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)

An early manifestation of alcoholic liver injury is the accumulation of protein, as well as fat, in the liver. The increase in soluble proteins is associated with retention of water and swelling of the hepatocyte, resulting in hepatomegaly. Though "in vitro" ethanol inhibits hepatic protein synthesis, no consistent effects have been found after acute alcohol administration "in vivo". Moreover, after chronic alcohol consumption, the synthesis of liver protein is increased rather than decreased. Alcohol consumption, however, delays the secretion of proteins from the liver into the plasma, promoting accumulation in the liver of proteins which are primarily destined for export. The altered secretion is associated with decreased hepatic content of polymerized tubulin and visible disruption of microtubules, an organelle which may maintain the architectural organization required for transport of macromolecules. The alteration of microtubules has been linked to consequences of ethanol oxidation in the liver.
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PMID:[Alcohol induced changes of protein metabolism (author's transl]. 35 64

Alcohol feeding to rats produced hepatomegaly, associated with enlargement of the hepatocytes. The increase in liver dry weight was accounted for not only by fat but also by protein accumulation, primarily in microsomes and cytosol, with a selective increase in export proteins: concentrations of both immunoreactive albumin and transferrin were augmented in liver microsomes and cytosol of ethanol-fed rats. To investigate the mechanism of this protein accumulation, [14C]leucine was injected intravenously and its incorporation into both liver and serum proteins was measured after various time intervals. Rates of synthesis and export were assessed from protein labeling and specific activities of leucyl-tRNA. Synthesis of liver protein and proalbumin were enhanced by chronic ethanol feeding, but this was not associated with a corresponding rise in serum albumin output. Actually, there was a significant retention of the label in liver albumin and transferrin with delayed appearance in the serum of ethanol-fed rats. This indicated that, regardless of the changes in synthesis, the export of protein from the liver into the plasma was impaired. This alteration in export was associated with a decreased amount of polymerized tubulin in the liver of ethanol-treated animals. Thus, both enhanced protein synthesis and defective export contribute to the ethanol-induced accumulation of liver protein, and the decrease in liver microtubules represents a possible site for impairment of protein export.
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PMID:Pathogenesis of alcohol-induced accumulation of protein in the liver. 56 Nov 18

Thirty-five Black patients with cirrhosis of the liver were admitted to the professorial unit over a 1-year period and were included in a carefully planned prospective study. Men predominated over women in a ratio of 3:1. Alcohol consumption in the form of African beer was significantly higher in cirrhotic patients than in a control population. The clinical picture was neither predominantly that of alcoholic nor of cryptogenic cirrhosis. Hepatomegaly, porphyria cutanea tarda, ascites, splenomegaly and oesophageal varices were common. There was a complete absence of gynaecomastia, spider naevi and liver palms. Histologically, the majority of patients had macronodular cirrhosis, and only 1 patient had micronodular cirrhosis and minimal fatty change. Hepatitis B surface antigen (HbsAg) was not detected in any patient, despite a positive HbAg rate of 4% in Black African blood donors, determined by means of the same laboratory technique.
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PMID:Cirrhosis of the liver in Rhodesian Blacks. 88 20

Hepatomegaly and abnormal liver function can occur in nonmetastatic malignancies. A patient with metastatic prostatic adenocarcinoma that had spared the liver and extrahepatic biliary tree is described. He had puzzling episodes of jaundice for a period of 2 1/2 years. The results of appropriate investigations and an exploratory laparotomy performed dlring the patient's four antemortem hospitalizations were indicative of "recurrent intrahepatic cholestasis," the cause of which remained an enigma even after exploratory laparotomy. At autopsy, no evidence of hepatic metastases or extrahepatic biliary obstruction was found. Alcohol, hepatotoxic drugs, toxins, viral and chronic active hepatitis, hemolysis, and extrahepatic biliary obstruction were eliminated as causes of the jaundice. We believe that the intermittent intrahepatic cholestasis is one of the nonmetastatic manifestations (nonmetastatic hepatopathy of malignancy) of the prostatic adenocarcinoma.
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PMID:Intermittent cholestatic jaundice and nonmetastatic prostatic carcinoma. 92 51

The hepatomegaly that appears after long-term feeding of ethanol results in accumulation of protein that is quantitatively as important as the increase in lipid. The bulk of protein accumulated in the soluble fraction of the cell. Hepatic albumin and transferrin concentrations increase and colchicine-binding protein decreases, thus suggesting an intrahepatic retention of export proteins.
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PMID:Alcoholic hepatomegaly: accumulation of protein in the liver. 119 96

The authors report the cases of 4 patients with heavy chronic alcoholic intake who presented with hepatomegaly and jaundice without obvious hepatic failure and who died rapidly. In all 4 cases, histological examination of the liver showed massive microvesicular and macrovesicular steatosis involving approximately 100% of hepatocytes and, in 2 cases, minimal lesions of alcoholic hepatitis. Histochemical study, performed in 3 cases, showed that steatosis was constituted of triglycerides only, and that hepatic glycogen was completely depleted in 2 of 3 cases. No obvious cause of death was found in these 4 patients. Shortly, before their death, the 4 patients had increased their ethanol and decreased their food intake. The authors suggest that death as well as microvesicular steatosis could have be due to acute mitochondrial dysfunction.
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PMID:[Severe hepatic steatosis: a cause of sudden death in the alcoholic patient]. 147 9

250 patients with fever, hepatomegaly and eosinophilia were investigated for parasitic infection by stool, urine, thick blood smear examination and sero-diagnosis (ELISA for anti-Toxocara and IFA for anti-Fasciola). Those with patent parasitic infections (41) and anti-Toxocara seropositivity (10) were excluded from follow up. The other were 3 months followed up. The detected infections were 10 Ascaris, 15 Strongyloides, 20 Toxocara, and 25 Schistosoma mansoni. Other 30 were positive for Fasciola eggs. No other infections were found in the remained 109 patients. IFA anti-Fasciola antibody titres were significantly higher among Fasciola group than any other groups. It is concluded that IFA anti-Fasciola antibody titre greater than or equal to 1/256 with ethanol fixed antigen sections is of value in diagnosis of acute fasciolitic hepatic syndrome.
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PMID:Indirect fluorescent antibody test in diagnosis of acute fasciolitic syndrome. 157 73

Protein supplemented diet was protective against the deleterious action of endosulfan on body growth and liver. Hepatomegaly and a reduction of body weight produced concurrently by endosulfan and ethanol were greater in male rats, suggesting that males are more susceptible than female rats to the metabolic stress caused by their interaction. Chronic endosulfan exposure resulted in a prolongation of ethanol sleeping time in female and not in male rats. This finding suggests failure of female rats to metabolize ethanol readily on account of their greater susceptibility than male rats to the hepatotoxic action of endosulfan.
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PMID:Evidence for a hazardous interaction between ethanol and the insecticide endosulfan in rats. 160 11

In the present study, the effect of chronic ethanol consumption in rats on the hepatic heme metabolism was investigated. Male Wistar rats were fed a nutritionally adequate liquid diet containing ethanol as 36% of the total calories for 5 weeks. After an overnight fast, the livers were excised and centrifuged to obtain mitochondrial and microsomal fractions. Chronic ethanol feeding of rats resulted in about 19% hepatomegaly as represented by the increased liver/body weight ratio. There was no difference in the mitochondrial protein content between the ethanol-treated and control rats, but the microsomal protein content was significantly increased in the ethanol-treated rats. Hepatic microsomal content of cytochrome P-450 (P-450) was markedly enhanced by chronic ethanol ingestion. Microsomal contents of cytochrome b5 (b5) and total heme were also increased to a lesser extent. After chronic ethanol abuse, the hepatic activity of delta-aminolevulinic acid (ALA) synthetase, which is a rate-limiting enzyme for heme production, was significantly increased and that of the heme oxygenase was slightly increased. These data indicate that ALA synthetase activity is induced by the negative feedback mechanism in order to compensate the depletion of heme caused by the utilization of heme for P-450. It is also speculated that, in response to excessive production of heme as described above, heme oxygenase activity is secondarily induced to regulate the amount of heme.
Alcohol
PMID:Alterations in hepatic delta-aminolevulinic acid synthetase and heme oxygenase activities after chronic ethanol consumption in rats. 178 21

A patient with multiple, pyogenic hepatic abscesses is described, and the pathophysiology, etiologies, clinical and laboratory manifestations, and management of the disease are reviewed. A 55-year-old man with a history of ethanol abuse and pancreatitis developed fever, chills, general malaise, and right upper quadrant abdominal pain two weeks before hospitalization. Baseline laboratory and hematology results included serum albumin concentration, 3.2 g/dL; serum alkaline phosphatase concentration, 239 mIU/mL; total serum bilirubin concentration, 1.3 mg/dL; white blood cell count, 18,400/cu mm; red blood cell count, 4.7 million/cu mm; hemoglobin, 12.5 g/dL; and hematocrit, 38.8%. Abdominal ultrasound showed echo-free cavities throughout the hepatic parenchyma; abdominal computed-tomography (CT) scan showed hepatomegaly and multiple radiolucent spaces. CT-guided needle aspiration of a hepatic mass yielded purulent material that grew Fusobacterium necrophorum under anaerobic conditions. On day 7, the patient was started on i.v. ampicillin sodium-sulbactam sodium. A CT scan two weeks later showed a reduction in the number and sizes of abscesses. The patient continued i.v. therapy for one month, then was discharged on a regimen of p.o. amoxicillin trihydrate-clavulanate potassium. Hepatic abscesses are either amebic or pyogenic; the latter usually has a higher mortality. The etiologies of pyogenic hepatic abscesses include ascending cholangitis, portal vein bacteremia, systemic bacteremia, extension from a contiguous focus of infection, and trauma. Diagnosis is difficult and relies highly on clinical suspicion. Clinical symptoms include hepatomegaly, fever, chills, and malaise. Abnormal laboratory values include leukocytosis, anemia, and hypoalbuminemia. The abscesses are frequently polymicrobial; Escherichia coli is the most commonly isolated species. CT is the best radiological technique for diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ampicillin-sulbactam therapy for multiple pyogenic hepatic abscesses. 229 77


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