BACKGROUND: Mechanisms involving obstructive sleep apnea (OSA) and nonalcoholic fatty liver disease (NAFLD) are under increasing assessment. This study evaluated the correlation of OSA with the severity of NAFLD. MATERIALS AND METHODS: Prospective study in which patients with at least one of metabolic syndrome (MS) criteria were initially assessed by the NAFLD fibrosis score and according to the outcome (intermediate or high risk of advanced fibrosis) underwent liver biopsy (exception of patients with clinical, ultrasound or endoscopic diagnosis of cirrhosis). All patients performed polysomnography. For statistical analysis, the patients were assembled into two groups: (1) without apnea or mild apnea and (2) moderate or severe apnea. In the correlation of OSA with the severity of NAFLD, the risk factors evaluated were: degree of steatosis, presence and severity of nonalcoholic steatohepatitis (NASH) and fibrosis. RESULTS: Fifty-one patients were evaluated, 80.4% had systemic arterial hypertension (SAH), 68.6% type 2 diabetes mellitus, 62.7% dyslipidemia and 96.1% MS. Regarding the histological evaluation (n = 48), all had steatosis, 95.8% steatohepatitis and 83.3% fibrosis. In polysomnography, 80.4% were group 1 and 19.6% group 2. In univariate analysis, no correlation was found between steatosis severity, NASH and presence or severity of fibrosis with OSA. A multivariate analysis adjusted for obesity level, found that patients with moderate to severe OSA had an increased risk of hepatic fibrosis (odds ratio 1.22, 95% confidence interval: 1.02-1.45, P = 0.027). CONCLUSION: The present study demonstrated an association between fibrosis and moderate to severe OSA, regardless of obesity.
BACKGROUND: Mechanisms involving obstructive sleep apnea (OSA) and nonalcoholic fatty liver disease (NAFLD) are under increasing assessment. This study evaluated the correlation of OSA with the severity of NAFLD. MATERIALS AND METHODS: Prospective study in which patients with at least one of metabolic syndrome (MS) criteria were initially assessed by the NAFLD fibrosis score and according to the outcome (intermediate or high risk of advanced fibrosis) underwent liver biopsy (exception of patients with clinical, ultrasound or endoscopic diagnosis of cirrhosis). All patients performed polysomnography. For statistical analysis, the patients were assembled into two groups: (1) without apnea or mild apnea and (2) moderate or severe apnea. In the correlation of OSA with the severity of NAFLD, the risk factors evaluated were: degree of steatosis, presence and severity of nonalcoholic steatohepatitis (NASH) and fibrosis. RESULTS: Fifty-one patients were evaluated, 80.4% had systemic arterial hypertension (SAH), 68.6% type 2 diabetes mellitus, 62.7% dyslipidemia and 96.1% MS. Regarding the histological evaluation (n = 48), all had steatosis, 95.8% steatohepatitis and 83.3% fibrosis. In polysomnography, 80.4% were group 1 and 19.6% group 2. In univariate analysis, no correlation was found between steatosis severity, NASH and presence or severity of fibrosis with OSA. A multivariate analysis adjusted for obesity level, found that patients with moderate to severe OSA had an increased risk of hepatic fibrosis (odds ratio 1.22, 95% confidence interval: 1.02-1.45, P = 0.027). CONCLUSION: The present study demonstrated an association between fibrosis and moderate to severe OSA, regardless of obesity.