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Query: UMLS:C0015695 (fatty liver)
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Still, very little is known about the precise pathogenetic mechanisms, the triggering events and in particular, the evolution and treatment of nonalcoholic steatohepatitis (NASH). It is part of the broad spectrum of nonalcoholic fatty liver diseases (NAFLDs). Mainly, it has been reported as a benign disease, associated with metabolic disorders commonly occurrence en the general population. Nevertheless, the syndrome can lead to cirrhosis, liver failure or hepatocellular carcinoma, requiring liver transplantation. We present one patient with diagnosis of NASH, who was treated initially for overweight, HTA and hyperlipaemia with incompleted response and who showed a quickly progress to cirrhosis but no cause of liver decompensated disease could be identified. Currently she is at end-stage waiting a liver transplantation. Controlled and multicentric studies with the same definition of NASH and the study end-points are needed, and will provide information about diagnosis features and novel therapies to early management of the disease.
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PMID:[Nonalcoholic steatohepatitis, the enigma of bad progression]. 1589 87

Patients with obstructive sleep apnea (OSA) are at risk for the development of fatty liver as a result of being overweight. Several data suggest that OSA per se could be a risk factor of liver injury; ischemic hepatitis during OSA has been reported, and OSA is an independent risk factor for insulin resistance. Therefore, we investigated liver damage and potential mechanisms in 163 consecutive nondrinking patients with nocturnal polysomnographic recording for clinical suspicion of OSA. Serum levels of liver enzymes were measured in all patients. Liver biopsy was offered to patients with elevated liver enzymes. Intrahepatic hypoxia was assessed by the expression of vascular endothelial growth factor (VEGF) on liver biopsy specimens. Severe OSA (apnea-hypopnea index [AHI] > 50/hr) was seen in 27% of patients; 52% had moderate OSA (AHI 10-50/hr), and 21% had no OSA. Overall, 20% had elevated liver enzymes. Independent parameters associated with elevated liver enzymes were body mass index (BMI) (OR: 1.13; CI: 1.03-1.2) and severe OSA (OR: 5.9; CI: 1.2-29). Liver biopsy was performed in 18 of 32 patients with elevated liver enzymes and showed steatohepatitis in 12 cases, associated with fibrosis in 7 cases. Patients with severe OSA were more insulin-resistant according to homeostasis model assessment, had higher percentage of steatosis as well as scores of necrosis and fibrosis, despite similar BMI. Hepatic immunostaining used as an indirect marker of hypoxia was not different between patients with or without severe OSA. In conclusion, severe OSA is a risk factor for elevated liver enzymes and steatohepatitis independent of body weight. Promotion of insulin resistance is probably involved. Further studies are needed to determine whether hypoxia contributes directly to liver injury.
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PMID:Chronic liver injury during obstructive sleep apnea. 1591 59

Childhood NAFLD has become an important childhood liver disease, and it is probably highly prevalent. The full of spectrum of NAFLD has been identified in children. It is not currently known whether or not simple hepatic steatosis in children is benign or whether it evolves to NASH over time. In contrast, childhood NASH certainly can have serious consequences. Cirrhosis is apparently rare in children with NAFLD, but it definitely occurs. Childhood NAFLD may occur in very young children, and there is no female predominance in the pediatric age bracket. Children present with vague abdominal pain, if they have any symptoms at all, but frequently hepatic steatosis is found incidentally on abdominal imaging. Laboratory studies show that serum aminotransferase abnormalities are rather moderate, with serum alanine aminotransferase (ALT) more elevated than serum aspartate aminotransferase (AST). Hypertriglyceridemia is the typical blood lipid abnormality, although hypercholesterolemia may occur. NASH may be more severe in children from certain ethnic groups, including Hispanics and Asians, or in association with certain metabolic disorders characterized by abnormalities in insulin receptor structure or signaling, such as lipodystrophy syndromes. Weight loss through dietary redesign and a regimen of regular exercise remains the mainstay for treatment for childhood NAFLD. A dietary strategy to minimize postprandial hyperinsulinemia and overall fat intake, such as a low glycemic index diet, may be the best dietary strategy. The real efficacy of drug treatments in children requires further investigation. The overriding message is that childhood obesity poses important health problems, including but not limited to potentially severe chronic liver disease. Early diagnosis of children who are only overweight is a worthy goal so that strategies to limit obesity can be instituted as early as possible. Identification of genetic risks is important, but management will invariably require changes in environmental factors. In addition to individual treatment, a multifaceted, societal initiative is required for solving the childhood obesity epidemic.
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PMID:Non-alcoholic fatty liver disease (NAFLD) in children. 1597 Apr 96

The number of obese and overweight Oklahomans and Americans has grown both steadily and rapidly in the last few decades. Along with this increase in weight, doctors now see a higher proportion of chronic, degenerative diseases such as cardiovascular disease, diabetes, cancer, and osteoarthritis. Poor diet, sedentary lifestyle, and poor stress and time management contribute to weight problems and illness. Lifestyle changes have no side effects or risks, other than the perceived challenge of implementing and maintaining them. Healthier habits offer multiple organ system benefits including weight control, less anxiety and depression, improved energy, better sleep, and lower rates of gastrointestinal problems, such as reflux, gallstones, and fatty liver. By providing accurate and comprehensible information, doctors can motivate and support patients to better safeguard their health and manage their weight. This article will suggest specific phrases to use in the framework of motivational interviewing, as discussed in the first article, Part I, in this 3-part series.
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PMID:Putting prevention into practice: counseling patients to prevent and decrease obesity. 1602 2

The majority of patients with nonalcoholic fatty liver disease are overweight and obese, lead relatively sedentary lifestyles, and have underlying insulin resistance. Treatment aimed at improving body weight and activity should be the cornerstone of our therapeutic armamentarium in combating this disease. Evidence suggests that diets low in processed carbohydrates and saturated fats with a goal to achieve a 500- to 1000-calorie/day deficit improve insulin sensitivity, reduce serum aminotransferases, and decrease hepatic steatosis. Encouragingly, improvements are seen with as little as a 5% reduction in body weight. Histopathologic parameters of steatohepatitis also appear to improve with weight loss. Antioxidant supplementation, specifically with vitamin E, may be considered as adjunctive therapy. Other antioxidants and the thiazolidinediones (pioglitazone and rosiglitazone) appear to be efficacious, but larger confirmatory studies are needed to ensure they are safe and beneficial in patients with nonalcoholic steatohepatitis. Novel agents such as renin-angiotensin system inhibitors may eventually prove to be efficacious as well. Future treatment for patients failing to achieve weight loss goals is likely to consist of combination therapy targeting insulin resistance, oxidative stress, and fibrogenesis.
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PMID:New treatments for nonalcoholic fatty liver disease. 1651 31

Researchers are only gradually becoming aware of the gravity of the risk that overweight and obesity pose for children's health. In this article Stephen Daniels documents the heavy toll that the obesity epidemic is taking on the health of the nation's children. He discusses both the immediate risks associated with childhood obesity and the longer-term risk that obese children and adolescents will become obese adults and suffer other health problems as a result. Daniels notes that many obesity-related health conditions once thought applicable only to adults are now being seen in children and with increasing frequency. Examples include high blood pressure, early symptoms of hardening of the arteries, type 2 diabetes, nonalcoholic fatty liver disease, polycystic ovary disorder, and disordered breathing during sleep. He systematically surveys the body's systems, showing how obesity in adulthood can damage each and how childhood obesity exacerbates the damage. He explains that obesity can harm the cardiovascular system and that being overweight during childhood can accelerate the development of heart disease. The processes that lead to a heart attack or stroke start in childhood and often take decades to progress to the point of overt disease. Obesity in childhood, adolescence, and young adulthood may accelerate these processes. Daniels shows how much the same generalization applies to other obesity-related disorders-metabolic, digestive, respiratory, skeletal, and psychosocial-that are appearing in children either for the first time or with greater severity or prevalence. Daniels notes that the possibility has even been raised that the increasing prevalence and severity of childhood obesity may reverse the modern era's steady increase in life expectancy, with today's youth on average living less healthy and ultimately shorter lives than their parents-the first such reversal in lifespan in modern history. Such a possibility, he concludes, makes obesity in children an issue of utmost public health concern.
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PMID:The consequences of childhood overweight and obesity. 1653 58

Nonalcoholic fatty liver disease (NAFLD) is a spectrum of liver disease whose hallmark is the accumulation of large-droplet fat in hepatocytes. This metabolic disorder occurs mainly in overweight or obese individuals. The disease mechanism involves hyperinsulinemia and hepatic insulin resistance, not ethanol abuse. NAFLD may be the hepatic manifestation of the "metabolic syndrome" classically associated with type 2 diabetes mellitus and cardiovascular disease. NAFLD ranges from simple steatosis, which is the least rapidly progressing disorder, to nonalcoholic steatohepatitis to cirrhosis, which can evolve to chronic liver failure. The high prevalence of NAFLD in children has been recognized only in the past 5 to 10 years, as rates of childhood obesity have soared. Accordingly, the best strategies for diagnosis and treatment of childhood NAFLD are a work in progress and remain controversial. Weight reduction through a healthy diet and regular medium-intensity exercise is the mainstay of current treatment. Few research data are available to guide pharmacologic therapy. Certain points regarding management of childhood NAFLD require emphasis: It is a serious liver disease that requires detailed clinical investigation. Other liver diseases causing fatty liver and/or abnormal liver tests, notably Wilson disease and chronic viral hepatitis, need to be excluded. Liver biopsy can provide critical diagnostic and staging information. Associated genetic or endocrine disorders need to be identified. Treatment should begin with a low-glycemic index diet that provides adequate nutrients but is low in harmful fats and eliminates foods causing postprandial hyperglycemia. Initially, this can target two to three problem foods so that it is easy for the adolescent to follow. Regular exercise suited to the capabilities and interests of the teenager should be added to the daily routine. Where possible, a team approach, including a dietician and psychologist, should be utilized, as adolescents do better in a supportive atmosphere. Optimal drug treatment requires further research: current front-runners are vitamin E and metformin. The roles of drugs that alter appetite and bariatric surgery for adolescents with NAFLD have not been determined.
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PMID:Nonalcoholic Fatty Liver Disease (NAFLD): Approach in the Adolescent Patient. 1694 68

Although population prevalence is very difficult to establish, nonalcoholic fatty liver disease (NAFLD) is probably the most common cause of liver disease in the preadolescent and adolescent age groups. There seems to be an increase in the prevalence of NAFLD, likely related to the dramatic rise in the incidence of obesity during the past 3 decades. Despite an increase in public awareness, overweight/obesity and related conditions, such as NAFLD, remain underdiagnosed by health care providers. Accurate diagnosis and staging of nonalcoholic steatohepatitis (NASH) requires liver biopsy. The development of noninvasive surrogate markers and the advancements in imaging technology will aid in the screening of large populations at risk for NAFLD. Two distinct histological patterns of NASH have been identified in the pediatric population, and discrete clinical and demographic features are observed in children with these 2 patterns. The propensity for NASH to develop in obese, insulin-resistant pubertal boys of Hispanic ethnicity or a non-Hispanic white race may provide clues to the pathogenesis of NAFLD in children. The natural history of pediatric NASH has yet to be defined, but most biopsies in this age group demonstrate some degree of fibrosis. In addition, cirrhosis can be observed in children as young as 10 years. While the optimal treatment of pediatric NAFLD has yet to be determined, lifestyle modification through diet and exercise should be attempted in children diagnosed with NAFLD. A large, multicenter trial of vitamin E and metformin is underway as part of the NASH clinical research network.
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PMID:Pediatric nonalcoholic fatty liver disease: a critical appraisal of current data and implications for future research. 1703 14

Polycystic ovary syndrome affects 6%-7% of reproductive-aged women, making it the most common endocrine disorder in this population. It is characterized by chronic anovulation and hyperandrogenism. Affected women may present with reproductive manifestations such as irregular menses or infertility, or cutaneous manifestations, including hirsutism, acne, or male-pattern hair loss. Over the past decade, several serious metabolic complications also have been associated with polycystic ovary syndrome including type 2 diabetes mellitus, metabolic syndrome, sleep apnea, and possibly cardiovascular disease and nonalcoholic fatty liver disease. In addition to treating symptoms by regulating menstrual cycles and improving hyperandrogenism, it is imperative that clinicians recognize and treat metabolic complications. Lifestyle therapies are first-line treatment in women with polycystic ovary syndrome, particularly if they are overweight. Pharmacological therapies are also available and should be tailored on an individual basis. This article reviews the diagnosis, clinical manifestations, metabolic complications, and treatment of the syndrome. A table summarizing treatment recommendations is provided.
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PMID:Polycystic ovary syndrome: diagnosis and treatment. 1727 49

The World Health Organization estimates that around one billion people throughout the world are overweight and that over 300 million of these are obese and if current trends continue, the number of overweight persons will increase to 1.5 billion by 2015. The number of obese adults in Australia is estimated to have risen from 2.0 million in 1992/93 to 3.1 million in 2005. The prevalence of obesity has been increasing due to a convergence of factors--the rise of TV viewing, our preference for takeaway and pre-prepared foods, the trend towards more computer-bound sedentary jobs, and fewer opportunities for sport and physical exercise. Obesity is not only linked to lack of self esteem, social and work discrimination, but also to illnesses such as the metabolic syndrome and hyperinsulinaemia (which increases the risk of developing heart disease, diabetes, hypertension, fatty liver), cancer, asthma, dementia, arthritis and kidney disease. It has been estimated that the cost of obesity in Australia in 2005 was $1,721 million. Of this amount, $1,084 million were direct health costs, and $637 million indirect health costs (due to lost work productivity, absenteeism and unemployment). The prevalence cost per year for each obese adult has been estimated at $554 and the value of an obesity cure is about $6,903 per obese person. Government efforts at reducing the burden remain inadequate and a more radical approach is needed. The Australian government, for example, has made changes to Medicare so that GPs can refer people with chronic illness due to obesity to an exercise physiologist and dietitian and receive a Medicare rebate, but so far these measures are having no perceptible effect on obesity levels. There is a growing recognition that both Public Health and Clinical approaches, and Private and Public resources, need to be brought to this growing problem. Australian health economist, Paul Gross, from the Institute of Health Economics and Technology Assessment claims there is too much reliance on health workers to treat the problem, especially doctors, who have not been given additional resources to manage obesity outside a typical doctor's consultation. Gross has recommended that further changes should be made to Medicare, private health insurance, and workplace and tax legislation to give people financial incentives to change their behaviour because obesity should not just be treated by governments as a public health problem but also as a barrier to productivity and a drain on resources. A Special Report of the WMCACA (Weight Management Code Administration Council of Australia) (www.weightcouncil.org) on the "Health Economics of Weight Management" has been published in the Asia Pacific Journal of Clinical Nutrition in September 2006. This report explores the cost benefit analysis of weight management in greater detail.
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PMID:Health economics of weight management: evidence and cost. 1739 29


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