Fatty liver is associated with recurrent bacterial infections independent of metabolic syndrome.

BACKGROUND: Diabetes mellitus and obesity are important components of metabolic syndrome (MetS) which are associated with infections. MetS is frequent in nonalcoholic fatty liver disease (NAFLD). AIMS: The objective of this study was to examine whether patients with NAFLD are at higher risk of recurrent bacterial infections (RBIs). METHODS: Two-hundred and forty-seven from 296 hospitalized NAFLD patients were assessed over a three-year period for the occurrence of RBIs and were compared with 100 age and gender-matched patients without NAFLD, who were hospitalized over the same period because of a bacterial infection. An RBI was defined as: ≥2 episodes of bacterial infections per year for a period of three consecutive years. NAFLD was diagnosed by ultrasonography. Biomarkers of inflammation, the level of oxidative stress, insulin resistance, and serum vitamin D levels were measured. RESULTS: NAFLD patients had significantly more RBIs than the patients without NAFLD (22% vs. 8%; P < 0.001). Univariate analysis showed that age, BMI, male waist circumference, serum 25(OH)D, triglycerides, serum malondialdehyde, and paraoxonase-1 are associated with RBIs in NAFLD patients. Multivariate analysis showed that NAFLD (odds ratio (OR) = 3.0, 95% confidence interval (CI) = 2.6-4.2, P < 0.001), serum 25(OH)D level <20 ng/mL (OR = 2.6; 95% CI 2.4-3.1, P = 0.01), obesity (BMI >30 kg/m(2) (OR = 2.2, 95% CI 1.8-2.9, P = 0.02) were associated with RBIs, irrespective of MetS. CONCLUSIONS: NAFLD is associated with increased risk of RBIs irrespective of MetS. Vitamin D insufficiency is frequent in NAFLD and is associated with increased risk of RBIs.

Presence of coronary plaques in patients with nonalcoholic fatty liver disease.

PURPOSE: To evaluate the relationship between nonalcoholic fatty liver disease (NAFLD) and coronary artery disease (CAD) and to define determinants of CAD in patients with or without metabolic syndrome. MATERIALS AND METHODS: This study was approved by the local ethics committee; informed consent was obtained. Twenty-nine subjects (mean age, 53 years +/- 7 [standard deviation]) with low to intermediate risk for CAD and with fatty liver were included. Thirty-two sex- and age-matched individuals without NAFLD served as controls. CAD was defined as a stenosis of more than 50% in at least one major coronary artery. Fatty liver was assessed by means of an attenuation of -10 HU or higher (calculated as liver attenuation minus spleen attenuation) by using computed tomography (CT), coronary plaques and stenosis by using CT coronary angiography, and biomarkers of insulin resistance, lipotoxicity, systemic inflammation, and oxidant and antioxidant status. A logistic regression analysis was performed to study multivariable associations. RESULTS: When compared with controls, NAFLD patients showed a higher prevalence of calcified and noncalcified coronary plaques (67% vs 34% and 52% vs 29%, respectively; both P < .001), higher prevalence of nonobstructive coronary stenosis (34% vs 14%; P < .008), higher homeostasis model assessment of insulin resistance (3.8 epsilonU/mL +/- 3.6 vs 2.6 epsilonU/mL +/- 3.2; P < .005) and higher triglyceride levels (208 mg/dL +/- 87 vs 148 mg/dL +/- 70; P < .005). Fatty liver proved to be a strong predictor of coronary atherosclerosis (odds ratio [OR], 2; P < .04), independent of indicators for metabolic syndrome (OR, 1.2; P > .2) and C-reactive protein levels (OR, 0.7; P > .4). CONCLUSION: Patients with NAFLD, even without metabolic syndrome, are at high risk for atherosclerosis. Assessment of NAFLD may be helpful for cardiovascular risk stratification.

Soft drink consumption is associated with fatty liver disease independent of metabolic syndrome.

BACKGROUND/AIMS: The independent role of soft drink consumption in non-alcoholic fatty liver disease (NAFLD) patients remains unclear. We aimed to assess the association between consumption of soft drinks and fatty liver in patients with or without metabolic syndrome. METHODS: We recruited 31 patients (age: 43+/-12 years) with NAFLD and risk factors for metabolic syndrome, 29 patients with NAFLD and without risk factors for metabolic syndrome, and 30 gender- and age-matched individuals without NAFLD. The degree of fatty infiltration was measured by ultrasound. Data on physical activity and intake of food and soft drinks were collected during two 7-day periods over 6 months using a food questionnaire. Insulin resistance, inflammation, and oxidant-antioxidant markers were measured. RESULTS: We found that 80% of patients with NAFLD had excessive intake of soft drink beverages (>500 cm(3)/day) compared to 17% of healthy controls (p<0.001). The NAFLD group consumed five times more carbohydrates from soft drinks compared to healthy controls (40% vs. 8%, p<0.001). Seven percent of patients consumed one soft drink per day, 55% consumed two or three soft drinks per day, and 38% consumed more than four soft drinks per day for most days and for the 6-month period. The most common soft drinks were Coca-Cola (regular: 32%; diet: 21%) followed by fruit juices (47%). Patients with NAFLD with metabolic syndrome had similar malonyldialdehyde, paraoxonase, and C-reactive protein (CRP) levels but higher homeostasis model assessment (HOMA) and higher ferritin than NAFLD patients without metabolic syndrome (HOMA: 8.3+/-8 vs. 3.7+/-3.7 mg/dL, p<0.001; ferritin: 186+/-192 vs. 87+/-84 mg/dL, p<0.01). Logistic regression analysis showed that soft drink consumption is a strong predictor of fatty liver (odds ratio: 2.0; p<0.04) independent of metabolic syndrome and CRP level. CONCLUSIONS: NAFLD patients display higher soft drink consumption independent of metabolic syndrome diagnosis. These findings might optimize NAFLD risk stratification.

Lower baseline ALT cut-off values and HBV DNA levels better differentiate HBeAg- chronic hepatitis B patients from inactive chronic carriers.

AIM: To determine whether new cut-off values for alanine aminotransferase (ALT) and baseline hepatitis B virus (HBV) DNA levels better differentiate HBeAg(-) chronic hepatitis B (CHB) patients from inactive chronic carriers. METHODS: Ninety-one patients [32 HBeAg(+) CHB, 19 inactive carriers and 40 HBeAg(-) CHB] were followed up for 2 years and were tested for HBV DNA levels by a PCR-based assay. ALT was tested twice during the last 6 mo using new cut-off values: ULN (upper limit of normal) 30 IU/L for males, 19 IU/L for females. Diagnostic accuracy, sensitivity, specificity, positive and negative predictive values were calculated by discriminant analysis. RESULTS: When using the revised ALT cut-off values, the lowest optimal HBV DNA level that differentiated HBeAg(-) CHB patients from inactive carriers was 50 000 copies/mL. The diagnostic accuracy of HBV DNA to determine inactive carriers with a cut-off of 50 000 copies/mL was similar to the previously recommended cut-off of 100 000 copies/mL (91%). HBV DNA levels were lower than the cut-off value in 95% of inactive carriers and in 28% of HBeAg(-) CHB patients. With ALT < 30 IU/L in men and < 19 IU/L in women and HBV DNA levels < 100 000 copies/mL, the risk of CHB is 5%. On the other hand, if ALT values were > 30 IU in men and > 19 IU in women and baseline HBV DNA levels were > 100 000 copies/mL, the risk is 86%. CONCLUSION: New cut-off values for ALT together with HBV DNA levels proposed by AASLD (American Association for the Study of Liver Diseases) and NIH (National Institute of Health) consensus seem appropriate to characterize inactive carriers.

Olive oil consumption and non-alcoholic fatty liver disease.

The clinical implications of non-alcoholic fatty liver diseases (NAFLD) derive from their potential to progress to fibrosis and cirrhosis. Inappropriate dietary fat intake, excessive intake of soft drinks, insulin resistance and increased oxidative stress results in increased free fatty acid delivery to the liver and increased hepatic triglyceride (TG) accumulation. An olive oil-rich diet decreases accumulation of TGs in the liver, improves postprandial TGs, glucose and glucagon-like peptide-1 responses in insulin-resistant subjects, and upregulates glucose transporter-2 expression in the liver. The principal mechanisms include: decreased nuclear factor-kappaB activation, decreased low-density lipoprotein oxidation, and improved insulin resistance by reduced production of inflammatory cytokines (tumor necrosis factor, interleukin-6) and improvement of jun N-terminal kinase-mediated phosphorylation of insulin receptor substrate-1. The beneficial effect of the Mediterranean diet is derived from monounsaturated fatty acids, mainly from olive oil. In this review, we describe the dietary sources of the monounsaturated fatty acids, the composition of olive oil, dietary fats and their relationship to insulin resistance and postprandial lipid and glucose responses in non-alcoholic steatohepatitis, clinical and experimental studies that assess the relationship between olive oil and NAFLD, and the mechanism by which olive oil ameliorates fatty liver, and we discuss future perspectives.

Soft drink consumption linked with fatty liver in the absence of traditional risk factors.

BACKGROUND: Little is known about dietary habits and their relationships with liver disease in nonalcoholic fatty liver disease (NAFLD) patients, particularly in the absence of obesity, diabetes or hyperlipidemia. OBJECTIVE: To assess the association between soft drink consumption and the presence of fatty liver in NAFLD patients who do not have classic risk factors. METHODS: Three hundred ten patients with NAFLD diagnosed by ultrasound were assessed for 36 months in a cross-sectional manner. Thirty-one patients (10%) who had NAFLD without classic risk factors were compared with 30 healthy controls. Physical activity was assessed during the preceding week and year, and every six months for 36 months. Data on daily dietary intake of food and soft drink, and the source of added sugar were collected during two seven-day periods, at the beginning of the study, and within two weeks after the metabolic tests by using a validated food questionnaire given by a trained dietician. Insulin resistance and lipid peroxidation were assessed by homeostasis model assessment-insulin resistance index (HOMA-IRI) and malondialdehyde (MDA) levels, respectively. RESULTS: Eighty per cent of patients (25 of 31) consumed an excessive amount of soft drink beverages (more than 50 g/day of added sugar) for 36 months, compared with 20% in healthy controls (P<0.001). Twenty per cent of patients consumed one drink per day, 40% consumed two to three drinks per day, and 40% consumed more than four drinks per day for most days during 36 months. The most common soft drinks consumed were regular Coca-Cola (40% of patients), Diet Coke (40%) and flavoured fruit juices (20%). Ultrasound findings revealed mild fatty liver in 44% of cases (n=14), moderate fatty liver in 38% (n=12), and severe fatty liver in 18% (n=5). HOMA-IRI and MDA levels were significantly higher in patients with NAFLD than in healthy controls (HOMA-IRI, 3.7 versus 1.7, P<0.001; and MDA, 420+/-300 micromol/mL versus 200+/-100 micromol/mL; P<0.001). When controlled for other factors, including dietary composition and physical activity, soft drink beverage consumption was the only independent variable that was able to predict the presence of fatty liver in 82.5% of cases with a sensitivity of 100%, a specificity of 76%, a positive predictive value of 57% and a negative predictive value of 100%. CONCLUSION: The present study may add important insight into the role of sugar-sweetened beverage consumption as a cause of fatty liver in patients without risk factors. Patients are encouraged to change their long-standing drinking behaviour.