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葡萄糖-6-磷酸脱氢酶缺乏症在乳糜泻患者中的高发率。

High Frequency of Glucose-6-Phosphate Dehydrogenase Deficiency in Patients Diagnosed with Celiac Disease.

机构信息

Dipartimento di Medicina, Chirurgia e Farmacia, University of Sassari, Viale San Pietro 8, 07100 Sassari, Italy.

Baylor College of Medicine, One Baylor Plaza Blvd, Houston, TX 77030, USA.

出版信息

Nutrients. 2022 Apr 26;14(9):1815. doi: 10.3390/nu14091815.

Abstract

UNLABELLED

Celiac disease (CD) is characterized by a proinflammatory state associated with the production of reactive oxygen species, i.e., a condition of oxidative stress. In this study, we tested the hypothesis that the inherited deficiency of glucose-6-phosphate dehydrogenase (G6PD), by causing impaired antioxidant defense, may increase the risk of CD.

METHODS

A retrospective monocentric case-control study was performed using the clinical records of 8338 outpatients (64.6% women) scheduled for upper endoscopy between 2002 and 2021 in Northern Sardinia. Overall, 627 were found to have CD (7.5%), and 1027 resulted to be G6PD-deficiency carriers (12.3%). Since randomization was impractical, the potential covariates imbalance between cases and controls was minimized using a 1:2 propensity-score-matched (PSM) analysis.

RESULTS

Overall, G6PD deficiency was associated with increased risk of CD (odds ratio (OR) 1.50; 95% confidence interval (CI) 1.19-1.90). The PSM procedure identified 1027 G6PD-deficient and 2054 normal patients. Logistic regression including the propensity score detected for G6PD deficiency an OR of 1.48 (95%CI 1.13-1.95; = 0.004).

CONCLUSIONS

Our findings show that the enzyme defect was significantly and positively associated with CD, in line with the pro-oxidant impact of the enzyme defect observed in animal models and humans.

摘要

目的

本研究旨在检验葡萄糖-6-磷酸脱氢酶(G6PD)遗传缺陷通过损害抗氧化防御,从而增加乳糜泻(CD)风险的假说。

方法

采用回顾性单中心病例对照研究,纳入 2002 年至 2021 年期间在撒丁岛北部接受上消化道内镜检查的 8338 名门诊患者(64.6%为女性)的临床记录。共发现 627 例 CD(7.5%),1027 例为 G6PD 缺乏携带者(12.3%)。由于随机化不切实际,采用 1:2 倾向评分匹配(PSM)分析最小化病例和对照组之间潜在混杂因素的不平衡。

结果

总体而言,G6PD 缺乏与 CD 风险增加相关(比值比(OR)1.50;95%置信区间(CI)1.19-1.90)。PSM 程序确定了 1027 例 G6PD 缺乏和 2054 例正常患者。包括倾向评分的逻辑回归检测到 G6PD 缺乏的 OR 为 1.48(95%CI 1.13-1.95; = 0.004)。

结论

我们的研究结果表明,该酶缺陷与 CD 显著正相关,与动物模型和人类观察到的酶缺陷的促氧化作用一致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aaac/9099929/2452400d01a8/nutrients-14-01815-g001.jpg

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