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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighty-five patients (81 males and 4 females) with significant alcoholic histories were studied. Alcohol misuse was directly or indirectly responsible for about 5-10% of hospital admissions in Sri Lanka. Prevalence of alcoholism in patients below 40 years (43% of cases) or with a strong family history (56% of cases) were demographic features simulating trends in developed nations. Although rarely an occupational hazard, the majority in this lower socio-economic group drank illicitly-manufactured brews with high alcohol content while many consumed a mixture of beverages. Lone drinkers were predominant (86%); features of psychological interest were sleep disturbance (64%), emotional problems (42%) and loneliness (34%); domestic problems (36%), social problems (24%) and financial problems (34%) were also noted. Many such factors, either singly or in combination, initiated or perpetuated the drinking habits of the patients. Drug misuse and suicidal tendencies were not observed. Severe hepatic damage was noted in 63% of 42 patients where the histology was demonstrated, and who usually presented with significant hepatomegaly; about 50% of patients below the age of 40 had hepatic damage of a serious or irreversible nature. Direct toxicity of ethanol, toxic contamination during the preparation of illicit brews and nutritional factors appear pertinent to hepatic damage in developing nations. Nutritional factors may cause variations in relation to abnormalities in liver function tests and also liver size among the population studied when compared to findings from the western world.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcohol Alcohol 1986
PMID:Recent aspects of alcoholism in Sri Lanka--an increasing health hazard. 349 12

Chronic consumption of ethanol often results in an increased rate of ethanol metabolism (metabolic tolerance) and in hepatomegaly. However, the extent of these changes is highly variable. We have found that these two phenomena are greatly influenced by age. We studied the effect of age on the development of metabolic tolerance and hepatomegaly and on the increase in hepatic oxygen consumption produced by chronic ethanol administration. The latter has been proposed to contribute to metabolic tolerance to ethanol. Ethanol was administered to female Sprague-Dawley rats with different initial ages (4, 6, 8, 11, and 17 weeks) for a 4-week period in a high-fat liquid diet. Control animals were pair-fed an isocaloric liquid diet in which ethanol was replaced with carbohydrate. Metabolic tolerance and hepatomegaly following chronic ethanol consumption were markedly dependent on the initial age of the animal, with young animals showing the largest increases. Although showing a similar general trend with age, the degree of metabolic tolerance was not linked proportionally with the degree of hepatomegaly. Perfused livers from young rats fed chronically with ethanol showed increases in ethanol metabolism and oxygen consumption, whereas no increase were observed in those from older animals. These findings support the hypothesis that an elevated rate of hepatic oxygen consumption contributes to metabolic tolerance. Total hepatic alcohol dehydrogenase activity was not increased by chronic ethanol consumption in any age group, demonstrating that an increase in the levels of this enzyme is not obligatory for metabolic tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcohol Clin Exp Res
PMID:Effect of age on metabolic tolerance and hepatomegaly following chronic ethanol administration. 639 2

It has been shown that alcohol consumption disrupts liver microtubules, impairs protein secretion and leads to ballooning of the hepatocytes in rats. Ethanol-induced hepatomegaly was accounted for by an increase of the hepatocytes volume. To study whether these changes occur in human alcoholic liver disease, hepatic tubular protein and export protein content were measured in 29 cases of alcoholic liver disease and were compared with those of 37 cases of non-alcoholic liver disease and 5 cases of non-hepatobiliary disease. Hepatic polymerized tubulin was significantly decreased in alcoholic liver disease compared to non-alcoholic liver disease (p less than 0.01), while free tubulin was increased in alcoholic liver disease. Hepatic transferrin (one of the export proteins) content was significantly higher (p less than 0.01) and serum transferrin level was significantly lower (p less than 0.05) in alcoholic liver disease than in non-alcoholic liver disease. These findings indicated that even in humans, chronic alcohol consumption decreased hepatic microtubules by impairing polymerization of tubular protein and increased hepatic export protein content. This decrease in hepatic microtubules by chronic alcohol consumption may play an important role in the development of human alcoholic liver disease.
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PMID:Changes of hepatic microtubules and secretory proteins in human alcoholic liver disease. 663 57

Both acute and chronic ethanol administration inhibit the secretion of albumin and glycoproteins from the liver. Impairment of posttranslational steps of the secretory process are mainly involved in this secretory defect, although in some instances altered synthesis of the protein moiety may be a factor. Decreased secretion following ethanol administration results in the intrahepatic retention of export proteins. The secretory defect is a consequence of the metabolism of ethanol and is likely mediated via acetaldehyde, although more conclusive proof is still required. The manner by which acetaldehyde impairs the secretory process is unknown, but may be related to its high reactivity with hepatocellular proteins. The specific posttranslational steps or processes involved in the secretory defect are still unclear; however, it appears that the final steps of secretion (post-Golgi events) may be the primary site of impairment. Impaired secretion of proteins from the liver could contribute to altered levels of plasma proteins and hepatomegaly as well as to the liver injury observed in the alcoholic.
Recent Dev Alcohol 1984
PMID:Effect of ethanol on hepatic secretory proteins. 672 60

In a prospective study of more than 10000 Yugoslav men it was found that consumption of alcoholic beverages was inversely related to non-sudden death from coronary heart disease (CHD) and positively related to death from trauma. The consequence was an apparently U-shaped relation between alcohol consumption and death, the lowest mortality being among moderate drinkers. Excess mortality from trauma was evident only among men under 55 and only for those who reported at entry to the study that they had been drunk during the preceding week. Alcohol consumption as reported at entry was unrelated to subsequent mortality from liver cirrhosis or any form of cancer. An enlarged liver, however, was associated with higher death rates for liver cirrhosis. This raises the possibility that some of the men were heavy drinkers preceding their entry to the study but were no longer drinking heavily at the time of entry. Enlarged liver, however, was also related to hypertension and to chronic obstructive pulmonary disease and thus was not a specific indicator of alcohol abuse in this population. Recent drunkenness but not frequency of drinking was related to death from trauma and liver cirrhosis and to sudden CHD death. In short, both the pattern of drinking and the usual level of alcohol consumption appear to be related to mortality in this population.
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PMID:Drinking habits and death. The Yugoslavia cardiovascular disease study. 687 7

In conclusion, the studies presented suggest that two factors commonly occurring in the alcoholic, namely, an increased rate of ethanol metabolism and hepatomegaly, may have important pathogenic implications in alcoholic liver disease. An increased rate of ethanol metabolism is linked to a greater oxygen demand, thus resulting in greater susceptibility to hypoxia in Zone 3 of the liver acinus, a factor which might be responsible for hepatocellular necrosis in alcoholic hepatitis. Propylthiouracil has been shown to have a protective effect against hypoxic necrosis in alcohol-fed animals and has been found to be most effective in accelerating the rate of recovery of alcoholics with active liver disease. On the other hand, hepatocyte expansion in hepatomegaly, in the face of a semi-rigid liver capsule, leads to constriction of extracellular volume and to an increase in intrahepatic and portal pressure. The latter, in turn, could produce a variety of haemodynamic alterations as those found in the alcoholic. To what extent the mechanisms described are responsible for or might add to the myriad of other disturbances observed in alcoholic disease should be further analysed.
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PMID:Hepatocyte demand and substrate supply as factors in the susceptibility to alcoholic liver injury: pathogenesis and prevention. 701 48

Alcohol inhibits the secretion of protein from the liver. Chronic abuse results in intrahepatic accumulation of export-type proteins and decreased plasma levels. These effects appear to be mediated by acetaldehyde, an oxidation product of ethanol. Acetaldehyde is capable of interfering with the assembly of microtubules, a component of the cytoskeleton, the integrity of which is required for normal secretion. Protein retention and cytoskeletal alterations may contribute to manifestations of alcoholic liver disease, such as hepatomegaly, ballooning of the hepatocyte, portal hypertension, and development of Mallory bodies.
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PMID:Effects of alcohol on hepatic transport of proteins. 704 72

A case report is presented of a young woman in whom symptomatic porphyria cutanea tarda (PCT) developed during copper chelation therapy for Wilson's disease. The 22 year old white woman was seen in the summer of 1978 because of development of blisters on the dorsa of the hands associated with focal atrophic hypopigmentation, generalized hyperpigmentation of the skin, and hpertrichosis of the lateral forehead and face. A sibling had died in childhood with Wilson's disease. When the patient developed hepatomegaly, ascites, and an acute hepatitis syndrome at the age of 11, penicillamine therapy was empirically started, with gradual symptomatic improvement. When evaluated at the age of 22, abnormal laboratory values included a total bilirubin of 1.2 mg%; alkaline phosphatase, 96 U; serum glutamic oxaloacetic transaminase (SGOT), 175 U; serum glutamic pyruvic transaminase (SGPT), 122 U; gamma glutamyl trans peptidase (GGTP), 64 U; and Bromsulphalein (BSP) retention, 21% at 45 minutes. Skin biopsy from the hand revealed a noninflammatory subepidermal bulla with prominently PAS positive vessel walls in the festooned dermal papillae at the base of the blister. A fragmented liver biopsy failed to reveal evidence of active hepatitis or cirrhosis, but considerable stainable iron was present in both hepatocytes and Kupffer cells. A rubeanic acid stain for copper was negative. The patient was diagnosed as having Wilson's disease, hepatic hemosiderosis, and PCT. Cessation of all ethanol consumption and discontinuation of the oral contraceptives which she had been taking for 6 years, was recommended. On examination 9 and 22 months after these modifications were instituted, the patient felt asymptomatic and was without evidence of any new blisters or scars of her skin. The hyperpigmentation and hypertrichosis persisted, but she rigidly adhered to a program of penicillamine, topical sunscreen application, and abnegation of alcohol. Liver function studies were normal, and urinary porphyrin levels returned toward normal values. The clinical onset of this patient's blistering disease was temporally associated with ethanol and exogenous estrogen medication.
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PMID:Porphyria cutanea tarda complicating Wilson's disease. 720 91

The effect of ethanol on hepatic regeneration after partial hepatectomy was studied. Ethanol was administered in a nutritionally adequate liquid diet 4 times daily by gastric intubation. The dose of ethanol was selected to maintain a continuous level of ethanol in the animals throughout the experiment. Treatment was started 24 hours before the operation and continued for 6 days. Control animals were pair-fed on a diet in which ethanol was isocalorically replaced by carbohydrate. On the 1st, 2nd, 3rd and 5th day after the operation the incorporation of [3H]-labelled thymidine into liver DNA and [14C]-labelled leucine into liver proteins and the mitotic index of the regenerating liver was assessed. On the 2nd and 3rd day the incorporation of labelled thymidine into DNA in the regenerating livers of alcohol-fed animals was significantly (P less than 0.05) lower than in pair-fed controls. The inhibition was most pronounced (60%) on the 2nd day after the operation. This was associated with a significant (P less than 0.01) decrease in mitotic activity, which was most pronounced in the periportal area. At the end of the experiment, however, DNA content was similar both in ethanol-treated and in control livers. It is concluded that the continuous presence of ethanol retards DNA synthesis and cell division of regenerating rat liver after partial hepatectomy. The incorporation of [14C]-leucine into liver proteins was inhibited by ethanol on the second day of regeneration (P less than 0.01), and at the end of the experiment the livers of ethanol-fed rats contained more protein than the control livers. This accumulation of proteins was accompanied by hepatomegaly.
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PMID:Effects of ethanol on liver regeneration after partial hepatectomy in rats. 723 Sep 14

Various metabolic studies were performed in a patient with the idiopathic Fanconi syndrome in whom constant ketonuria suggested that organic acidemia might contribute to the metabolic acidosis. Glucose intolerance with a diminished insulin release was found after PO or IV glucose loads and after glucagon administratio. An insulinopenic "diabetes-like" state has not previously been described in such patients. The patient had impaired galactose-glucose interconversion, elevated blood lactate levels, reduced pyruvate levels, and an increased lactate:pyruvate ratio. Hepatomegaly and hypoglycemia were not present, and liver and muscle biopsies revealed no enzymatic evidence of glycogenosis. The erythrocyte UDP galactose transferase activity was normal. The patient failed to convert fructose to glucose and had a rise in blood lactate after ethanol administration. Further studies revealed no production of glucose after alanine or glycerol administraion, each test being associated with elevated blood lactate levels and, after alanine, an increased lactate:pyruvate ratio. The lactate:pyruvate ratio was elevated after glucagon administration with increased lactate and reduced pyruvate concentrations.
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PMID:Abnormalities of carbohydrate metabolism in idiopathic Fanconi syndrome. 738 41


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