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Cortez-Pinto H.,Unidade de Nutricao e Metabolismo | Gouveia M.,Catholic University of Portugal
Alcoholism: Clinical and Experimental Research | Year: 2010

Background and Aims: The World Health Organization estimated that 3.2% of the burden of disease around the world is attributable to the consumption of alcohol. The aim of this study is to estimate the burden of disease attributable to alcohol consumption in Portugal. Methods: Burden and costs of diseases attributable to alcohol drinking were estimated based on demographic and health statistics available for 2005, using the Disability-Adjusted Life Years (DALY) lost generated by death or disability. Results: In Portugal, 3.8% of deaths are attributable to alcohol (4,059 of 107,839). After measuring the DALY generated by mortality data, the proportion of disease attributable to alcohol was 5.0%, with men having 5.6% of deaths and 6.2% of disease burden, while female figures were, respectively, 1.8 and 2.4%. Considering the sum of death and disability DALYs, liver diseases represented the main source of the burden attributable to alcohol with 31.5% of total DALYs, followed by traffic accidents (28.2%) and several types of cancer (19.2%). As for the cost of illness incurred by the health system, our results indicate that €95.1 millions are attributable to alcohol-related disease admissions (liver diseases, cancer, traffic accidents, and external causes) while the ambulatory costs of alcohol-related diseases were estimated in €95.9 million, totaling €191.0 million direct costs, representing 0.13% of Gross Domestic Product and 1.25% of total national health expenditures. An alternative analysis was carried out using higher consumption levels so as to replicate aggregate alcohol consumption statistics. In this case, DALYs lost increased by 11.7% and health costs by 23%. Conclusion: Our results confirm that alcohol is an important health risk factor in Portugal and a heavy economic burden for the health system, with hepatic diseases ranking first as a source of burden of disease attributable to alcohol. Copyright © 2010 by the Research Society on Alcoholism. Source

Machado M.V.,Unidade de Nutricao e Metabolismo | Goncalves S.,Hospital Santa Maria | Carepa F.,Hospital Santa Maria | Coutinho J.,Hospital Santa Maria | And 2 more authors.
Liver International | Year: 2012

Introduction and aims:: Obesity is a common risk factor for nonalcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD). NAFLD and CKD have been associated in many epidemiological studies. We hypothesize that more severe liver disease, namely nonalcoholic steatohepatitis (NASH), is related with further renal impairment. We aimed to evaluate if changes in renal function were present in morbid obese patients with NAFLD. Methods: Prospective and consecutive recruitment of morbid obese patients with biopsy proven NAFLD obtained during bariatric surgery. Renal function was evaluated with CKD-Epidemiology Collaboration estimated glomerular filtration rate (eGFR). Plasmatic adiponectin, leptin and active ghrelin concentrations were determined. Results: One hundred and forty-eight patients were included of whom 25% had NASH and 75% simple steatosis. NASH patients were older, with higher body mass index and had more frequently metabolic syndrome and lower eGFR (97 ± 22 vs 106 ± 16 ml/min/1.73 2, P = 0.035). NASH conferred an odds ratio (OR) 3.0 (1.3-7.0) for eGFR < 90 and OR 9.7 (1.0-96.4) for eGFR < 60 ml/min/1.73 2. eGFR < 90 ml/min/1.73 2 associated with aspartate aminotransferase [OR 2.9 (1.1-7.6)] and γ-glutamyl transpeptidase elevation [OR 3.0 (1.3-7.2)], NASH [OR 3.0 (1.3-7.0)], any lobular inflammatory activity [OR 3.0 (1.3-7.0)] and severe fibrosis [OR 3.4 (1.1-10.8)]. Neither eGFR nor liver histology was associated with adipokines levels. Conclusions: In morbid obese patients, NASH, particularly lobular inflammation and advanced fibrosis, associates with mild decreases in eGFR, suggesting a common inflammatory link between liver and renal lesion. © 2011 John Wiley & Sons A/S. Source

Carvalhana S.,Unidade de Nutricao e Metabolismo | Leitao J.,Centro Hospitalar iversitario Of Coimbra | Alves A.C.,Institute Nacional Of Saude Dr Ricardo Jorge | Bourbon M.,Institute Nacional Of Saude Dr Ricardo Jorge | Cortez-Pinto H.,Unidade de Nutricao e Metabolismo
Liver International | Year: 2014

Background & Aims: Liver steatosis measurement by controlled attenuation parameter (CAP) is a non-invasive method for diagnosing steatosis, based on transient elastography. Its usefulness as screening procedure for hepatic steatosis in general population has not been previously evaluated. The aim of this study was to evaluate the diagnostic accuracy of CAP and fatty liver index (FLI) for detection and quantification of steatosis in general population. Methods: Recruitment was done from a prospective epidemiological study of the general adult population. Steatosis was evaluated using CAP, FLI and ultrasound (US). Steatosis scored according to Hamaguchi's US scoring, from 0 (S0) to 6 (S6) points. Hepatic steatosis defined by score ≥2 (S≥2) and moderate/severe steatosis by score ≥4 (S≥4). Performance of CAP and FLI for diagnosing steatosis compared with US was assessed using areas under receiver operating characteristic curves (AUROC). Results: From 219 consecutive individuals studied, 13 (5.9%) excluded because of failure/unreliable liver stiffness measurements. Steatosis prevalence: S≥2 38.4% and S≥4 12.1%. CAP significantly correlated with steatosis (ρ = 0.73, P < 0.0001), steatosis score (ρ = 0.76; P < 0.0001), FLI (ρ = 0.69), waist circumference (ρ = 0.62), body mass index (ρ = 0.55), triglyceride (ρ = 0.49), HOMA-IR (ρ = 0.26), alcohol consumption (ρ = 0.24) and cholesterol (ρ = 0.19), not with liver stiffness measurements. Using CAP and FLI, AUROC's were 0.94 (95% CI 0.91-0.97, P < 0.001) and 0.91 for S≥2; 0.95 (95% CI 0.90-0.99, P < 0.001) and 0.93 for S≥4 respectively. Optimal cut-off value of CAP and FLI were 243 dB/m and 48 for S≥2; 303.5 dB/m and 62 for S≥4 respectively. Conclusion: Controlled attenuation parameter and FLI seem promising tools for screening and steatosis quantification in the general population. Larger studies are needed for validation. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. Source

Carvalhana S.,Unidade de Nutricao e Metabolismo | MacHado M.V.,Unidade de Nutricao e Metabolismo | Cortez-Pinto H.,Unidade de Nutricao e Metabolismo
Current Opinion in Clinical Nutrition and Metabolic Care | Year: 2012

PURPOSE OF REVIEW: Nonalcoholic fatty liver disease (NAFLD) is the liver epidemic of our time. Diet strongly influences its development and should be a component of any treatment plan. It is crucial to standardize diet recommendations in an evidence-based manner. RECENT FINDINGS: Calorie restriction per se seems beneficial regardless of macronutrients composition. However, fat consumption, mainly cholesterol and saturated fatty acids are particularly steatogenic. There is increasing evidence that fructose, mainly consumed as soft drinks, is highly deleterious to the liver. Controversial results regarding modest alcohol consumption, suggest that although alcohol should not be advised, it should not be strictly forbidden. Recent studies suggest beneficial effects of coffee and tea in NAFLD. SUMMARY: Patients with NAFLD should have an individualized diet recommendation, in order to lose at least 7% of their weight if overweight, reducing caloric intake, mainly at cost of cholesterol and saturated fatty acids. Simple sugars should be avoided, and soft drinks discouraged. © 2012 Wolters Kluwer Health. Source

Machado M.V.,Unidade de Nutricao e Metabolismo | Ferreira D.M.S.,University of Lisbon | Castro R.E.,University of Lisbon | Silvestre A.R.,Hospital Santa Maria | And 6 more authors.
PLoS ONE | Year: 2012

Introduction: Nonalcoholic fatty liver disease (NAFLD) can be seen as a manifestation of overnutrition. The muscle is a central player in the adaptation to energy overload, and there is an association between fatty-muscle and -liver. We aimed to correlate muscle morphology, mitochondrial function and insulin signaling with NAFLD severity in morbid obese patients. Methods: Liver and deltoid muscle biopsies were collected during bariatric surgery in NAFLD patients. NAFLD Activity Score and Younossi's classification for nonalcoholic steatohepatitis (NASH) were applied to liver histology. Muscle evaluation included morphology studies, respiratory chain complex I to IV enzyme assays, and analysis of the insulin signaling cascade. A healthy lean control group was included for muscle morphology and mitochondrial function analyses. Results: Fifty one NAFLD patients were included of whom 43% had NASH. Intramyocellular lipids (IMCL) were associated with the presence of NASH (OR 12.5, p&0.001), progressive hepatic inflammation (p = 0.029) and fibrosis severity (p = 0.010). There was a trend to an association between IMCL and decreased Akt phosphorylation (p = 0.059), despite no association with insulin resistance. In turn, hepatic steatosis (p = 0.015) and inflammation (p = 0.013) were associated with decreased Akt phosphoryation. Citrate synthase activity was lower in obese patients (p = 0.047) whereas complex I (p = 0.040) and III (p = 0.036) activities were higher, compared with controls. Finally, in obese patients, complex I activity increased with progressive steatosis (p = 0.049) and with a trend with fibrosis severity (p = 0.056). Conclusions: In morbid obese patients, presence of IMCL associates with NASH and advanced fibrosis. Muscle mitochondrial dysfunction does not appear to be a major driving force contributing to muscle fat accumulation, insulin resistance or liver disease. Importantly, insulin resistance in muscle might occur at a late point in the insulin signaling cascade and be associated with IMCL and NAFLD severity. © 2012 Machado et al. Source

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