From Section II (S.X.), Department of Neurology (Z.O., Y.C., J.L., F.O., G.L., S.T., W.H., J.Z.), The First Affiliated Hospital, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Guangzhou; Department of Epidemiology and Biostatistics (X.G.), School of Public Health, Guangdong Pharmaceutical University; Department of Neurology and Stroke Center (Y.Z.), The First Affiliated Hospital of Jinan University, Guangzhou; Department of Neurology (Z.L.), The First Affiliated Hospital of Guangxi Medical University, Nanning; and Department of Neurology (W.D.), Meizhou Hospital Affiliated to Sun Yat-sen University, China.
Neurology. 2020 Sep 15;95(11):e1471-e1478. doi: 10.1212/WNL.0000000000010245. Epub 2020 Jul 10.
To assess the risk of glucose-6-phosphate dehydrogenase (G6PD) on stroke prognosis, we compared outcomes between patients with stroke with and without G6PD deficiency.
The study recruited 1,251 patients with acute ischemic stroke. Patients were individually categorized into G6PD-deficiency and non-G6PD-deficiency groups according to G6PD activity upon admission. The primary endpoint was poor outcome at 3 months defined by a modified Rankin Scale (mRS) score ≥2 (including disability and death). Secondary outcomes included the overall mRS score at 3 months and in-hospital death and all death within 3 months. Logistic regression and Cox models, adjusted for potential confounders, were fitted to estimate the association of G6PD deficiency with the outcomes.
Among 1,251 patients, 150 (12.0%) were G6PD-deficient. Patients with G6PD deficiency had higher proportions of large-artery atherosclerosis (odds ratio [OR] 1.53, 95% confidence interval [CI] 1.09-2.17) and stroke history (OR 1.93, 95% CI 1.26-2.90) compared to the non-G6PD-deficient group. The 2 groups differed significantly in the overall mRS score distribution (adjusted common OR 1.57, 95% CI 1.14-2.17). Patients with G6PD deficiency had higher rates of poor outcome at 3 months (adjusted OR 1.73, 95% CI 1.08-2.76; adjusted absolute risk increase 13.0%, 95% CI 2.4%-23.6%). The hazard ratio of in-hospital death for patients with G6PD-deficiency was 1.46 (95% CI 1.37-1.84).
G6PD deficiency is associated with the risk of poor outcome at 3 months after ischemic stroke and may increase the risk of in-hospital death. These findings suggest the rationality of G6PD screening in patients with stroke.
评估葡萄糖-6-磷酸脱氢酶（G6PD）对卒中预后的影响，我们比较了卒中伴和不伴 G6PD 缺乏患者的结局。
这项研究纳入了 1251 例急性缺血性卒中患者。根据入院时 G6PD 活性，将患者单独分为 G6PD 缺乏组和非 G6PD 缺乏组。主要终点是 3 个月时改良 Rankin 量表（mRS）评分≥2（包括残疾和死亡）定义的不良结局。次要结局包括 3 个月时的总体 mRS 评分以及住院期间死亡和 3 个月内的全因死亡。采用逻辑回归和 Cox 模型，调整潜在混杂因素后，评估 G6PD 缺乏与结局的关系。
在 1251 例患者中，150 例（12.0%）为 G6PD 缺乏。与非 G6PD 缺乏组相比，G6PD 缺乏组患者大动脉粥样硬化（优势比[OR] 1.53，95%置信区间[CI] 1.09-2.17）和卒中史（OR 1.93，95% CI 1.26-2.90）的比例更高。两组患者总体 mRS 评分分布差异显著（校正常见 OR 1.57，95% CI 1.14-2.17）。G6PD 缺乏患者 3 个月时不良结局发生率更高（校正 OR 1.73，95% CI 1.08-2.76；校正绝对风险增加 13.0%，95% CI 2.4%-23.6%）。G6PD 缺乏患者住院期间死亡的风险比为 1.46（95% CI 1.37-1.84）。
G6PD 缺乏与缺血性卒中后 3 个月的不良结局风险相关，并且可能增加住院期间死亡的风险。这些发现提示对卒中患者进行 G6PD 筛查具有合理性。
