Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
Alcohol Alcohol 1990
PMID:Validity of post-mortem alcohol reports. 233 92

T-2 toxin (T-2), a trichothecene mycotoxin, produced by several members of the genus Fusarium is a cytotoxic feed contaminant and has been shown to by immunomodulatory. It is suspected that T-2 associated immunomodulation is mediated partly through the hypothalamic-pituitary-adrenal (HPA) axis. T-2, prepared in 4% ethanol/corn oil, was administered orally to male CD-1 mice. Endotoxemia was evident 24 h after a single, oral exposure to T-2. Blood levels of corticosterone, indicative of the stress-response, increased 24 h after T-2 exposure. Hypothalamic norepinephrine and serum corticosterone levels increased in a dose-related manner after 2 weeks of T-2 exposure. Endotoxin, detected in the serum of animals exposed to 2.5 mg/kg T-2 for 1 week, was not associated with bacteremia. Neither endotoxin nor bacteremia were detectable after 2 or 4 weeks of T-2 exposure. Exposure to 2.5 mg/kg T-2 also affected several organs. The forestomach was ulcerated, with lymphocytic infiltration, epithelial proliferation, and hyperkeratinization. Increased spleen weight was associated with a proliferative red pulp. No histological changes were observed in the enlarged liver. Gastritis has been associated with increased corticosteroid production; cortical depletion and reduced mass of the thymus are phenomena attributable to increased corticosteroid levels. An increased corticosteroid level has been associated with thymic involution leading potentially to decreased T-dependent antibody response, a known effect of T-2.
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PMID:Relationship of the hypothalamic-pituitary-adrenal axis with chemically induced immunomodulation. I. Stress-like response after exposure to T-2 toxin. 254 45

The (+)-cyanidanol-3 is used as an antihepatotoxic and hepatoprotective drug in both men and animals against alcoholic and experimental liver injury. Histologic staining techniques give mostly qualitative or semiquantitative description of liver damages. Experiments have been carried out to determine the hepatoprotective effects of (+)-cyanidanol-3 on alcoholic liver damage (i.e., fatty liver and hepatomegaly) by morphometric measurement of the liver tissue sections. Ethanol was administered ad lib to CFY rats to cause mild alcoholic liver damage together with 200 mg/kg/day (+)-cyanidanol-3 to prevent the tissue deterioration. The changes of hepatic lobule and hepatocytes were measured morphometrically. The chronic ethanol consumption results in hepatocellular hypertrophy, a significant increase in size of the hepatocytes and a mild increase of the intralobular extrahepatocytic space as well when compared with controls. The volume of cytoplasm was increased while the parameters of nuclei were unchanged. The (+)-cyanidanol-3 prevents changes and the morphometric parameters in the treated group were almost the same as in the controls. The treatment with (+)-cyanidanol-3 alone does not affect the hepatic tissue parameters. The results show the hepatoprotective effect of (+)-cyanidanol-3 and the suitability of the morphometric method for quantitative comparison of normal and experimentally-altered liver cells.
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PMID:Some morphometric evidence of hepatoprotective effects of (+)-cyanidanol-3. 258 92

In the present study, the effects of chloroquine and ethanol administration during gestation have been investigated on the developing rat fetus. Intragastric administration of chloroquine (700 mg/kg body weight) resulted in several structural abnormalities. The incidence of hepatomegaly was increased by 30%, the liquification of visceral organs was increased by 15% and a 9% higher incidence of cleft palate, wrist drop, clubbed foot and brain liquification was observed in the fetuses from the chloroquine-treated group compared to the corresponding controls. Fetuses from the chloroquine-treated group also showed a decrease of about 40% in the body weight and a 30% reduction in the ossification of the sternum. The teratogenic effects of oral ethanol administration in several respects were similar to those of the chloroquine. Ethanol, when administered as 30% of the total daily calories, resulted in growth retardation, resorption, still births, liquification of the brain, wrist drop and clubbed foot. Additionally, ethanol resulted in the inhibition of several metabolic pathways in the liver and brain of the developing fetuses. This included the inhibition of protein, RNA and DNA metabolism in the fetal livers and brains. The feto-toxic effects of these two xenobiotics and their possible molecular mechanisms have been discussed.
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PMID:Toxicological consequences of chloroquine and ethanol on the developing fetus. 262 56

Intake of opium is very common in India. The contraband material is generally contaminated with arsenic. Most often opium eaters present with neuropathy and hepatomegaly. Arsenic was estimated in serum, urine, nails and hair of opium eaters with and without neuropathy. Arsenic was also estimated in various opium samples. Arsenic was significantly higher in serum, urine, nails and hair of opium addicts when compared to controls. The opium samples analysed showed varyingly high amounts of arsenic.
Drug Alcohol Depend 1987 Nov
PMID:Levels of arsenic in Indian opium eaters. 282 59

Clinical examination and measurement of MCV and GGT were carried out on 124 self-referred 'healthy' Drinkwatchers, all of whom had consumed at least 80 g alcohol/day for more than 2 years. The majority (66.1%) were in social classes II and III. Sixty-three subjects (54.1%) had a raised MCV, GGT or hepatomegaly. A raised MCV was significantly more likely to occur in men. Forty-five subjects (36.3%) had an enlarged liver of whom 17 had a normal MCV and GGT. This study shows that MCV and GGT are poor screening tests for excessive alcohol consumption in 'healthy' subjects but, if used at all, MCV appears to be more sensitive in women and GGT in men. Neither test is an adequate substitute for a careful history and full clinical examination.
Alcohol Alcohol 1987
PMID:Drinkwatchers--description of subjects and evaluation of laboratory markers of heavy drinking. 288 68

Centrilobular hypoxia mediated by enhanced hepatic consumption of oxygen has been hypothesized to be a factor of pathogenetic importance in ethanol-induced liver injury. In the present study, this hypothesis was tested in a rat model which developed alcoholic centrilobular liver necrosis. Male Wistar rats were infused with high fat diet plus ethanol or isocaloric glucose for 7 weeks, a duration which resulted in induction of balloon cell degeneration, focal necrosis, and inflammation in the centrilobular region of the liver of the ethanol-fed animals. Hepatic blood flow, oxygen consumption and oxygen delivery were determined by the radiolabeled microsphere method and measurement of oxygen content in arterial, portal venous, and hepatic venous blood. Hepatic oxygen consumption was markedly increased by 159% in the ethanol-fed animals compared to that in the controls when results were expressed as relative to body weight. Even after these results were standardized per gram of liver weight, hepatic oxygen consumption was still significantly elevated in the ethanol-fed group, but the magnitude of the elevation was reduced to 70%, due to marked hepatomegaly observed in these animals. There was a concomitant 59% increase in hepatic oxygen delivery in the ethanol-fed rats when expressed per kilogram of body weight, and this effect was attributable entirely to increased portal blood flow. However, the increment of this increase in oxygen delivery was much too small to compensate for the 159% increase in oxygen consumption. In addition, this increase in hepatic oxygen delivery was no longer observable when the results were reexpressed based on the liver weight.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Incomplete compensation of enhanced hepatic oxygen consumption in rats with alcoholic centrilobular liver necrosis. 291 30

Prolonged administration of either lithium (7 mg/kg body wt.) or ethanol (30% of daily caloric intake) for 10 days to pregnant rats results in several anatomical abnormalities in the fetus. Intragastric administration of lithium carbonate to pregnant rats immediately after confirmation of pregnancy resulted in high incidence of cleft palate, growth retardation, brain liquification and pulpy brain, hepatomegaly and digital abnormalities, when compared to the saline-treated controls. Furthermore, lithium administration during gestation also resulted in other less frequently observed abnormalities in the fetus, e.g., cardiomegaly, hydronephrosis, ankle-joint defects, syndactyly, defected ribs and sternum ossification defects. Chronic ethanol consumption by pregnant rats during early gestation also resulted in several anatomical abnormalities of prenatal growth retardation, resorption and still births, cleft palate, hydrocephaly and hydronephrosis. The severity and frequency of several of the fetal abnormalities were compounded when lithium and ethanol were administered simultaneously. The possible mechanisms of lithium and ethanol teratogenicity and their synergistic effects have been explained on a biochemical basis.
Alcohol
PMID:Teratogenic effects of lithium and ethanol in the developing fetus. 308 78

To study the acute and chronic effects of ethanol on hepatic fatty acid-binding protein, rats were pair-fed with liquid diets containing 36% of energy either as ethanol or as additional carbohydrate for 4 to 5 weeks. Animals were killed 90 min after intragastric administration of diets with or without ethanol. Alcohol feeding markedly increased liver triglycerides, with a modest rise in nonesterified fatty acids. Alcohol-fed rats developed hepatomegaly, with a 48% increase in hepatic cytosolic proteins. Fatty acid binding was first assessed by the kinetics of [14C]palmitate binding to cytosolic proteins. The maximal binding capacity more than doubled in the cytosol of the ethanol-fed rats compared to pair-fed controls, whereas the dissociation constant increased by 64%. Acute ethanol administration (3 gm per kg body weight) either to ethanol-fed or control rats did not have a significant effect. To identify the fatty acid-binding protein, labeled cytosolic proteins were fractionated by gel filtration: most of the cytosolic fatty acids eluted as a single peak in the 12,000 to 18,000 molecular weight region corresponding to the hepatic fatty acid-binding protein. The increase in this protein, confirmed by radial immunodiffusion (27.0 +/- 1.4 mg per 100 gm body weight vs. 11.2 +/- 1.6, in controls; p less than 0.01), accounted for 22% of the total rise in cytosolic protein induced by chronic ethanol feeding.
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PMID:Fatty acid-binding protein: a major contributor to the ethanol-induced increase in liver cytosolic proteins in the rat. 311 83

An unresolved controversy is whether exposure to organic solvents in the workplace causes hepatotoxicity. From a medical surveillance study of 289 printing factory employees who were exposed primarily to toluene, we identified eight workers who had persistently abnormal serum transaminase and/or alkaline phosphatase values. The eight men were generally healthy and gave no history of taking medications or of drinking ethanol to excess. None was obese or diabetic. Six patients had hepatomegaly based on physical examination. All eight had mild elevations (less than 2 to 3 times the upper value of normal) of serum transaminases [alanine (ALT) and aspartate aminotransferase (AST)]. However, there was a marked increase in the ratio of ALT/AST (mean = 1.61). In each case, liver biopsy revealed mild, pericentral fatty change. Our results, consistent with those previously published by some others, suggest that pericentral fatty liver with mild "reactive hepatitis" is the most likely diagnosis in workers exposed to solvents for whom common causes of mild liver test abnormalities have been excluded. An increased ALT/AST ratio may represent a convenient, previously unrecognized indicator of this condition.
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PMID:Liver structure and function in print workers exposed to toluene. 261 34


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