Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From a group of 424 patients with histologically verified fatty liver 92 patients without diabetes mellitus and alcohol abuse were subjected to follow-up examination for 3 1/2 years. 56 patients underwent second liver biopsy at this time; 20 of these patients had shown marked fatty liver at the initial liver biopsy examination. These 20 patients with marked fatty liver and 25 further patients with moderarte fatty liver could be followed up 5 and 7 1/2 years later; the clinical examination, the various liver function tests, liver scan and blind liver biopsy did not show any evidence of progression of fatty liver towards chronic inflammatory liver disorders or precirrhotic states. This clinical study therefore suggests the harmlessness of non-alcoholic fatty liver.
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PMID:Follow-up study on patients with non-alcoholic and non-diabetic fatty liver. 49 27

A distict alcoholic withdrawal syndrome in chronic alcoholics cannot only be induced upon withdrawal of alcohol or dose reduction but also occurs upon continuous and long lasting consumption of larger quantities of alcohol. In the latter case we deal with an alcoholic predelirium which is characterized by simultaneous occurence of neurologic, vegetative and gastrointestinal disturbances as well as mental symptoms like anxiety, increased irritability and disturbance of sleep. In parallel to this alcoholic withdrawal syndrome from internal medical view a characteristic symptomatology can be observed in patients with chronic alcohol abuse. In most cases younger patients are concerned who, concomitantly with predelirant symptoms frequently display a labile hyperlipidemia and additional obesity, fatty liver, hyperlipidemia and often also hyperuricemia. Based on ten typical cases the combination of symptoms as described above is introduced. This combination can according to Feuerlein be defined as "alcohol-syndrome". The difficulties of diagnosis are shown because in many cases not the alcohol abuse but primarily vegetative and other functional disturbances dominate the clinical appearance. Additionally the pathogenetic connection between the described symptoms and alcohol abuse are discussed.
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PMID:[The "alcohol-syndrome" from internal medical view (author's transl)]. 86 89

Malnutrition is common among alcoholics because alcohol displaces protein-, vitamin-, and mineral-containing foods in the diet, and chronic alcohol consumption results in maldigestion and malabsorption of essential nutrients. In addition, alcohol exerts direct toxic effects on both the liver and gut, resulting in structural alterations in the intestine and the development of fatty liver, alcoholic hepatitis, and cirrhosis. Liver injury is preceded by an adaptive phase characterized by accelerated metabolism of drugs (including ethanol), and hyperlipemia, secondary to hypertrophy and hyperactivity of the smooth endoplasmic reticulum. Side effects include enhanced hepatotoxicity of CCI4 and possibly energy wastage. Alcoholics should not be led to beleive that correction or prevention of nutritional deficiency will prevent liver damage in the face of continued alcohol abuse.
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PMID:Alcohol and malnutrition in the pathogenesis of liver disease.. 117 54

The present paper is devoted to overview the basic concepts of ethanol-induced hepatic injury and therapeutic modalities by which alcoholic liver disease can be alleviated. The role of alcohol dehydrogenase of both hepatic and gastric origin as well as the importance of the number one metabolite acetaldehyde are discussed, furthermore the effects of microsomal ethanol oxidizing system are also described. The features of the major clinicopathological consequences of alcohol abuse fatty liver, alcoholic hepatitis are briefly outlined, and the basic pathogenetic mechanisms that lead to cirrhosis--cell necrosis, regeneration and fibroplasia--are shown. The understanding of the pathophysiology of alcohol-induced liver injury may improve the therapy with drugs and nutritional factors, and allow successful prevention through the early recognition of heavy drinkers before their social or medical disintegration. In the management of alcoholic liver diseases, among the true hepatoprotective agents a naturally occurring flavonoid silymarin and an active methyl-donor metabolite S-adenosyl-L-methionine seem to be promising. An antifibrotic treatment with colchicine might also be of importance. Further prospective, well-designed, controlled clinical trials are still warranted to evaluate real efficacy of these drugs. The hepatic consequences of alcohol abuse may be treatable, however, prevention would be the true resolution of the major global health problem of alcoholism.
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PMID:Pathogenesis and management of alcoholic liver injury. 134

Excessive consumption of ethanol results in reversible redox changes in the liver that are mainly responsible for the accumulation of triglycerides and the fatty liver of the alcoholic patient. In spite of continuing alcohol abuse, only a fraction of all alcoholics will develop alcoholic hepatitis and eventually cirrhosis. Genetic predisposition and environmental factors (in particular the often poor nutrition of the alcoholic) probably play an important role in the evolution of these complications. The generation of reactive oxygen species increases during the metabolism of ethanol, but their pathogenetic role in alcoholic liver disease in man is not clear. Acetaldehyde, a metabolite of ethanol, can react with proteins and form stable adducts. Such neoantigens may elicit an immunologic response which could in part be responsible for the liver cell damage associated with excessive alcohol consumption. Since no satisfactory animal model for alcoholic liver disease exists, the relative importance of the various factors involved in alcoholic liver disease is difficult to assess.
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PMID:[Pathogenesis of alcoholic liver disease]. 158 33

Having briefly analyzed the metabolism of ethanol in man, the author describes hepatocellular damage induced by alcohol abuse and histological, clinical and biohumoral features of steatosis and fibrosis. One hundred clinical cases of hepatic steatosis and fibrosis are also illustrated, studied and observed during five years.
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PMID:[Steatosis and fibrosis: first stage of liver damage induced by chronic alcoholism. Our experience in 100 cases]. 182 26

Plasma endotoxin concentration was measured in 85 patients with alcoholic liver disease (alcoholic cirrhosis (n = 64), alcoholic hepatitis without cirrhosis (n = 11), fatty liver (n = 10), and in patients with non-alcoholic cirrhosis (n = 15]. Endotoxin concentration was determined with an improved chromogenic substrate assay, using individual standard curves for each plasma sample. In patients with alcoholic cirrhosis the mean endotoxin concentration was significantly higher than in patients with non-alcoholic cirrhosis (p less than 0.05). In addition, distinctly higher endotoxin concentrations (greater than 20 pg/ml) were more frequently observed in patients with alcoholic cirrhosis than in non-alcoholic cirrhosis (34.4 vs. 14.3%, p less than 0.05). Mean endotoxin concentration was not significantly higher in cirrhotics with ascites or esophageal varices as compared with the subgroup without ascites or esophageal varices. The endotoxin concentration did not correlate with serum bilirubin, prothrombin concentration or serum enzyme activities. In patients with alcoholic liver disease, however, endotoxin concentration revealed a negative correlation (p less than 0.05) with the concentration of high density lipoprotein cholesterol. On admission endotoxin concentrations in alcoholics with fatty liver were similarly elevated as observed in alcoholic cirrhosis. In six out of 12 patients with fatty liver or alcoholic hepatitis, in whom a second sample of plasma was investigated after 6 to 8 days, endotoxemia was no longer detectable; in the remaining patients, the endotoxin concentration decreased markedly. The results indicate that, irrespective of the stage of liver disease, alcohol abuse favours the development of endotoxemia. They support the hypothesis that gut-derived endotoxins might play a role in the initiation and aggravation of alcohol-induced liver disease.
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PMID:Plasma endotoxin concentrations in patients with alcoholic and non-alcoholic liver disease: reevaluation with an improved chromogenic assay. 205 Sep 95

Alcohol abuse is widespread and alcoholic liver disease represents a major medical and social problem. The spectrum of alcoholic liver injury is currently grouped into three clinical forms: fatty liver, alcoholic hepatitis and cirrhosis. The rational management of alcoholic liver disease can be divided in non-specific therapy and in specific treatment. The most important aspect of non-specific therapy is cessation of alcohol consumption: the abstinence diminishes symptoms and improves signs, and significantly increases survival. As to specific treatment, a number of controlled clinical trials of various forms of therapy have been carried out. Steatosis is spontaneously reversible after cessation of alcohol consumption, and therefore no treatment is necessary. For hepatitis, a number of protocols have been studied with both low and high doses of corticosteroids, cyanidanol, penicillamine, synthetic thyroid antagonists, hormones, and amino acids. Results have been negative, disappointing, or contradictory. In cirrhosis, corticosteroids and colchicine have been used: the former were ineffective while clinical and histological improvement as well as reduced mortality were obtained with the latter. Especially interesting results were registered after treatment with polyunsaturated phosphatidylcholine which has been used for steatosis, acute hepatitis and cirrhosis with good clinical, histological, and biohumoral findings.
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PMID:[Alcoholic liver diseases and their treatment]. 248 Aug 64

Recently numerous reports show deleterious effects of alcohol abuse on pregnant women giving their children a high risk of stillbirth and/or several developmental abnormalities and mental retardation, i.e. the Fetal alcohol syndrome (FAS). In the present study, the effects of maternal alcohol consumption on lipid metabolism in the litter liver were investigated in rats. These rats showed not only quite less lipid deposition in spite of large amount of alcohol consumption up to adulthood, but also showed increased FFA oxidation in the livers. In addition, increased level of very low density lipoprotein and hypoglucagonemia were found. 40 micrograms/kg of glucagon which is known as an inhibitory factor of apoprotein production in the liver, was injected for 2 weeks into the rat tail vein and resulted in apparent fatty liver and hypolipoproteinemia. Norepinephrine injection (1 mg/kg) caused plasma glucagon to be depressed in the rat as compared with adult alcohol rats. Plasma cyclic AMP response to glucagon was also depressed in these rats. From these results, it is suggested that the deranged glucagon secretion from the pancreas and lowered glucagon-induced cyclic AMP response would relate to the abnormal lipoprotein metabolism in the rat.
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PMID:[Experimental studies on lipoprotein metabolism in rats reared with liquid alcohol diet from the fetal life]. 298 81

Reye's syndrome (RS) is generally considered a childhood disease. We report our experience with RS in adults in the metropolitan Milwaukee area. Reye's syndrome was diagnosed in seven 18- to 46-year-old adults. The diagnostic criteria were as follows: viral prodrome followed by vomiting and encephalopathy without focal neurological signs, normal cerebrospinal fluid values, increased levels of serum aminotransferases (transaminase), prolonged prothrombin time, elevated blood ammonia levels, and characteristic microvesicular fatty liver and mitochondrial changes. None of the patients was hypoglycemic. The diagnosis of RS was entertained in 22 but confirmed in only seven patients. In cases of non-Reye's encephalopathy, drug ingestion presented as one of the most difficult differential diagnostic problems, which also included alcohol abuse, collagen vascular disease, and hepatitis B surface antigenemia. Clinical jaundice, distinctly uncommon in RS, was present in only one patient who presented to us in stage V coma. In adults, RS is more difficult to diagnose and should be suspected more frequently in patients with unexplained altered behavior following a viral illness and vomiting. Liver biopsy can be performed safely and is usually mandatory in adults. Patients with RS diagnosed during stage I or II coma and treated experienced an uneventful recovery.
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PMID:Reye's syndrome in adults. Diagnostic considerations. 380 May 31


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