Chin-Li Lu1, Ya-Hui Chang2, Yu Sun3, Chung-Yi Li4. 1. Graduate Institute of Food Safety, College of Agriculture and Natural Resources, National Chung Hsing University, Taichung, Taiwan. 2. Department of Public Health, College of Medicine, National Cheng Kung University, Tainan, Taiwan. 3. Department of Neurology, En Chu Kong Hospital, Sanxia District, New Taipei City, Taiwan. 4. Department of Public Health, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Department of Public Health, College of Public Health, China Medical University, Taichung, Taiwan. Electronic address: cyli99@mail.ncku.edu.tw.
Abstract
AIMS: This study was conducted to investigate potential link between type 2 diabetes mellitus (T2DM) and epilepsy, and the role of severe hypoglycaemia (SH) might play in the relationship. METHODS: This was a cohort study based on Taiwan's National Health insurance claims. Totally 751,792 people with T2DM and 824,253 matched controls were identified in 2002-2003 and followed to incidence of epilepsy or end of 2011. We used Cox proportional hazard model to relate epilepsy incidence to separate and joint effects of T2DM and SH. A possible mediation effect of SH on the association between T2DM and epilepsy was analyzed. RESULTS: Over a 10-year follow-up, patients with T2DM had a higher incidence rate of epilepsy than controls (35.0 vs 21.9 per 10,000 person-years). After controlling for potential confounders including SH, T2DM increased the hazard of epilepsy by some 50%. The stratified analysis further indicated that T2DM (hazard ratio (HR)=1.44, 95% confidence interval (CI) = 1.40-1.47), and SH (HR = 2.22, 95% CI = 1.76-2.81) were both independent risk factors for epilepsy. SH did not modify but mediated 12% of the association between T2DM and epilepsy. CONCLUSION: Our findings supported that SH may increase the risk of epilepsy, and that T2DM may increase risk of epilepsy independent of SH.
AIMS: This study was conducted to investigate potential link between type 2 diabetes mellitus (T2DM) and epilepsy, and the role of severe hypoglycaemia (SH) might play in the relationship. METHODS: This was a cohort study based on Taiwan's National Health insurance claims. Totally 751,792 people with T2DM and 824,253 matched controls were identified in 2002-2003 and followed to incidence of epilepsy or end of 2011. We used Cox proportional hazard model to relate epilepsy incidence to separate and joint effects of T2DM and SH. A possible mediation effect of SH on the association between T2DM and epilepsy was analyzed. RESULTS: Over a 10-year follow-up, patients with T2DM had a higher incidence rate of epilepsy than controls (35.0 vs 21.9 per 10,000 person-years). After controlling for potential confounders including SH, T2DM increased the hazard of epilepsy by some 50%. The stratified analysis further indicated that T2DM (hazard ratio (HR)=1.44, 95% confidence interval (CI) = 1.40-1.47), and SH (HR = 2.22, 95% CI = 1.76-2.81) were both independent risk factors for epilepsy. SH did not modify but mediated 12% of the association between T2DM and epilepsy. CONCLUSION: Our findings supported that SH may increase the risk of epilepsy, and that T2DM may increase risk of epilepsy independent of SH.
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