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)

Forty five cases of chronic pancreatitis have been diagnosed between January 1966 to July 1983 in the Hospital A. Posadas. The diagnosis was confirmed by the presence of one or more of the following data: pancreatic calcifications positive in 35, abnormal secretin test 37, ultrasonography and computed tomography pathological findings 10. Surgical operations were carried out in 25 patients and biopsy taken in 5. Thirty nine (86.6%) were males, 6 (13.3%) females, the mean age in each group was 47.4 and 39.8 years. Chronic alcoholism was certain in 41 (91.9) patients, in the remainder 4 no other etiologic factors were found. The main clinical data were: Weight loss 38 (84.4%) diabetes 34 (75.5%) pain 33 (73.3% in 7 as acute pancreatitis) Steatorrhea 23 (51.1%) jaundice 16 (35.5%- 11 by extrahepatic biliary tree obstruction, 5 by hepatic cirrhosis) pseudocysts 12 (26.6%). The more common associated diseases were: hepatic cirrhosis 6, fatty liver 2 (17.7%) gastroduodenal ulcer 6 (13.3%) cancer 4 (8.8%--gastric 1, pancreatic 3). In order to study the frequency of the clinical data the patients were grouped according to the presence or absence of calcifications and the etiologic factor Symptoms and signs were matched and statistic analysis (coefficient association phi) was made. Only a moderate association between acute pancreatitis in no calcified group and diabetes in calcified group were found. The chronologic study of certains clinical data shows that acute pancreatitis, jaundice, pseudo-cyst and surgical operations were significative more frequent in the first five years while diabetes has little more frequency in the second five year period. Twenty six surgical operations were carried out in 25 patients; 20 (76.9%) due to complications, 6 (23.1%) secondary to pain (pancreatic resection 3, pancreatoyeyunostomy 2, exploration 1). Twenty three patients were lost to follow-up, 12 died and 10 are still alive. This last group was followed at regular period, 8 remained asymptomatic and 2 have intermittent abdominal pain related to alcoholic ingestion.
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PMID:[Chronic calcified pancreatitis. Our experience]. 639 6

Since alcoholism is a major health problem, mechanisms responsible for various forms of alcoholic liver disease (e.g., fatty liver, alcoholic hepatitis, and cirrhosis) require elucidation. Knowledge of these mechanisms is needed to provide a sound framework to treat alcoholic liver disease, to prevent its occurrence and to identify those most susceptible to it. Israel and co-workers proposed that ethanol-induced necrosis results from hypoxia to centrilobular hepatocytes as a consequence of an alcohol-induced increase in hepatic oxygen utilization (Y. Israel, H. Kalant , H. Orrego , J. M. Khanna , L. Videla , and J. M. Phillips, 1975, Proc. Natl. Acad. Sci. USA, 72(3), 1137-1141). We have employed several new techniques to evaluate this hypothesis. Procedures have been developed to make measurements of hepatic metabolism within the hepatic lobule in the isolated, perfused liver using miniature light guides and oxygen electrodes. By comparing these lobular measurements to global metabolism and to hepatic morphology determined by light and electron microscopy, a coherent, quantitative description of lobular oxygen metabolism is emerging. With these techniques, the lobular oxygen gradient was measured directly in isolated, perfused rat livers. This gradient was elevated in livers from ethanol-treated rats, an effect which was blocked by the antithyroid drug, propylthiouracil. Restriction of oxygen delivery to the isolated liver produced stable, circumscribed zones of virtual anoxia localized around the central vein. Anoxic stress led within minutes to centrilobular injury with complete sparing of periportal areas. Cellular injury was characterized by the formation of membranous blebs on the surface of centrilobular hepatocytes. When hypoxic tissue was reoxygenated , blebs were released into the circulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is hypoxia involved in the mechanism of alcohol-induced liver injury? 672 87

The first step in ethanol metabolism is carried out by two enzyme systems: Alcohol dehydrogenase and cytochrome P-450. The cytochrome P-450 system also detoxifies a wide variety of foreign compounds. On the basis of recent evidence, metabolic reasons are suggested for four well-known consequences of alcoholism: (a) The development of fatty liver; (b) the development of metabolic tolerance; (c) the occurrence of interactions between drugs and alcohol; and (d) the fact that many of the kilocalories attributable to ethanol do not seem to "count "count "count" when ethanol forms a major part of the diet.
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PMID:Metabolism of ethanol. 677 4

Six main types of histopathological changes were found in 463 patients with chronic alcoholism admitted during the 10-year period from 1966 to 1975: group I, normal liver in 2.6%; group II, fatty liver in 8.4%; group III, acute alcoholic hepatitis (AAH) in 7.6%; group IV, cirrhosis with or without steatosis in 68.7%; group V, cirrhosis with AAH in 12.8%; group VI, liver cell carcinoma (LCC) in 1.9% (all of the latter patients were also included in group IV). Seventy-three % were males and 27% were females. Females tended to be older than males. Cirrhosis was found in 68% of the group between 21 and 30 yr and in 85% between 51 and 60 yr. Normal histology or steatosis was less frequent after the age of 50 yr. Ascites and jaundice were more frequent in patients with AAH than in patients with steatosis. The majority of patients had SGOT under 100 karmen units/ml; SGPT was normal in 80% of patients with cirrhosis and higher than 100 karmen units/ml in 10%. SGPT was higher than SGOT in only 11.9% of the patients. Mortality was 46.7% according to the followup until 1978. Survival was 38.4% at the end of the first year and decreased very slowly afterwards to 32.8% in males and 11.5% in females after a 5-yr period.
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PMID:Alcoholic liver diseases in Portugal. Clinical and laboratory picture, mortality, and survival. 704 74

The prevalence of serum markers, HBsAg, anti-HBsAg, HBcAg and anti-HBeAg in a group of subjects affected by chronic alcoholism with fatty liver or with cirrhotic stages is reported. An incidence of chronic HBsAg carriers, similar to that found in healthy subjects, was noticed, while an elevated incidence of other serological markers of previous contact with HBV were found. The Authors discuss the significance of this report, on the basis of a greater possibility of contact with HBV, for social-economic situations of those patients. The etiopathogenetic role of HBV in the cirrhotic evolution of alcoholic liver diseases was excluded.
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PMID:[HBV serologic markers in the chronic alcoholism (author's transl)]. 726 76

We compared the weights of the brain, heart, spleen, lungs, liver, and kidneys, uncorrected and corrected for body surface area (BSA) and body mass index (BMI), of 50 alcoholics with 50 forensic controls matched for sex, age, and body weight. With the exception of combined renal weight corrected for BSA and BMI, no significant differences were found in organ weights between the two groups. Glomerular diameter corrected for BSA was significantly greater in alcoholics than controls. It appears that nephromegaly and glomerulomegaly are both population markers for alcoholism. In alcoholics, there was no correlation between the microscopic degree of steatosis and glomerulomegaly. In controls, renal glomerular diameter was greater with increasing severity of hepatic steatosis, probably as a reflection of obesity.
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PMID:Organomegaly in chronic alcoholics. 749 69

The purpose of this study was to determine if the ketone body beta-hydroxybutyrate (beta-HBA) is a useful positive marker for sudden deaths in chronic alcoholics, thought to be due to hypoglycemia. Beta-HBA can be reliably measured in postmortem samples of vitreous humour and urine. In fatalities where there is a history of chronic alcoholism and routine investigations, including autopsy and routine toxicology, yield only a fatty liver as positive findings, a raised level of beta-HBA can be used as an indicator for alcoholic ketosis. Alcoholic ketosis is often associated with antemortem hypoglycemia. Caution should be observed in attributing the significance of ketosis exclusively to alcohol in those conditions where it would otherwise be expected (i.e. diabetic ketoacidosis and chronic starvation). A measurement of this marker of alcoholic ketosis may also help in the investigation of cases where hypothermia or alcohol withdrawal fits are suspected.
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PMID:The investigation of beta-hydroxybutyrate as a marker for sudden death due to hypoglycemia in alcoholics. 830 32

Autonomic neuropathy has been evaluated by various cardiovascular bedside tests in 172 patients with chronic alcoholism (36 alcoholics without liver disease, 50 patients with fatty liver and 86 with cirrhosis), in 21 patients with HBsAg-positive chronic liver disease, in 14 patients with primary biliary cirrhosis, in 14 patients with cirrhosis of other origin and in 86 healthy controls. Parasympathetic integrity was evaluated by beat-to-beat variation during deep breathing, Valsalva manoeuvre and standing up, sympathetic function by blood pressure response to standing and to sustained handgrip test. Autonomic reflex damage was found in all groups examined. Patients with alcoholic cirrhosis exhibited the most severe alterations. Our results suggest, that chronic hepatopathy itself presents a pathogenetic factor of autonomic neuropathy. Autonomic failure has to be considered as a possible cause of symptoms in liver diseases with all its prognostic consequences.
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PMID:[Autonomic neuropathy in chronic liver diseases]. 846 64

Urinary porphyrins and their metabolites aminolevulinic acid (ALA) and porphobilinogen (PBG) were determined in 15 normal volunteers and in 45 alcoholics, subdivided into three groups according to their liver function tests and histology: alcoholics exhibiting no evidence of hepatocellular damage; alcoholics with fatty liver and impaired function of liver enzymes; and alcoholics with proven liver cirrhosis. The dominant trend observed in those alcoholics devoid of any evidence of liver disease was increased ALA, PBG, and uroporphyrin. Coproporphyrinuria was shared by the patients exhibiting liver damage. The data shown enabled us to differentiate between the direct, primary effect of alcohol on the heme biosynthetic pathway and the secondary indirect effect, which is probably related to liver damage that follows alcohol consumption. Evaluation of the results led to the suggestion that urinary ALA could possibly serve as a marker of alcoholism. The specificity and sensitivity of the test were found to be 87% and 80%, respectively.
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PMID:Alcohol-induced changes in urinary aminolevulinic acid and porphyrins: unrelated to liver disease. 883 36

Decades ago it was suggested that nutritional factors are important in the development of alcoholic liver disease (ALD). However, several models of experimental alcoholism considered that the diets fed to animals were nutritionally adequate, complete and balanced. Therefore, a concept prevailed that the effects observed were due to alcohol per se and that they occurred despite a nutritionally adequate status in the animal. Examination of various models revealed that animals were malnourished because they ingested reduced levels of macro- and micronutrients. Furthermore, they consumed only small amounts of carbohydrate and a high level of unsaturated fat for long periods during the development of ALD. Alcoholic rats show many effects of inadequate nutritional status, such as a slow growth, depressed levels of liver glycogen and pancreatic amylase, enhanced protein degradation and circulating levels of branched-chain amino acids, and increased levels of enzymes involved in gluconeogenesis and alterations in the activities of enzymes related to the metabolism of carbohydrate as compared with controls. Chronic consumption of alcohol did not result in fatty liver, high blood alcohol concentration (BAC) or other observed effects when intake of energy, carbohydrate and other nutrients was increased. Furthermore, pre-existing effects of alcohol consumption, such as fatty liver, BAC and delayed gastric emptying, were reversed in rats receiving increased energy and carbohydrate intakes while continuing alcohol ingestion. Thus, nutritional status of the animal determines the production or prevention of ALD or other effects that were considered to be due to alcohol alone.
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PMID:Nutritional factors required for alcoholic liver disease in rats. 916 58


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