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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors summarize and update the most recent knowledge in the field of prevalence, natural history and incidence of Non Alcoholic Fatty Liver Disease (NAFLD) and Non Alcoholic Steatohepatitis (NASH). These novel diseases, firstly recognized at the beginning of the second millennium, arose suddenly to the attention of the clinicians, because they are the hepatic expression of the "so-called" metabolic syndrome. Due to the epidemic burden of obesity, diabetes, and metabolic diseases, NAFLD and NASH will become soon probably the most common hepatic disease worldwide, and they surely will keep busy our future young hepatologists.
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PMID:Epidemiology and natural history of non-alcoholic fatty liver disease (NAFLD). 1938 Nov 18

With the growing epidemic of obesity and diabetes, more attention has been placed on metabolic syndrome and its associated hepatic manifestation, non-alcoholic fatty liver disease (NAFLD). Within the spectrum of clinico-pathologic conditions known as NAFLD, only a minority of patients has the histological features characteristic of non-alcoholic steatohepatitis (NASH), which has the potential to progress to cirrhosis and hepatocellular carcinoma. Therefore, diagnosis and therapy should target patients with NASH. Current treatment recommendations include weight loss and the reversal of other components of metabolic syndrome, but several other treatment modalities are under investigation. To date, no pharmacologic treatment has been reliably shown to be effective for NASH. This article reviews all available treatment modalities, including lifestyle changes, bariatric surgery, weight loss medications, insulin sensitizers, lipid lowering agents, antioxidants, cytoprotective agents, and other novel treatments.
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PMID:Treatment regimens for non-alcoholic fatty liver disease. 1938 Nov 25

Hepatitis C virus (HCV) infection has been associated with insulin resistance or diabetes mellitus, but data are controversial on the role of different HCV genotypes in causing insulin resistance. We have designed a study aimed at determining insulin resistance in patients with chronic hepatitis C with predominant genotype 3. Insulin resistance was measured using a homeostasis model of assessment for insulin resistance in 85 non-diabetic, non-cirrhotic patients with chronic hepatitis C (genotype 3 = 54). The results were compared with 38 biopsy-proven patients with non-alcoholic fatty liver disease and 25 age- and body mass index-matched healthy volunteers. Patients with chronic hepatitis C had a higher fasting insulin and homeostasis model of assessment for insulin resistance values than healthy volunteers (P = 0.0001). A large number of patients with chronic hepatitis C showed evidence of insulin resistance than healthy controls [53 (62.3%) vs. 4 (16%), respectively] (P < 0.0001). Of the various risk factors studied for insulin resistance in patients with chronic hepatitis C, higher waist (P = 0.010) and higher serum triglycerides (P = 0.002) were found to correlate with HOMA-insulin resistance. There was no difference in insulin resistance amongst patients with genotype 1 or 3, respectively. Based on these results, we conclude that insulin resistance is common among non-diabetic, non-cirrhotic patients with chronic hepatitis C. A majority of these patients had genotype 3, but there was no difference in insulin resistance between genotype 1 and genotype 3 patients.
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PMID:Insulin resistance is common in patients with predominantly genotype 3 chronic hepatitis C. 1951 42

Sialadenosis is a unique form of non-inflammatory, non-neoplastic bilateral salivary gland disorder characterized by recurrent painless swelling which usually occurs in parotid glands. Alcoholism is one of the main causes of sialadenosis along with diabetes, bulimia, and other idiopathic causes. The prognosis is verified according to the degree of liver function. We present a case of a 46 year-old man who had alcoholic fatty liver disease diagnosed as alcoholic sialadenosis based on clinical points of recurrent bilateral parotid swelling after heavy alcohol drinking, computed tomography, and fine-needle aspiration biopsy. After stopping alcohol drinking and treated with conservative treatment, he got improved without specific sequela.
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PMID:[Sialadenosis in a patient with alcoholic fatty liver developing after heavy alcohol drinking]. 1969 51

NAFLD (non-alcoholic fatty liver disease) represents a spectrum of fatty liver diseases associated with an increased risk of Type 2 diabetes and cardiovascular disease. The spectrum of fatty liver diseases comprises simple steatosis, steatosis with inflammation [i.e. NASH (non-alcoholic steatohepatitis)], fatty liver disease with inflammation and fibrosis (severe NASH) and cirrhosis. The molecular mechanisms contributing to NASH are the subject of considerable investigation, as a better understanding of the pathogenesis of NASH will lead to novel therapies for a condition that hitherto remains difficult to treat. In the present issue of Clinical Science, Piguet and co-workers have investigated the effects of hypoxia in the PTEN (phosphatase and tensin homologue deleted on chromosome 10)-deficient mouse, a mouse model that develops NAFLD. The authors show that a short period (7 days) of exposure to hypoxia aggravates the NAFLD phenotype, causing changes in the liver that are in keeping with NASH with increased lipogenesis and inflammation.
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PMID:Hypoxia and non-alcoholic fatty liver disease. 1990 Jan 66

Owing to increased obesity, non-alcoholic fatty liver disease (NAFLD) is now the most prevalent liver disease in the United States. NAFLD is considered a component of metabolic syndrome, a cluster of disorders that also includes diabetes mellitus, dyslipidemia, arteriosclerosis, and hypertension. Exposure to ambient air particulate matter with aerodynamic diameters < 2.5 microm (PM(2.5)) is a risk factor for arteriosclerosis and lung disease, but its effect on NAFLD is unknown. PM(2.5) induces pulmonary dysfunction via Toll-like receptor (TLR) activation on alveolar macrophages. TLR activation of Kupffer cells, resident hepatic macrophages, and subsequent pro-inflammatory cytokine production have been shown to play a key role in NAFLD progression. We hypothesized that PM(2.5) exposure is a significant risk factor for the progression of NAFLD. Thus, following exposure of male C57BL/6 mice fed high fat chow (HFC) to concentrated air particulate matter (CAPs) or filtered air for 6 weeks, progression of NAFLD was evaluated by standardized histological assessment of hepatic inflammation and fibrosis. In mice fed HFC, the hepatic inflammatory grade (3.00 +/- 0.00 vs. 1.50 +/- 0.71, P < 0.001) and fibrosis stage (1.00 +/- 0.00 vs. 0.60 +/- 0.52, P = 0.023) were both significantly higher in mice exposed to CAPs versus filtered air, respectively. Increased numbers of Kupffer cells contained PM in CAPs-exposed mice scores of (2.00 +/- 0.94 vs. 0.20 +/- 0.42, respectively, P < 0.001). PM exposure increased IL-6 secretion up to seven-fold in a dose-dependent manner by isolated wild-type but not TLR4(-/-) Kupffer cells (P < 0.050). In conclusion, ambient PM(2.5) exposure may be a significant risk factor for NAFLD progression.
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PMID:Kupffer cell activation by ambient air particulate matter exposure may exacerbate non-alcoholic fatty liver disease. 1990 45

The most frequent liver disorder in metabolic syndrome is the nonalcoholic fatty liver disease. Its pathogenesis is a complex, multifactorial process, characterized by insulin resistance and involvement of the endocrine system. Hypothyroidism may lead to nonalcoholic steatohepatitis via hyperlipidemia and obesity. Adult patients with growth hormone deficiency have a metabolic syndrome-like phenotype with obesity and many characteristic metabolic alterations. The chronic activation of the hypothalamic-pituitary-adrenal axis results in metabolic syndrome as well. Cushing's syndrome has also features of metabolic syndrome. Mild elevation of transaminase activities is commonly seen in patients with adrenal failure. Non-alcoholic steatosis is twice as common in postmenopusal as in premenopausal women and hormonal replacement therapy decreases the risk of steatosis. Insulin resistance, diabetes mellitus type 2, sleeping apnoe syndrome, cardiovascular disorders and non-alcoholic fatty liver disease are more frequent in polycystic ovary syndrome. Hypoandrogenism in males and hyperandrogenism in females may lead to fatty liver via obesity and insulin resistance. Adipokines (leptin, acylation stimulating protein, adiponectin) have a potential role in the pathogenesis of nonalcoholic fatty liver. The alterations of endocrine system must be considered in the background of cryptogenic liver diseases. The endocrine perspective may help the therapeutic approaches in the future.
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PMID:[Role of the endocrine system in the pathogenesis of non-alcoholic fatty liver disease]. 1992 96

Psoriasis is a chronic inflammatory, immune-mediated skin disease, which may cause significant deterioration in the quality of life. Recent evidence indicates that psoriasis and psoriatic arthritis are frequently associated with cardiometabolic diseases including myocardial infarction, stroke, diabetes, obesity, dyslipidemia and non-alcoholic fatty liver disease. Although the causal relationship between cardiometabolic comorbidities and psoriasis has not yet been completely proven, it appears that obesity is a relevant risk factor for the development of psoriasis and metabolic syndrome. In addition, moderate to severe psoriasis itself is a risk factor for cardiovascular disease and the metabolic syndrome. Some common genetic traits as well as inflammatory mechanisms may underlie the development of psoriasis and cardiometabolic comorbidities. The presence of comorbidities has important implications in the global approach to patients with psoriasis. Traditional systemic anti-psoriatic agents could negatively affect cardiometabolic comorbidities, and may have important interactions with drugs commonly used by psoriasis patients. In contrast, the recent findings that the risk of myocardial infarction is markedly reduced in rheumatoid arthritis patients who respond to anti-TNF-alpha therapy compared with non-responders supports the hypothesis that the anti-inflammatory effect of TNF-alpha blockers might potentially reduce the cardiovascular risk also in psoriasis patients. Finally, patients with moderate to severe psoriasis should be treated promptly and effectively, should also be encouraged to drastically correct their modifiable cardiovascular risk factors, in particular obesity and smoking habit.
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PMID:Cardiometabolic comorbidities and the approach to patients with psoriasis. 2009 57

There is abundant and accumulating evidence on the classification of psoriasis as a systemic disease that exhibits a host of co-morbidities. As a consequence, the second Interdisciplinary Conference on Co-morbidities and Lifestyle Modification, convened by the International Psoriasis Council, has concluded that specialist physicians, primary care physicians and dermatologists are faced with an opportunity to impact, not just psoriasis disease understanding and management, but overall patient well-being. The conference panel was represented by the disciplines of dermatology, cardiology, rheumatology, epidemiology, endocrinology, hepatology and gastroenterology, and medical specialists with particular expertise in obesity, diabetes mellitus, inflammation and genetics. The multiple co-morbidities associated with psoriasis were reviewed with a view to identify possible mechanisms linking psoriatic disease with obesity, metabolic syndrome, diabetes, cardiovascular disease and non-alcoholic fatty liver disease. Consensus was established on the association of psoriasis with other co-morbidities and disease states. Consequently, there is a significant opportunity for specialist and primary care physicians to collaborate with dermatologists in the management of the overall health of psoriasis patients. First, there is an important need for physicians to routinely screen psoriasis patients for the multiple susceptibility risk factors and co-morbidities associated with psoriasis. Second, the design and implementation of lifestyle modification plans including exercise, diet and the limitation of alcohol and tobacco intake, will not only benefit their general medical health but also their psoriasis.
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PMID:Exploring the association between cardiovascular and other disease-related risk factors in the psoriasis population: the need for increased understanding across the medical community. 2038 92

Incretin-based therapies have shown promise in the treatment of type 2 diabetes. Here we review our current understanding of TGR5 as a target to induce glucagon-like peptide-1 (GLP-1) secretion. These new observations suggest that TGR5 agonists may constitute a novel approach to treat type 2 diabetes, as well as complications of diabetes, such as non-alcoholic fatty liver disease.
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PMID:Targeting the TGR5-GLP-1 pathway to combat type 2 diabetes and non-alcoholic fatty liver disease. 2044 64


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