Increased risk for diabetes mellitus in patients with carbon monoxide poisoning
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Chien-Cheng Huang1,2,3,4,5, Chung-Han Ho6,7, Yi-Chen Chen6, Hung-Jung Lin1,8,9, Chien-Chin Hsu1,8, Jhi-Joung Wang6, Shih-Bin Su5,10,11 and How-Ran Guo2,12
1Department of Emergency Medicine, Chi Mei Medical Center, Tainan, Taiwan
2Department of Environmental and Occupational Health, College of Medicine, National Cheng Kung University, Tainan, Taiwan
3Bachelor Program of Senior Service, Southern Taiwan University of Science and Technology, Tainan, Taiwan
4Department of Geriatrics and Gerontology, Chi Mei Medical Center, Tainan, Taiwan
5Department of Occupational Medicine, Chi Mei Medical Center, Tainan, Taiwan
6Department of Medical Research, Chi Mei Medical Center, Tainan, Taiwan
7Department of Pharmacy, Chia Nan University of Pharmacy and Science, Tainan, Taiwan
8Department of Biotechnology, Southern Taiwan University of Science and Technology, Tainan, Taiwan
9Department of Emergency Medicine, Taipei Medical University, Taipei, Taiwan
10Department of Leisure, Recreation and Tourism Management, Southern Taiwan University of Science and Technology, Tainan, Taiwan
11Department of Medical Research, Chi Mei Medical Center, Tainan, Taiwan
12Department of Occupational and Environmental Medicine, National Cheng Kung University Hospital, Tainan, Taiwan
How-Ran Guo, email: [email protected]
Keywords: brain, carbon monoxide, endocrine, diabetes mellitus, poisoning
Received: February 06, 2017 Accepted: June 04, 2017 Published: June 29, 2017
Carbon monoxide poisoning (COP) causes hypoxic injury and inflammatory and immunological reactions in the brain and local organs including the pancreas. Therefore, it is plausible that COP may increase the risk for developing diabetes mellitus (DM), but studies on this possible association are limited. We conducted a nationwide study in Taiwan to fill the data gap. We used the Nationwide Poisoning Database and the Longitudinal Health Insurance Database 2000 to identify all COP patients diagnosed between 1999 and 2012 (the study cohort) and then construct a comparison cohort of patients without COP through matching at 1:3 by the index date and age. The risk for DM between the two cohorts was compared by following up until 2013. We also investigated the independent predictors for DM in all the patients. During the study period, 22,308 COP patients were identified, and 66,924 non-COP patients were included in the comparison cohort accordingly. Patients with COP had an increased risk for DM with an adjusted hazard ratio (AHR) of 1.92 (95% confidence interval [CI]: 1.79–2.06) after adjusting for age, sex, comorbidities, and monthly income, especially in the subgroups of age <35 years, age ≥ 65 years, female sex, and comorbidities with congestive heart failure, hyperthyroidism, and polycystic ovary syndrome. Cox proportional hazard regression analysis showed that the increased risk for DM was highest in the first month after COP (AHR= 3.38; 95% CI: 2.29–4.99) and lasted even after 4 years (AHR= 1.82; 95% CI: 1.62–2.04). We found that COP, older age, male sex, hypertension, hyperlipidemia, hyperuricemia, and low monthly income were independent predictors for DM. Intervention studies are needed to validate the results and delineate the detailed mechanisms.
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