探讨了G6PD缺乏症患者药物性溶血性贫血（DIHA）的分子基础，重点关注氨苯砜、阿莫西林和伯氨喹。这些药物对于治疗麻风病和疟疾等感染至关重要。然而，它们可通过不同于传统免疫介导途径的复杂机制损害红细胞（RBC）膜。有证据表明，药物代谢产物，如氨苯砜羟胺和5-羟基伯氨喹，会诱导氧化应激并破坏RBC膜的完整性。带3蛋白是RBC细胞骨架的关键组成部分，在这一过程中成为关键因素，经历酪氨酸磷酸化和聚集，导致膜重塑和不稳定。这篇综述强调需要进一步研究，以阐明G6PD缺乏症中药物诱导溶血所涉及的精确分子相互作用。了解这些机制可能为开发靶向治疗方法铺平道路，包括辅助治疗和新型药物制剂，以降低这一脆弱人群溶血性贫血的风险。
