Jia-Chao Qi1, Jian-Chai Huang1, Qi-Chang Lin2, Jian-Ming Zhao1, Xin Lin1, Li-Da Chen3, Jie-Feng Huang1, Xiao Chen1. 1. Fujian Provincial Sleep-Disordered Breathing Clinic Center, Laboratory of Respiratory Disease of the Fujian Medical University, Department of Respiratory Medicine, the First Affiliated Hospital of Fujian Medical University, No. 20, Chazhong Rd., Taijiang, Fuzhou, 350005, Fujian Province, People's Republic of China. 2. Fujian Provincial Sleep-Disordered Breathing Clinic Center, Laboratory of Respiratory Disease of the Fujian Medical University, Department of Respiratory Medicine, the First Affiliated Hospital of Fujian Medical University, No. 20, Chazhong Rd., Taijiang, Fuzhou, 350005, Fujian Province, People's Republic of China. chang4e@126.com. 3. Department of Respiratory Medicine, Zhangzhou Affiliated Hospital of Fujian Medical University, No. 59, West Shengli Rd., Xiangcheng, Zhangzhou, 363000, Fujian Province, People's Republic of China.
Abstract
PURPOSE: Obstructive sleep apnea (OSA) is closely related to nonalcoholic fatty liver disease (NAFLD), though the mechanism is not conclusive as obesity is a confounder. The objective of this observational study was to investigate the correlation between these disorders in nonobese subjects. METHODS: We consecutively enrolled nonobese individuals undergoing polysomnography and abdominal ultrasonography and analyzed differences in NAFLD patients grouped by the apnea-hypopnea index (AHI) and in OSA patients according to the presence or absence of NAFLD. Multivariate regression analysis was used to evaluate the independent risks of NAFLD in OSA patients. RESULTS: A total of 175 participants were included. The 106 ultrasound-diagnosed NAFLD patients were classified into four groups by AHI. There were no significant differences in triglycerides (TG), serum aminotransferase levels of alanine aminotransferase and aspartate aminotransferase, high-sensitivity C-reactive protein, and homeostasis model assessment of insulin resistance (HOMA-IR) with worsening OSA. In both OSA patients with NAFLD and those without NAFLD, body mass index (BMI), the lowest oxygen saturation (LaSO2), HOMA-IR, and TG were significantly associated. Additionally, BMI, LaSO2, and TG independently predicted the development of NAFLD after adjustments (odds ratio [OR] = 1.562, p = 0.003; OR = 0.960, p = 0.03; OR = 3.410, p < 0.001, respectively). CONCLUSIONS: In nonobese subjects, OSA itself does not appear to induce significant changes in liver enzymes. With reference to lipid metabolism, weight control and OSA-related hypoxemia are key factors in reducing the risk of NAFLD in OSA patients. Additional large-scale, prospective studies are warranted to investigate the impact of OSA on liver injury in nonobese adults.
PURPOSE:Obstructive sleep apnea (OSA) is closely related to nonalcoholic fatty liver disease (NAFLD), though the mechanism is not conclusive as obesity is a confounder. The objective of this observational study was to investigate the correlation between these disorders in nonobese subjects. METHODS: We consecutively enrolled nonobese individuals undergoing polysomnography and abdominal ultrasonography and analyzed differences in NAFLD patients grouped by the apnea-hypopnea index (AHI) and in OSA patients according to the presence or absence of NAFLD. Multivariate regression analysis was used to evaluate the independent risks of NAFLD in OSA patients. RESULTS: A total of 175 participants were included. The 106 ultrasound-diagnosed NAFLD patients were classified into four groups by AHI. There were no significant differences in triglycerides (TG), serum aminotransferase levels of alanine aminotransferase and aspartate aminotransferase, high-sensitivity C-reactive protein, and homeostasis model assessment of insulin resistance (HOMA-IR) with worsening OSA. In both OSA patients with NAFLD and those without NAFLD, body mass index (BMI), the lowest oxygen saturation (LaSO2), HOMA-IR, and TG were significantly associated. Additionally, BMI, LaSO2, and TG independently predicted the development of NAFLD after adjustments (odds ratio [OR] = 1.562, p = 0.003; OR = 0.960, p = 0.03; OR = 3.410, p < 0.001, respectively). CONCLUSIONS: In nonobese subjects, OSA itself does not appear to induce significant changes in liver enzymes. With reference to lipid metabolism, weight control and OSA-related hypoxemia are key factors in reducing the risk of NAFLD in OSA patients. Additional large-scale, prospective studies are warranted to investigate the impact of OSA on liver injury in nonobese adults.
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