Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antiretroviral medications have significantly improved the prognosis of subjects infected by human immunodeficiency virus (HIV). However, long-term complications of these drugs are increasingly recognized as significant causes of morbidity and mortality. Non-alcoholic fatty liver disease (NAFLD), which can evolve into non-alcoholic steato-hepatitis (NASH), cirrhosis and ultimately hepatic failure is one of the more often observed complications in the current clinical practice and the correlation with liver enzyme elevations is controversial. Multiple factors have been considered as possibly correlated to this event in the HIV-infected population, including metabolic abnormalities (such as hyperlipidaemia, hyperglycaemia and being overweight), chronic inflammation, concurrent infection with hepatitis C and B viruses, and treatment with certain nucleoside reverse transcriptase inhibitors (NRTI). HIV-associated syndromes such as lactic acidosis and lypodystrophy are frequently associated with fatty liver disease and a mitochondrial injury has been considered as its possible pathogenetic factor. In particular, treatment containing stavudine and didanosine have proven to be the most commonly implicated in the occurrence of mitochondrial abnormalities. Epidemiologic data to better define the role of predictive factors and drugs associated with the development of NAFLD are still lacking. Furthermore, it remains unclear the better therapeutic management for this condition, even if the current best therapeutic option for NAFLD is the treatment of the underlying disease. Other studies are mandatory to better elucidate the pathogenesis of NAFLD and the optimal therapeutic strategy for the underlying conditions.
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PMID:Steatohepatitis in HIV-infected subjects: pathogenesis, clinical impact and implications in clinical management. 1789 69

Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) are gaining increasing recognition as components of the emerging epidemic of obesity in North America and in other parts of the world. These entities are considered the hepatic manifestations of the insulin resistance syndrome and represent the spectra of fatty liver disease associated with it. All features of metabolic syndrome are associated with NAFLD/NASH, including obesity, type 2 diabetes, arterial hypertension, and hyperlipidemia in the form of elevated triglyceride levels. NAFLD/NASH can progress to liver cirrhosis and has been reported as a cause of hepatocellular carcinoma. In this review, the histopathologic features of NAFLD/NASH and differential diagnostic considerations are discussed. In addition, grading and staging schema proposed and currently in use are reviewed. Finally, other aspects for consideration by practicing pathologists, such as sampling issues, histopathologic findings after therapeutic interventions, and recurrence after liver transplantation, are addressed.
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PMID:Pathology of nonalcoholic fatty liver disease. 1795 Dec 8

Non-alcoholic steatohepatitis (NASH), the metabolic syndrome of the liver, characterised by the consequences of obesity (insulin resistance, production of free radicals, chronic inflammation) has become a new epidemic in the United States as in Europe. Diagnosis is suspected in patients with obesity, denying alcohol abuse, having typical co-morbitities (Hypertension, Diabetes mellitus, Hyperlipidemia). Liver histology confirms the diagnosis of NASH. Fatty liver without inflammation bears a good prognosis. Liver fibrosis, however, in NASH patients signalizes progression to liver cirrhosis and even HCC. Treatment modalities are limited. Reduction of body weight, physical activity, treatment of co-morbitities, specially Hypertension and Diabetes are of paramount importance. At the moment it remains unclear whether glitazone treatment could be introduced in the therapeutic armentarium.
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PMID:[Non-alcoholic steatohepatitis--a new epidemic]. 1806 58

Nonalcoholic fatty liver disease (NAFLD) is considered to be a hepatic manifestation of metabolic syndrome. The clinicopathologic spectrum ranges from simple steatosis to nonalcoholic steatohepatitis (NASH). Simple steatosis has a relatively benign clinical course, but NASH can progress to cirrhosis and hepatocellular carcinoma. As yet there is no convincingly effective treatment for NAFLD and the best option for these patients might be a multimodal treatment plan targeting obesity, insulin resistance, diabetes mellitus, hyperlipidemia and hypertension.
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PMID:[Treatment of fatty liver disease]. 1840 89

Non-alcoholic fatty liver disease (NAFLD) is a major complication linked with the metabolic syndrome associated with dyslipidemia, inflammation, and oxidative stress. Impact of type 2 diabetes with hyperlipidemia in NAFLD has to be established, as well as the utility of commonly prescribed anti-diabetic and lipid-lowering agents in improving liver injury markers. Genetic type 2 diabetic Goto-Kakizaki rats were fed with a high-fat diet to test hepatic effects of type 2 diabetes with hyperlipidemia and the effect of atorvastatin and insulin, individually and in combination, in systemic and hepatic inflammatory and oxidative stress markers. High-fat diet aggravated fasting glycemia, systemic and liver lipids, and inflammatory and oxidative stress markers. Individual treatments improved glycemic and lipid profiles, but failed to improve inflammatory markers, whereas insulin was able to reduce liver oxidative stress parameters. Combination of insulin and atorvastatin further improved glycemic and lipid profiles and decreased circulating C-reactive protein levels and liver inflammatory and oxidative stress markers. Insulin and atorvastatin combination leads to better glycaemic and lipid profiles and to better protection against liver inflammation and oxidative stress, giving a superior level of liver protection in type 2 diabetic with hyperlipidemia.
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PMID:A role for atorvastatin and insulin combination in protecting from liver injury in a model of type 2 diabetes with hyperlipidemia. 1893 12

Non-alcoholic fatty liver disease includes a broad spectrum of liver abnormalities ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), which can progress to cirrhosis and hepatocellular carcinoma. Patients with primary NASH have the metabolic (or insulin resistance) syndrome, condition typically associated with obesity, diabetes, hyperlipidemia and hypertension. To understand the mechanisms implicated in development of NASH, animal models of non-alcoholic fatty liver disease have been generated. These have greatly improved our understanding of some of the aspects of this disease. The challenge now is to identify the common mechanisms between the animal models and humans, which could eventually lead to a better prognosis and development of novel therapeutic strategies.
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PMID:Non-alcoholic steatohepatitis and animal models: understanding the human disease. 1902 69

Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases and may progress to advanced hepatic fibrosis and cirrhosis in some patients. Cirrhosis due to NAFLD is considered extremely rare in children in the Asia-Pacific region. We report the characteristics of 5 children with advanced hepatic fibrosis and cirrhosis due to NAFLD. Four of them were obese, and all of them had high alanine transaminase levels and ultrasonographic evidence of fatty liver. None had diabetes mellitus or hyperlipidemia. The calculated HOMA-IR was more than two in all five cases. Liver biopsy showed stage III fibrosis in 2 patients and stage IV fibrosis (cirrhosis) in 3.
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PMID:Advanced hepatic fibrosis and cirrhosis due to nonalcoholic fatty liver disease in Sri Lankan children: a preliminary report. 1966 6

Non-alcoholic steatohepatitis (NASH) is characterised by steatosis, liver cell injuries, the presence of a mixed inflammatory lobular infiltrate, and variable degrees of fibrosis. Werner syndrome (WS) is a rare autosomal recessive disease characterised by the premature onset of multiple age-related disorders. Central obesity and insulin resistance are common symptoms of both NASH and WS. Three cases were studied to evaluate the association between WS and NASH. NASH was diagnosed by liver biopsies and imaging studies following the exclusion of alcohol consumption, viral disease or autoimmune liver disease. Liver histology was compatible with NASH in all cases. Liver dysfunction, hyperlipidaemia, insulin resistance and regional increase of intra-abdominal fat even though the body mass indices were all normal or low, were observed. Metabolic disorders due to WS may complicate and cause NASH. Hence, the observed clinical association between WS and NASH suggests that patients with WS should also be screened for NASH.
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PMID:Werner syndrome as a possible cause of non-alcoholic steatohepatitis. 1972 Jun 29

Non-alcoholic fatty liver disease (NAFLD) has recently been recognized as a leading cause of abnormal liver function tests. Its spectrum ranges from simple steatosis, which is usually a benign and non progressive condition, to non-alcoholic steatohepatitis (NASH), which may progress to cirrhosis and hepatocellular carcinoma. NASH is thought to be almost 10% of NALFD and part of metabolic syndrome. NASH patients usually have insulin resistance, frequently combined with hypertension, hyperlipidemia and diabetes. The etiology of NASH remains unclear, but most investigators agree that the development of NASH requires underlying steatosis followed by a "second hit" that induces inflammation, fibrosis, or necrosis. The interaction of adipocytokines (TNF-alpha, adiponectin) with oxidative stress and lipid peroxidation has been postulated to play a key role in NASH. The basic therapy for NASH is an improved of lifestyle, including exercise and diet. Drug therapy should be considered as additional therapy.
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PMID:[Diagnosis and therapy in NASH]. 1986 Feb 10

Nonalcoholic fatty liver disease (NAFLD), first described in 1980, is now recognized as one of the most common causes of elevated liver enzymes and chronic liver disease in Western countries. The incidence of NAFLD in both adults and children is rising, in conjunction with the burgeoning epidemics of obesity and type 2 diabetes mellitus. NAFLD often coexists with other sequelae of the metabolic syndrome: central obesity, type 2 diabetes, hypertension, and hyperlipidemia. NAFLD encompasses a spectrum of pathologic liver diseases ranging from simple hepatic steatosis to a predominant lobular necro-inflammation, with or without centrilobular fibrosis (called nonalcoholic steatohepatitis or NASH). NASH can progress to cirrhosis, decompensated liver disease, and hepatocellular carcinoma. Though the natural history of NASH is still not clearly defined, it has been observed to progress to cirrhosis in 15%-220% of those affected. Insulin resistance is nearly universal in NASH and is thought to play an important role in its pathogenesis leading to dysregulated lipid metabolism. The prevalence of insulin resistance is reported in the general population to be approaching 45%, suggesting that NAFLD and NASH will contin nue to be an important public health concern. To date, NASH has proven to be a difficult disease to treat. Front-line therapy with lifestyle modifications resulting in weight loss through decreased caloric intake and moderate exercise is generally believed to be beneficial in patients with NASH, but is often difficult to maintain long term. Given that insulin resistance plays a dominant role in the pathogenesis, many studies have examined the use of insulin sensitizers: the biguanides (metformin), thiazolidinediones (pioglitazone, troglitazone, and rosiglitazone), glucagon-like peptide-1-receptor agonists, or incretins (exenatide)in NASH. This review will provide an overview of insulin resistance in NAFLD and provide a detailed summary on the clinical data regarding the use of insulin sensitizers in NASH.
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PMID:Insulin sensitizers in nonalcoholic fatty liver disease and steatohepatitis: Current status. 1992 Nov 18


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