Nonalcoholic fatty liver disease in primary aldosteronism: a pilot study.

BACKGROUND: An impairment of glucose metabolism, contributing to the increased cardiovascular risk, has been shown in primary aldosteronism (PA). Insulin resistance is associated with nonalcoholic fatty liver disease (NAFLD) and may play a role in its pathophysiology. The aim of this study was to investigate the association between NAFLD and PA, and to identify determinants of NAFLD in this condition. METHODS: A total of 40 patients with PA, 40 sex-, age-, and body mass index matched patients with low-renin essential hypertension (LREH) and 40 normotensive subjects were studied. According to ultrasound detection of fatty liver, each group was subdivided in two subsets: with NAFLD and without NAFLD. Patients with diabetes, obesity, and hyperlipidemia were excluded. RESULTS: Prevalence of NAFLD in PA was similar to that observed in LREH patients, and higher (P < 0.01) than in normotensive controls. Serum potassium was lower in PA than in LREH patients with NAFLD (P < 0.001), while it was similar in PA and LREH patients without NAFLD. At univariate analysis, plasma aldosterone, homeostasis model assessment (HOMA) index and hypokalemia were determinants of NAFLD in PA (P < 0.05), while HOMA index was associated with NAFLD in LREH (P < 0.05). At multivariable analysis, only hypokalemia remained associated with NAFLD in PA (P = 0.02). CONCLUSIONS: The results of this pilot study suggest that, in the absence of major risk factors for liver disease, NAFLD is a frequent finding in PA. Patients with PA and hypokalemia are more insulin resistant and have higher prevalence of NAFLD than those with normokalemia, indicating greater risk for metabolic and liver disease in this subgroup.

Nonalcoholic fatty liver disease, adiponectin and insulin resistance in dipper and nondipper essential hypertensive patients.

OBJECTIVE: The pathogenesis of nonalcoholic fatty liver disease (NAFLD) is multifactorial, and the presence of insulin resistance is recognized as the pathophysiological hallmark of this condition. Arterial hypertension is referred as an insulin-resistant state, and insulin resistance may substantially contribute to the cardiovascular risk in this disorder. We examined the inter-relationship between insulin sensitivity, adiponectin levels, and NAFLD in hypertensive patients with different circadian blood pressure profiles. METHODS: Eighty never-treated patients with essential hypertension were selected for having a nocturnal decrement of blood pressure that was at least 10% (dippers, n=47) or less than 10% (nondippers, n=33) of daytime values. No patient had diabetes mellitus, obesity, hyperlipidemia, or other risk factors for hepatic disease. The two groups were similar as to sex, age, and BMI. Abdominal fat distribution and NAFLD were assessed by ultrasonography. RESULTS: Hepatic steatosis was detected in 57.5% of all patients. Nondippers showed a higher prevalence of NAFLD than dippers (81.8 vs. 40.4%, P<0.005). Insulin and the homeostasis model of assessment index were higher (P<0.001) and adiponectin was lower (P<0.001) in nondippers than in dippers, whereas no difference was found in regional fat, liver enzymes, and other metabolic parameters. At multivariate analysis, factors independently associated with nondipping were insulin (P<0.05) and adiponectin (P<0.01) with the homeostasis model of assessment index being of borderline significance. CONCLUSION: In the absence of major risk factors for the development of NAFLD, a high prevalence of liver steatosis was associated with insulin resistance and low adiponectin levels in essential hypertensive patients with a nondipping profile.