Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic ingestion of ethanol (5 g/kg/day) for 6 weeks increased the hepatotoxicity of a single injection of D-galactosamine (330 mg/kg) in rats. Plasma transaminases, alkaline phosphatase, gamma glutamyl transpeptidase and sulphobromophthalein retention were consistently high in alcohol-fed rats compared to sucrose-fed controls, 25 hours after galactosamine administration. Liver histology in sucrose-fed rats revealed typical inflammatory changes and cytoplasmic vacuolation without cell necrosis was seen. Propylthiouracil treatment had no beneficial or protective effect in alcohol-fed rats in this animal model of hepatitis.
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PMID:Potentiation of hepatotoxicity by ethanol in galactosamine-induced hepatitis in rats: role of propylthiouracil protection. 684 26

Chronic alcoholism is accompanied by systemic involvement of the internal organs. Clinico-morphological forms of chronic alcoholism are distinguished on the basis of the prevailing organ pathology, Morphological data are presented, and pathogenesis of the lesions of the liver, heart, pancreas, and kidneys in patients with chronic alcoholism is analysed. The hepatic form may present alcoholic dystrophy, hepatitis or cirrhosis which are stages of progressing hepatopathy. The toxic and metabolic effect of ethanol is important in the pathogenesis of liver lesion. The cardiac form is characterized by the development of alcoholic myocardiodystrophy. In addition to the toxic influence of ethanol, hormonal and electrolyte changes and microcirculatory disorders play a role in its pathogenesis. Chronic calcifying pancreatitis in chronic alcoholism is associated with the effect of ethanol on the mediatory system. The renal form any present necronephrosis, hepatorenal syndrome, glomerulonephritis or pyelonephritis. Their pathogenesis is determined by toxicity of ethanol, circulation of immune complexes in the blood, or immunosuppression.
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PMID:[Morphology and pathogenesis of visceral manifestations of chronic alcoholism]. 711 39

We studied the effects of acute and chronic ethanol feeding on hepatic regeneration in rats following partial hepatectomy and toxic liver injury produced by D-galactosamine. Ethanol, when administered as a single dose (6 gm/kg), inhibited 3H-thymidine incorporation into hepatic DNA; this effect depended in part on the time of ethanol feeding following partial hepatectomy. Multiple ethanol feedings produced an even greater inhibition, which persisted for at least 48 hr after partial hepatectomy. Rats chronically fed ethanol for 30 days also failed to achieve a hepatic proliferative response to either partial hepatectomy or D-galactosamine induced hepatitis comparable to isocaloric pair-fed controls. These investigations suggest that there may be a certain metabolic state in the hepatocyte cell cycle which is most susceptible to the action(s) of ethanol; inhibition of liver regeneration by acute or chronic ethanol consumption may result in delayed recovery from prior or coincident liver injury.
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PMID:Effect of acute and chronic ethanol intoxication on hepatic regeneration. 719 26

Ethanol is easily absorbed from the intestine and diffuses quickly throughout body water. The bulk of ethanol is metabolized in the liver, where alcohol dehydrogenase, a complex mixture of isoenzymes, oxidizes ethanol to acetaldehyde. Ethanol abuse produces functional and structural changes in the gastrointestinal tract, such as in the stomach, small intestine, liver, and pancreas. Accumulating evidence suggests direct toxicity of ethanol and possibly of acetaldehyde. Fatty liver, alcoholic hepatitis, liver cirrhosis, acute and chronic gastritis, deranged structure and function of the small intestine, acute and chronic pancreatitis, and pancreatic lithiasis are some of the sequelae of ethanol abuse. Recent investigations have enhanced our understanding of the functional and structural changes of the gastrointestinal tract produced by the abuse of ethanol.
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PMID:Ethanol, the liver, and the gastrointestinal tract. 719 92

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

Due to a combination of ingested ethanol and inhaled trichloroethylene (Tri) a 28 year old man developed toxic hepatitis and acute oliguric renal failure, both of which had a favorable evolution. Tri has been described as a cause of hepatic disfunction and acute renal failure due to acute tubular necrosis, although some of the cases described are controversial, because Tri was either contaminated by other dissolvents or could not be proven pure, with the exception of one case. In many there was ethanol ingestion. The Tri inhaled by our patient was found to contain less than 1% of carbon tetrachloride (C-Tchl). This would suggest the C-Tchl to be responsible for the clinical picture although the combination Tri/ethanol cannot be discarded as the causal agent, due to the small amount of contaminant present.
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PMID:[Toxic hepatitis and acute renal failure after inhalation of chloride solvents: report of one case (author's transl)]. 732 30

An alcoholic patient developed severe hepatitis and renal failure after ingesting the contents of a 300 ml. bottle of Nyquil for its ethanol content. This illness was presumably related to the 6 gm. of acetaminophen contained in this nonprescription preparation. Although hepatic damage with or without renal failure is usually described after a massive overdose of acetaminophen, the changes in drug metabolism induced by chronic ethanol consumption may increase the risk for acetaminophen toxicity. The large number of nonprescription acetaminophen-ethanol preparations available should be considered in evaluating an alcoholic patient seen with acute hepatic and renal dysfunction.
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PMID:Alcoholism, nonprescription drug and hepatotoxicity. The risk from unknown acetaminophen ingestion. 733 85

Caffeine elimination was studied in 419 patients with cirrhotic and noncirrhotic liver disease of different etiology (hepatitis B virus infection n = 79; hepatitis NANB virus infection n = 74; ethanol-induced liver damage n = 143; primary biliary cirrhosis I-IV n = 63; cryptogenic liver cirrhosis n = 60) following oral administration of 366 mg caffeine. Caffeine clearance in the control group was 69 +/- 33 ml/min (age-matched healthy volunteers and patients without liver disease). Caffeine clearance in acute hepatitis B (70 +/- 60 ml/min) chronic persistent hepatitis B (81 +/- 56 ml/min), chronic aggressive hepatitis B (107 +/- 66 ml/min), posthepatitic liver cirrhosis B (84 +/- 62 ml/min), acute hepatitis NANB (94 +/- 69 ml/min), chronic persistent hepatitis NANB (122 +/- 60 ml/min), chronic aggressive hepatitis NANB (87 +/- 52 ml/min) and posthepatitic cirrhosis NANB (59 +/- 26 ml/min) is not reduced in comparison with controls. In patients with alcoholic fatty liver (127 +/- 71 ml/min, p < 0.05) caffeine clearance is enhanced, in alcoholic hepatitis (57 +/- 72 ml/min) comparable to controls and in alcoholic cirrhosis reduced (36 +/- 44 ml/min, p < 0.05). In primary biliary cirrhosis I-IV caffeine clearance is higher than in controls (117 +/- 59 ml/min, p < 0.05). In cirrhotic liver disease of different origin caffeine clearance is inversely related to the serum bilirubin level. However, the absolute value is determined in addition by the underlying disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Caffeine elimination in cirrhotic and non-cirrhotic liver disease of different etiology. 748 16

Acetaldehyde, the first metabolite of ethanol, is capable to bind various proteins followed by the formation of acetaldehyde adducts. This condensate is supposed to act as a neoantigen. We have recently demonstrated the appearance of acetaldehyde adducts in liver of experimental animals after chronic ethanol treatment, and we produced an experimental hepatitis in guinea pig by immunization with acetaldehyde adducts and treatment with free access to ethanol. However the structure of acetaldehyde adducts and its characteristics are still vague. To elucidate the binding site of anti-adducts antibody against the epitope on adducts, we established a cell line of hybridoma producing monoclonal antibody. This monoclonal antibody recognized protein condensate modified with high concentration of acetaldehyde (1-10 mM) but not those modified with low concentration of it (20-200 microM), whereas the polyclonal antibody produced by conventional method recognized both of them. Using the affinity-purified adducts by monoclonal or polyclonal antibody-liganded column, we examined the antibody titers by ELISA. The elevation of antibody titer was more specific in chronic alcoholics, especially in patients with hepatic inflammatory change, when antibody was measured against the adducts purified by monoclonal antibody than against the adduct purified by polyclonal antibody. Namely, there exist different types of antibody according to the concentration of acetaldehyde to form the adducts. The concentration of acetaldehyde is thought to be much greater in the liver of alcoholics compared to the patient with non alcoholic liver disease. Actually we have immunohistochemically detected the adduct related to high concentration of acetaldehyde in the liver specimen of alcoholics. In conclusion, the appearance of adduct related to high concentration of acetaldehyde and the acquisition of immunity against it appear to be a characteristic feature in alcoholics with hepatic inflammation. Therefore, evaluation of circulating antibodies against protein epitope related to high concentration of acetaldehyde is helpful to know conditions of such types of liver disease seen in alcoholics.
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PMID:[Immune response against protein epitopes modified with acetaldehyde and its clinical significance in alcoholic liver diseases]. 751 Apr 76

Hepatitis viruses and alcohol are major causes of liver disease. This study was aimed at investigating the effect of alcohol intake on the replication of hepatitis C virus and the efficacy of interferon therapy. Fifty-three patients who were histologically proved to have chronic hepatitis C were tested. Of these, 16 were diagnosed as habitual drinkers whose cumulative total consumption of alcohol was more than 100 kg or who had consumed at least 60 gm of ethanol daily for at least 5 yr. The quantities of hepatitis C virus RNA in serum were measured with a competitive assay that combined reverse transcription and polymerase chain reaction. The subjects received a 26-wk course of interferon-alpha therapy. There were no significant differences in age and ALT levels between habitual drinkers and nonhabitual drinkers. The titer of viral RNA (logarithmic transformed copy numbers per milliliter of serum) of habitual drinkers (8.5 +/- 0.5) was higher than that of nonhabitual drinkers (7.7 +/- 0.8) (p < 0.01). Neopterin levels in serum, a marker for the activation of cell-mediated immunity, were lower for habitual drinkers (5.7 +/- 1.5 pmol/ml) than for nonhabitual drinkers (8.1 +/- 5.0 pmol/ml) (p < 0.01). Eleven of the nonhabitual drinkers (30%) were long-term responders whose alanine aminotransferase levels remained within normal range during the 24 wk after interferon therapy, whereas only one (6%) of the habitual drinkers was a long-term responder (p = 0.06). These findings suggest that alcohol intake increases hepatitis C virus RNA levels in serum--at least in part--impairment of cellular immunity, and modulates the efficacy of interferon therapy.
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PMID:Increased serum hepatitis C virus RNA levels among alcoholic patients with chronic hepatitis C. 752 70


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