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

Clinical features and liver biopsy findings were studied in six patients with nonalcoholic steatohepatitis associated with hyalin. A comparative study was made on the ultrastructure of the hyalin in one patient with nonalcoholic steatohepatitis and in one patient with alcoholic hepatitis. The patients, all over 50 years old, comprised two females and one male with steatohepatitis and three females with micronodular cirrhosis. They showed obesity, hepatomegaly, and mild abnormalities on laboratory tests. Three of them showed maturity-onset diabetes. The hyalin was found in the cytoplasm of swollen hepatocytes of the centrilobular or in the peripheral region of nodules and was accompanied by necrosis. Ultrastructurally, the hyalin comprised filamentous structures and vesicular or angular structures resembling disorganized circular or branched rough endoplasmic reticulum. It resembled that found in the liver of patients with alcoholic hepatitis.
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PMID:Nonalcoholic steatohepatitis and cirrhosis with Mallory's hyalin with ultrastructural study of one case. 617 90

Male rats treated with a single dose of 1,2-dibromo-3-chloropropane (DBCP) were tested for their ability to carry out the synthesis of liver proteins. In animals treated for 12 h, we found no changes in the uptake of [14C]orotic acid into liver RNA or the uptake of [3H]leucine into liver or serum protein. Uptake of [3H]leucine into the soluble fraction of the enlarged liver increased in proportion to liver size, while the uptake of [14C]orotic acid was unchanged. Examination of the ultrastructure of liver cells from rats treated for 12, 24, or 48 h revealed that the structure of the rough and smooth endoplasmic reticulum (RER; SER) were modified. An absence of ordered stacks of the RER and the presence of tangled nets of SER were noted.
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PMID:The integrity of liver protein synthesis in male rats treated with 1,2-dibromo-3-chloropropane. 618 May 25

Glucocorticoid treatment in dogs is known to cause hepatocellular swelling due to accumulation of cytoplasmic compounds which variably have been identified histochemically as fat, glycogen, or water. In the present study changes in dog liver, after treatment for 15 days with two different doses of oral or intramuscular prednisone, were examined using histological, histochemical, and ultrastructural techniques as well as quantitative chemical analysis. Thirty mongrel dogs were divided into two control groups and three treatment groups of six dogs each. Dogs which received prednisone orally at 1.2 mg/kg body weight/day, or 4 mg/kg body weight/day, respectively, or received intramuscular prednisone injections of 4 mg/kg body weight/day had hepatomegaly due primarily to hepatocellular accumulation of glycogen. Compared to controls, no changes in the hepatic water concentration were observed, whereas the relative amounts of liver fat were decreased slightly and those of protein were decreased markedly. Hepatocellular glycogen could be demonstrated histochemically in tissues fixed in absolute alcohol, but not in tissues treated with aqueous fixative, such as 10% buffered formalin or Bouin's solution. Glycogen deposition occurred predominantly in the midzone of hepatic acini. Affected hepatocytes varied in size and shape. The most severely affected cells were enlarged five to ten fold with glycogen occupying most of the cytoplasmic space restricting the mitochondria, endoplasmic reticulum, and other organelles to a narrow zone around the cell periphery and the nucleus. It was concluded that treatment with prednisone causes hepatomegaly due to glycogenosis in the dog.
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PMID:Prednisone-induced morphologic and chemical changes in the liver of dogs. 646 1

It has been shown in experiments on male rats that administration of cordiamine per os in a dose of 73 mg/kg for 45 days provokes hepatomegaly, proliferation of smooth endoplasmic reticulum in hepatocytes, an increase in the microsomal fraction release, rise in the content of cytochrome P450 and in the rate of N-demethylation of ethylmorphine and p-hydroxylation of aniline in liver microsomes. The spectral magnitude of cytochrome P450 binding with aniline and cordiamine does not change under the effect of the latter drug, while interaction of the enzyme with ethylmorphine decreases. The rate of the recovery of the cytochrome P450-ethylmorphine complex increases 3-fold. It is assumed that an increase in the content of cytochrome and in the rate of xenobiotic hydroxylation in microsomes after prolonged administration of cordiamine might be regarded as substrate induction in nature.
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PMID:[Changes in the hydroxylating function and structure of the hepatic endoplasmic reticulum of the rat as affected by long-term kordiamin administration]. 665 65

The administration of lipid-lowering drugs to rodents, notably those related to clofibrate, rapidly provokes a hepatic response characterized by hepatomegaly, proliferation of smooth endoplasmic reticulum and proliferation of peroxisomes in hepatocytes. In some studies hepatocellular carcinoma has been found in rats or mice exposed for their entire life-span to high dose levels of various fibrates. In the present study liver biopsy samples were obtained from 38 hyperlipidemic patients, 28 of whom had been receiving fenofibrate for between 2 months and approximately 3 years (mean values: males 1.79, females 1.98 years). The remaining 10 patients had never been treated with a lipid-lowering drug. Examination of the biopsy samples by a variety of optical techniques and by electron microscopy failed to reveal any difference between the groups. Peroxisomes were relatively rare, there being no evidence of the clear proliferation seen in rodent studies. Other microscopic features of interest were some variation of nuclear size, mitochondria containing paracrystalline inclusions, dilated endoplasmic reticulum associated with reduced amounts of rough endoplasmic reticulum, and the presence of lipid droplets in the liver cells. However, these variations from normal were in general not much more apparent in samples from the fenofibrate-treated patients than in the untreated group. Light- and electron-microscopic observations did not suggest liver intoxication or a carcinogenic pattern.
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PMID:Influence of fenofibrate on cellular and subcellular liver structure in hyperlipidemic patients. 683 87

Phenobarbital was injected intraperitoneally into male white NMRI mice aged 0.5, 1. 1.5, 3, 6 and 12 months at a dose of 120 mg/kg body weight for 10 consecutive days. The 0.5 month-old mice did not tolerate the phenobarbital dose and died. The experimental animals and one of the controls were sacrificed 1, 3, 5, 10, 15 and 20 days after phenobarbital administration was started. Liver weights were recorded and liver cells were isolated. The number of nuclei per cell was determined and the DNA-content of each single nucleus was measured by Feulgen fluorescence cytophotometry. Liver weights showed an increase of 25--30% during phenobarbital treatment and returned slowly to lower values after cessation of drug application. The hepatic enlargement was accompanied by an excessive and likewise reversible nuclear and whole cell DNA-polyploidization, i.e. polyploidization beyond the physiological age-dependent ploidy level; for example, mean values of 7.7 c per nucleus (versus 4.2 c in the controls) and 14.3 c for whole liver cells (versus 7.5 c in the controls) were found in 3 months-old animals after 5 days of treatment. As with the induction of microsomal enzymes, the augmentation of smooth endoplasmic reticulum, and the increase of RNA- and protein-synthesis, excessive DNA-polyploidization of liver cell nuclei appears to be an expression of hepatocellular hypertrophy due to the functional or metabolic stress imposed upon the liver by large quantities of phenobarbital. After cessation of drug administration the abnormally high ploidy cells are eliminated - probably by necrobiosis - and the liver cells return to their normal age-dependent DNA-ploidy level. The liver cells of the one-month-old animals revealed the physiological polyploidization to be slightly inhibited. This is probably due to some toxic effect of phenobarbital. Phenobarbital did not alter the number of nuclei per liver cell.
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PMID:Excessive reversible phenobarbital induced nuclear DNA-polyploidization in the growing mouse liver. 728 18

Ultrastructural changes in mitochondria from hepatocytes of male Swiss Webster mice were observed during the course of porphyria induced by ingestion of a powdered diet containing 2.5 percent griseofulvin (GF). A variety of sporadic mitochondrial alterations were noted between three days and 22 weeks. Mitochondria appeared intact in hepatocytes from control mice fed powdered diet alone. The abundance and prominence of altered mitochondria increased after seven weeks and was particularly apparent after 15 weeks, concurrent with pronounced hepatomegaly and Mallory body (MB) formation. One or more changes observed in some mitochondria of several hepatocytes included: swelling, associated myelin bodies, increased matrix density, disoriented cristae, intracristal swelling, bizarre shapes, paracrystalline inclusions and elongated or spherulated giant forms. Many mitochondria showed intimate association with rough surface endoplasmic reticulum (RER) adjacent to smooth surface endoplasmic reticulum (SER). GF-induced mitochondrial defects appear to represent nonspecific morphologic alterations similar to many reported in human hepatocytes in alcoholic liver disease, porphyria and various other toxic and metabolic liver diseases. They may reflect another common site of metabolic insult between two such diverse processes as GF-induced mouse porphyria and human alcoholic liver disease.
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PMID:Hepatocyte mitochondrial alterations in griseofulvin fed mice. 736 97

The activity of microsomal cytochrome P-450 monooxygenase and ultrastructure of the liver have been studied in rats exposed dynamically to 50, 500, and 20,000 ppm of vinyl chloride (VC) over 10 months. After 1 and 3 months of exposure to 500 and 20,000 ppm of VC, the level of cytochrome P-450 was slightly lower than in the control animals and upon continuation of exposure it was restored to the original level accompanied by slight increase of activity of aniline p-hydroxylase. Liver enlargement, developed in the course of the exposure, was accompanied by ultrastructural alterations beginning in the 3rd month of exposure to all concentrations of VC. Development of hepatic alterations (hypertrophy of smooth and rough endoplasmic reticulum, swelling of mitochondria, accumulation of lipid droplets, focal cytoplasmic degradation) is discussed with regard to the activity of microsomal monooxygenase system in metabolizing VC to toxic metabolites.
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PMID:Monooxygenase activity and ultrastructural changes of liver in the course of chronic exposure of rats to vinyl chloride. 745 Aug 89

Rats subjected to inhalation of 3500 ppm o-xylene for 6 weeks were found to increase their body-weight at a lower rate than did the controls, despite an increased food and fluid intake, and to develop hepatic enlargement. Post mortem studies revealed no other abnormality. The distribution of the hepatocellular nuclei according to size was, however, modified. The proportion of large nuclei was higher in the test animals than in the controls, and the number of cells per unit area was lower, as a sign of cellular hypertrophy. Electron microscopic studies revealed a loss of glycogen, and increase of rough and smooth endoplasmic reticulum and of peroxisomes. These changes which are typical of the adaptational phase of poisoning may be connected with the induction of the mixed function oxidase system. Enzyme histochemical and ultrastructural studies also revealed a slight hepatocellular damage.
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PMID:Changes induced by O-xylene inhalations in the rat liver. 745 28

Age-related changes in the susceptibility to clofibric acid were investigated in male F344 rats of 8, 52, and 117 weeks old. Hepatomegaly, decrease of serum total cholesterol and triglyceride, increase of the total cytochrome P-450 contents, induction of the activities of microsomal omega-hydroxylation and peroxisomal beta-oxidation, proliferation of smooth endoplasmic reticulum and peroxisomes were detected in 8- and 52-week-old rats. In 117-week-old rats clofibric acid treatment resulted in decrease of serum total cholesterol, elevation of the activities of microsomal and peroxisomal enzymes, and slight proliferation of peroxisomes. These results suggest that the susceptibility of the male F344 rat liver to clofibric acid decreases in 117-week-old rats, though the effect is still recognizable.
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PMID:Age-related changes in the susceptibility to clofibric acid, a hypolipidemic agent, of male rat liver. 761 79


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