Aspirin adherence in subjects with glucose-6-phosphate-dehydrogenase deficiency having an acute coronary syndrome

Sanna, Giuseppe D; Uras, Marco; Murgia, Alessandro; Talanas, Giuseppe; Moccia, Eleonora; Corda, G; Mura, Erica; Saba, Pier Sergio; Parodi, Guido

doi:10.1093/ehjcvp/pvaa060

Cited by 6 publications

(14 citation statements)

References 10 publications

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“…In southern China, the prevalence of G6PD deficiency reportedly varies from 4% to 10% 2 . Aspirin is the most extensively used antiplatelet agent for secondary stroke prevention, 2 but its safety in patients with G6PD deficiency is controversial 1,3‐10 . Our previous study revealed a higher risk of moderate‐to‐severe bleeding after aspirin used in patients with G6PD deficiency, 3 which might lead to a decline in hemoglobin.…”

Section: Introductionmentioning

confidence: 98%

“… 2 Aspirin is the most extensively used antiplatelet agent for secondary stroke prevention, 2 but its safety in patients with G6PD deficiency is controversial. 1 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 Our previous study revealed a higher risk of moderate‐to‐severe bleeding after aspirin used in patients with G6PD deficiency, 3 which might lead to a decline in hemoglobin. However, the hemoglobin decline was accompanied by a significant bilirubin increase after aspirin treatment in the G6PD‐deficient patients, suggesting hemolysis.…”

Section: Introductionmentioning

confidence: 98%

“…Glucose‐6‐phosphate dehydrogenase (G6PD) deficiency is the most common human enzyme defect, affecting more than 500 million individuals worldwide. 1 In southern China, the prevalence of G6PD deficiency reportedly varies from 4% to 10%. 2 Aspirin is the most extensively used antiplatelet agent for secondary stroke prevention, 2 but its safety in patients with G6PD deficiency is controversial.…”

Section: Introductionmentioning

confidence: 99%

“…Glucose‐6‐phosphate dehydrogenase (G6PD) deficiency is the most common human enzyme defect, affecting more than 500 million individuals worldwide 1 . In southern China, the prevalence of G6PD deficiency reportedly varies from 4% to 10% 2 .…”

Section: Introductionmentioning

confidence: 99%

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Association between aspirin‐induced hemoglobin decline and outcome after acute ischemic stroke in G6PD‐deficient patients

Chen

et al. 2021

CNS Neurosci Ther

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Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Association between aspirin‐induced hemoglobin decline and outcome after acute ischemic stroke in G6PD‐deficient patients

Chen

et al. 2021

CNS Neurosci Ther

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“…However, the small number of studies does not allow a definitive conclusion about the safety of ASA [ 157 ]. Recently, Sanna et al, examining an unselected population of acute coronary syndrome patients from Northern Sardinia with normal or deficient G6PD activity, treated with low doses (100 mg/day) of ASA, did not observe any case of hemolysis [ 158 ]. Unfortunately, these results cannot be generalized, as the risk of hemolysis is linked to the severity of the deficient phenotype and, ultimately, to the specific gene variant that caused it [ 154 ].…”

Section: Metabolic Implications Of G6pd Deficiency In Various Organs and Tissuesmentioning

confidence: 99%

The Controversial Role of Glucose‐6‐Phosphate Dehydrogenase Deficiency on Cardiovascular Disease: A Narrative Review

Dore

Parodi

Portoghese

2021

Oxidative Medicine and Cellular Longevity

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Cardiovascular disorders (CVD) are highly prevalent and the leading cause of death worldwide. Atherosclerosis is responsible for most cases of CVD. The plaque formation and subsequent thrombosis in atherosclerosis constitute an ongoing process that is influenced by numerous risk factors such as hypertension, diabetes, dyslipidemia, obesity, smoking, inflammation, and sedentary lifestyle. Among the various risk and protective factors, the role of glucose-6-phosphate dehydrogenase (G6PD) deficiency, the most common inborn enzyme disorder across populations, is still debated. For decades, it has been considered a protective factor against the development of CVD. However, in the recent years, growing scientific evidence has suggested that this inherited condition may act as a CVD risk factor. The role of G6PD deficiency in the atherogenic process has been investigated using in vitro or ex vivo cellular models, animal models, and epidemiological studies in human cohorts of variable size and across different ethnic groups, with conflicting results. In this review, the impact of G6PD deficiency on CVD was critically reconsidered, taking into account the most recent acquisitions on molecular and biochemical mechanisms, namely, antioxidative mechanisms, glutathione recycling, and nitric oxide production, as well as their mutual interactions, which may be impaired by the enzyme defect in the context of the pentose phosphate pathway. Overall, current evidence supports the notion that G6PD downregulation may favor the onset and evolution of atheroma in subjects at risk of CVD. Given the relatively high frequency of this enzyme deficiency in several regions of the world, this finding might be of practical importance to tailor surveillance guidelines and facilitate risk stratification.

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

Li,

Chen,

Deng

et al. 2024

Clinical Case Reports

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Key Clinical MessageAspirin‐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.AbstractAspirin‐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.

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Aspirin adherence in subjects with glucose-6-phosphate-dehydrogenase deficiency having an acute coronary syndrome

Cited by 6 publications

References 10 publications

Association between aspirin‐induced hemoglobin decline and outcome after acute ischemic stroke in G6PD‐deficient patients

Association between aspirin‐induced hemoglobin decline and outcome after acute ischemic stroke in G6PD‐deficient patients

The Controversial Role of Glucose‐6‐Phosphate Dehydrogenase Deficiency on Cardiovascular Disease: A Narrative Review

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

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