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)

An autopsy survey of 441 cases of alcoholic liver disease from the first year of each of the last three decades in the Los Angeles area of the United States was studied. This study includes 326 cases of cirrhosis, 57 cases of fatty liver, 27 cases of alcoholic hepatitis, and 31 cases of fibrosis associated with excessive alcoholic use. Criteria for the histologic classification and the clinical features of alcoholic liver disease are discussed. This survey shows a trend of slight increase in the frequency of alcoholic liver disease and a threefold increase in alcohol related deaths in women in the autopsied population in the early 1980s. Overall, almost half of the patients with alcohol related death showed hypertrophic livers in each subcategory of alcoholic live disease. The whole spectrum of alcoholic liver disease is observed in this series. All the cases with hepatocellular carcinoma are cirrhotic and these patients expired 10 years older than the alcoholic hepatitis group. This study indicates alcohol is probably not carcinogenic but alcohol is cirrhogenic with malignant potentials which could lead to the development of hepatocellular carcinoma in the cirrhoto-regenerative process.
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PMID:The clinicopathological spectrum of alcoholic liver disease--an autopsy survey of 441 cases. 217 37

Alcoholic liver disease presents a wide spectrum of clinical manifestations ranging from mild asymptomatic fatty liver to alcoholic hepatitis and severe life-threatening liver failure with ascites, hemorrhaging esophageal varices, and encephalopathy. Although still poorly understood, the mechanism of this injury is probably the result of numerous direct toxic and metabolic effects of alcohol on the hepatocyte. Therapy consists primarily of abstinence and supportive care. However, several newer treatments are actively being studied. These include prednisolone, anabolic steroids, glucagon and insulin, propylthiouracil, and cyanidanol. Colchicine is promising as an agent to inhibit fibrosis. Complications of cirrhosis, including ascites and variceal hemorrhage, are the result of end stage disease. A return to old techniques of ascitic fluid management suggests that therapeutic large-volume paracentesis with albumin infusion is a safe and effective form of therapy. Variceal hemorrhage is best treated with sclerotherapy, vasoconstrictors, and balloon tamponade. Little has been done to alter the ultimately dismal prognosis and long-term survival of alcoholic liver disease.
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PMID:Alcoholic liver disease. 222 93

The drinking behaviour of 95 consecutive men subjected to medicolegal autopsy in Helsinki was studied by interviewing a relative or friend of the deceased. Sufficient data for estimating the daily alcohol dose were obtained in 61 (64%) of the cases. Of these men, 21 (34%) were reported to drink at least an average of 80 g of alcohol daily. The validity of post-mortem alcohol reports was assessed by comparing the occurrence of alcohol-related diseases, toxicological data as well as the cause and manner of death with the reported alcohol consumption. Men whose reported daily alcohol consumption exceeded 80 g (mean 230 g) differed from men reported to drink less than 10 g (mean 3 g) in their more common incidence of positive post-mortem alcohol test (P less than 0.0005), fatty liver (P less than 0.001), enlarged liver (P less than 0.01), alcoholic hepatitis (P less than 0.05), chronic pancreatitis (P less than 0.01), and in their lower rate of death from cardiovascular diseases (P less than 0.05). The present results indicate that interviews with relatives or friends provide reliable data on the drinking behaviour of the deceased. At autopsy, the most sensitive tests coinciding with high consumption of alcohol in post-mortem alcohol reports but not with each other were positive post-mortem blood alcohol and the occurrence of fatty liver.
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PMID:Validity of post-mortem alcohol reports. 233 92

By means of consecutive pancreatic stimulation, we have investigated the presence of changes of pancreatic function in alcoholic patients, with and without alcoholic liver disease, in order to detect functional alterations and possible association of hepatic and pancreatic disease. The patients were 49 chronic alcoholics (8 patients without liver disease, 11 hepatic steatosis, 9 alcoholic hepatitis and 21 alcoholic cirrhosis) and 15 non alcoholic subjects (8 normal controls and 7 cases of non alcoholic cirrhosis). In all the cases two consecutive stimulations were carried out: first with secretin and cholecystokinin (CCK) and second with CCK alone. The total volume and concentration as well as the output of bicarbonate, trypsin, amylase and total proteins were measured in the duodenal juice. Patients with alcoholic cirrhosis had larger volumes of duodenal juice and lower concentrations of bicarbonate, enzymes and proteins. There was also a tendency to larger volume and lower bicarbonate concentration as the hepatic lesion was more severe. Bicarbonate output was significatively higher in patients with alcoholic cirrhosis but for the remaining parameters the outputs were similar in all the groups. In conclusion, the alterations in pancreatic function parallel the severity of the liver disease. None of the patients had changes consistent with chronic pancreatitis.
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PMID:[Changes in pancreatic secretion in alcoholic liver disease]. 237 59

We report the free, acyl-, and total carnitine contents of 49 clinically healthy volunteers and 167 chronic alcoholics with various clinically and/or anatomopathologically identified degrees of hepatic affection. There was a gradual upward trend in carnitine levels as the degree of hepatic affection increased. In cirrhotic patients, both free and acylcarnitine levels were significantly higher than normal, but there was no systematic hypercarnitinemia in other stages of alcoholism; on the contrary, noncirrhotic alcoholic patients accounted for 82.6% of all hypocarnitinemia cases. Hypercarnitinemia among cirrhotic alcoholics was due chiefly to increased free carnitine concentrations. Acylcarnitine levels in patients with hepatic steatosis were significantly higher than those in normal subjects (P less than 0.001), but there were no other statistically significant differences in either acyl- or free carnitine levels between normals on the one hand and, on the other, patients with hepatic steatosis, alcoholic hepatitis, slight hepatopathy, or chronic hepatopathy without portal hypertension.
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PMID:Free carnitine and acylcarnitine levels in sera of alcoholics. 239 Feb 92

Hepatocytes and bile duct epithelium express several types of cytokeratins, the characteristic intermediate-filament proteins of epithelial cells. The cytokeratin antigen expression was studied in normal and diseased livers, intrahepatic cholangiocarcinomas, and hepatocellular carcinomas by immunohistochemical methods using a panel of polyclonal and monoclonal antibodies to cytokeratins. Ten percent formaldehyde solution-fixed, paraffin-embedded sections obtained from ten patients without liver disease, 18 patients without liver disease, 18 patients with different stages of primary biliary cirrhosis, 14 patients with alcoholic hepatitis, ten patients with fatty liver hepatitis secondary to diabetes mellitus or morbid obesity, five patients with hepatocellular carcinomas, and five patients with cholangiocarcinomas were examined. The results suggested that hepatocytes and bile duct epithelium retain their distinct cytokeratin profiles in liver disease, including malignant transformation. Therefore, demonstration of cytokeratins in the liver is useful in establishing the cellular origin of neoplasms and understanding the pathogenesis of liver diseases.
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PMID:Expression of cytokeratins in normal and diseased livers and in primary liver carcinomas. 246 75

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

Hypertrophic osteoarthropathy (HOA) may be an idiopathic condition or may be secondary to other diseases, the most common of which is bronchogenic carcinoma. Among non neoplastic etiologies, it is commonly associated with chronic liver disease, usually cirrhosis and chronic active hepatitis. The concomitant occurrence of HOA and hepatic steatosis is another association that has recently been reported. We report here a 70-year-old male with periostitis, clubbing of the fingers and alcoholic hepatitis stenosis. We emphasize the need to perform observational studies to validate this association.
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PMID:[Hypertrophic osteopathy and acropachy associated with noncirrhotic alcoholic liver disease. Apropos a case]. 249 73

Increased levels of serum procollagen III peptide (P-III-P) have been found in patients with alcoholic hepatitis and cirrhosis. Serum P-III-P was increased (greater than 15 micrograms/l) in 38 of 44 (86%) patients with alcoholic liver cirrhosis, in 6 of 20 (30%) with fatty liver, in 1 of 13 (8%) with non-alcoholic fatty liver, and in 3 of 14 (21%) with other chronic liver diseases. Median serum P-III-P was almost three times higher in alcoholic liver cirrhosis than in alcoholic fatty liver (p less than 0.001). Serum P-III-P was increased in three of six patients with alcoholic fatty liver and periportal fibrosis. In the total material (n = 91), a statistically significant negative correlation between serum P-III-P and albumin (r = -0.71, p less than 0.001) and Normotest (r = -0.63, p less than 0.001), respectively, and a positive correlation between serum P-III-P and bilirubin (r = 0.65, p less than 0.001) were found. The serum level of P-III-P had no prognostic value concerning the mortality in patients with alcoholic cirrhosis.
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PMID:Serum procollagen III peptide in alcoholic and other chronic liver diseases. 260 4

80 patients (P) (68 men and twelve women) with the diagnosis of delirium tremens were retrospectively analyzed and reexamined over a period of ten years (1974 to 1984). Included were only patients who--after failure of oral medication--required intravenous therapy with Chlomethiazol and thereby intensive care treatment. Mean age was 46.2 (26 to 75) years. During the observation period delirium tremens increased in frequency by 11% each year. Nine patients had two, six patients three and two patients four episodes of delirium tremens. In 86.7% delirium tremens occurred with fatty liver and alcoholic hepatitis, epileptic seizures, cirrhosis and hepatic coma, gastrointestinal hemorrhage and pancreatitis. Eight patients (10%) died in hospital at a mean age of 53.2 years. None of the deceased had less than three (on average four) complicating or associated diseases. These were mostly pneumonia, cirrhosis, hepatic coma, and gastrointestinal hemorrhage. The mean duration of intravenous Chlomethiazol therapy was 4.7 (0.25 to 20) days, the applied dose 26.2 (0.8 to 78.6) grams, there being no significant difference between survivors and non-survivors. Of the 72 survivors 62 were invited for follow-up examination after an average of five years. During this period another twelve patients (15%) died of pneumonia, gastrointestinal bleeding, cardiocirculatory failure and accidents. Life expectancy was only 9.3 years. Of 29 patients who came for follow-up, 55% showed clinical evidence of alcohol dependency, 65% had elevated gamma-glutamyl-transferase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Severe course of delirium tremens. Results of treatment and late prognosis]. 262 19


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