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)

The carcinogenic potential of cycasin and methylazoxymethanol (MAM) acetate was investigated in nonhuman primates. Old-world monkeys (rhesus, cynomolgus, and African green monkeys) received cycasin and/or MAM acetate by oral or ip routes up to 11 years. Eighteen monkeys survived longer than 2 months after initiation of treatment with cycasin (50-75 mg/kg) or MAM acetate (1.5-3.0 mg/kg) given orally 5 days/week; 9 of the animals were necropsied. Histopathologic examination of a liver tumor from 1 of these monkeys revealed well-differentiated hepatocellular carcinoma. A second monkey had multiple tumors, including hepatocellular carcinoma, intrahepatic bile duct adenocarcinoma, renal carcinoma and adenomas, and adenomatous polyps of the colon. Although liver tumors were not observed in the other monkeys, all but 1 monkey had hepatic lesions such as toxic hepatitis and cirrhosis. These monkeys had received cycasin and/or MAM acetate for an average of 57 months (range, 2-133 mo). A group of 10 monkeys received MAM acetate by weekly ip injections (3-10 mg/kg). Six of these animals developed tumors after receiving an average of 6.14 g (range, 3.58-9.66 g) of MAM acetate for an average of 75 months (range, 50-89 mo). Four of the monkeys developed hepatocellular carcinomas, and 2 had multiple primary tumors including hepatocellular carcinomas, renal carcinomas, squamous cell carcinomas of the esophagus, and adenocarcinomas of the small intestine. Our results showed that long-term administration of cycasin and/or MAM acetate by oral and ip routes was hepatotoxic and carcinogenic in old-world monkeys.
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PMID:Carcinogenicity and hepatotoxicity of cycasin and its aglycone methylazoxymethanol acetate in nonhuman primates. 624 73

Hepatic encephalopathy in patients with severe liver disease was associated with marked elevation of either serum methionine or blood ammonia levels or with simultaneous moderate increases in both parameters. CSF methionine levels also increased in encephalopathic patients with fulminant hepatitis and liver cirrhosis. Increased influx of methionine into the brain over the theoretical values predicted from Pardridge's equation suggested that accelerated transport of serum methionine across the blood-brain barrier was observed in these cases with hepatic encephalopathy. Hepatic encephalopathy in acute carbon tetrachloride liver injury could be obtained experimentally following intraperitoneal injection of ammonium acetate in rats, which already received intragastric administration of methionine. However, similar encephalopathy could not be observed by the administration of glycine or leucine in place of methionine. These results suggest at least that methionine and ammonia act synergistically on inducing hepatic encephalopathy.
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PMID:Impaired metabolism of methionine in severe liver diseases. II. Clinical and experimental studies on role of impaired methionine metabolism in pathogenesis of hepatic encephalopathy. 710 99

Inherited coagulation protein deficiencies associated with bleeding diatheses may present with spontaneous bleeding early in life, or may not be recognized until the development of hemorrhage after trauma or surgery. Diagnostic evaluation with coagulation screening tests, followed by confirmation with coagulation factor assays, is essential for appropriate management. For moderate-to-severe hemophilia, treatment includes coagulation factor replacement with purified, plasma-derived coagulation factor, or in the case of hemophilia A, factor VIII concentrate produced with recombinant techniques. Increased use of pharmacologic agents such as desmopressin acetate for patients with mild hemophilia A or type 1 von Willebrand's disease has allowed physicians to treat patients without the risk of infectious complications from plasma-derived factor concentrates. In addition to the management of the inherited bleeding disorders, patients may also require management of human immunodeficiency virus infection, hepatitis, and coagulation factor inhibitors. Issues for the coming years will include continued work to ensure product safety, the role of prophylactic treatment to prevent longterm disabilities, and the application of gene therapy to the management of bleeding disorders.
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PMID:Treatment of inherited coagulation disorders. 887 17

Amodiaquine, a 4-aminoquinoline antimalarial, has been associated with hepatitis and agranulocytosis in humans. Drug hypersensitivity reactions, especially agranulocytosis, have been attributed to reactive intermediates generated by the oxidants discharged from stimulated polymorphonuclear leucocytes (PMN). The metabolism of amodiaquine to both stable and chemically reactive metabolites by human PMN has been investigated in vitro. Incubation of [14C]-amodiaquine with PMN resulted in irreversible binding of radiolabel to protein and depletion of intracellular reduced glutathione, which were enhanced by phorbol myristate acetate (PMA), a PMN activator. Two metabolites were identified: the C-5' glutathione adduct of amodiaquine, derived from both endogenous and exogenous glutathione, and 4-amino-7-chloroquinoline, which was presumed to be formed by hydrolysis of amodiaquine quinoneimine. Desethylamodiaquine, the major plasma metabolite of amodiaquine in humans, also underwent bioactivation to a chemically reactive species in the presence of PMA-stimulated PMN. Substitution of the 4'-hydroxyl group in amodiaquine with fluorine significantly reduced irreversible binding to protein and abolished depletion of intracellular glutathione in the presence of PMA. These findings indicate that the bioactivation of amodiaquine by PMN is associated with the formation of a quinoneimine intermediate. Such a reactive metabolite, if produced in PMN or bone marrow in vivo, may be responsible for the drug's myelotoxicity.
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PMID:The bioactivation of amodiaquine by human polymorphonuclear leucocytes in vitro: chemical mechanisms and the effects of fluorine substitution. 757 70

Obstetricians and Gynecologists care for many patients with conditions potentially requiring blood transfusions. Cesarean section and hysterectomy are the two surgeries performed most frequently and both have the potential for blood loss requiring transfusion. Other examples include postpartum hemorrhage, placenta previa, and ruptured ectopic pregnancy. Obstetricians and gynecologists need to become knowledgeable about the ever-changing aspects of blood transfusion and apply it in their clinical practice. This review intends to update obstetricians and gynecologists and other health care professionals about the basic as well as the latest technologies of blood transfusion. The different types of blood components are discussed including their preparation, indications, risks, and benefits. The complications of blood transfusion and their management are reviewed, including infections, noninfectious, and immunological etiologies. HIV and hepatitis are explored, these being the most serious infectious risks of transfusion. Autologous blood transfusion, an underutilized option, is examined. Hemodilution and intraoperative blood salvage, other techniques for using the patient's own blood, are discussed. Finally, synthetic agents such as erythropoietin, granulocyte colony-stimulating factors, factors, desmopressin acetate, gonadotropin-releasing hormone agonists, and new products are introduced as potential replacements to blood transfusion in the future.
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PMID:Transfusion medicine in obstetrics and gynecology. 765 95

The survival rate for acute hepatic failure induced by Propionibacterium acnes and lipopolysaccharide (LPS) was increased when a hot water extract from the flowers of Inula britannica L. subsp. japonica Kitam. was injected into the experimental hepatitis mice, and anti-hepatitis substances could be extracted with CHCl3. The CHCl3 extract from I.britannica was fractionated and anti-hepatitis fractions IB-3-2 and IB-3-3 were obtained. IB-3-3 had the most potent anti-hepatitis activity among the fractions but further purification of the active compound was not achieved because of the low yield. IB-3-2 contained only one substance which was identified to be taraxasteryl acetate by 1H- and 13C-NMR and MS. Taraxasteryl acetate showed potent preventive activity against acute hepatic failure induced by P.acnes and LPS in a dose-dependent manner, however deacetylation and modification of the olefinic bonds significantly decreased the anti-hepatitis activity of taraxasteryl acetate. Taraxasteryl acetate also inhibited the increment of plasma transaminase on acute hepatic failure induced by carbon tetrachloride (CCl4) or D-galactosamine. From a histological study it appeared that degeneration and necrosis, which were observed in the liver from CCl4 mice, were not found in the liver cells from taraxasteryl acetate treated mice. These results indicates that taraxasteryl acetate shows preventive effects on experimental hepatitis caused by either immunologically induced injuries or hepatotoxic chemicals.
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PMID:Preventive effect of taraxasteryl acetate from Inula britannica subsp. japonica on experimental hepatitis in vivo. 1725 90

The induction of macrophage procoagulant activity (PCA) has been shown to correlate with the development of fulminant hepatic necrosis after infection with murine hepatitis virus strain 3 (MHV-3). However, comparatively little is known about the early events in cells after viral infection leading to PCA expression. Accordingly, we investigated the early cellular events in the induction of macrophage PCA by MHV-3. MHV-3 stimulation of macrophages did not result in a detectable increase in intracellular calcium levels nor did stimulation of macrophages by calcium ionophores result in induction of PCA, suggesting that calcium transients were neither necessary nor sufficient for induction of PCA by MHV-3. Treatment of cells with phorbol myristate acetate had no effect on PCA induction; however, inhibition of protein kinase C (PKC) by staurosporine or H7 resulted in attenuation of macrophage PCA following MHV-3 stimulation (P < 0.05 compared with untreated macrophages), suggesting that although activation of PKC alone is insufficient for PCA induction, PKC may be an integral component of PCA induction by MHV-3. We have previously demonstrated that dimethyl prostaglandin E2 inhibited induction of PCA by MHV-3. In this study, treatment of cells by agents that increase intracellular cAMP (forskolin, isobutylmethyl xanthine) significantly inhibited PCA induction (P < 0.02). These results demonstrate that induction of macrophage PCA by MHV-3 involves PKC, but proceeds independently of changes in intracellular calcium, and that PCA expression is down-regulated by increases in intracellular cAMP.
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PMID:Effect of alterations in early signal transduction events on the induction of procoagulant activity by murine hepatitis virus strain 3 in vitro. 773 Aug 2

We investigated the effect of inflammatory cytokines on the intercellular adhesion molecule-1 expression on primary cultured murine hepatocytes. Tumor necrosis factor-alpha, interferon-gamma and interleukin-1 alpha up-regulated the intercellular adhesion molecule-1 expression on hepatocytes in a dose-dependent fashion; however, interleukin-6 did not. On the basis of kinetic analysis, the expression level reached a peak 24 hr after stimulation, and both cycloheximide and actinomycin D inhibited the expression. Furthermore, T lymphocytes bind more to interferon-gamma-stimulated hepatocytes than to unstimulated hepatocytes. The binding was dependent on the concentration of interferon-gamma. The binding was also up-regulated by stimulating T lymphocytes with phorbol myristate acetate. Tumor necrosis factor-alpha and interleukin-1 alpha demonstrated the same effect as interferon-gamma, whereas interleukin-6 did not increase T-lymphocyte adhesion to the hepatocytes. The adhesion induced by interferon-gamma or tumor necrosis factor-alpha was inhibited by antibody against either intercellular adhesion molecule-1 or lymphocyte function-associated antigen-1, a ligand for intercellular adhesion molecule-1, but was not inhibited by CD44 antibodies. These results demonstrate that inflammatory lymphokines enhance the T-lymphocyte adhesion to primary cultured hepatocytes by up-regulating the intercellular adhesion molecule-1 expression on the stimulated hepatocytes by activating the de novo pathway. This mechanism may play an important role in the pathogenesis of hepatitis.
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PMID:Inflammatory cytokines up-regulate intercellular adhesion molecule-1 expression on primary cultured mouse hepatocytes and T-lymphocyte adhesion. 790 80

Endometriosis is a disease observed in women in fertile age, it causes pelvic pain characterized by dysmenorrea and dyspareunia. Moreover, there is an association with infertility. Between the alternative of the medical therapeutics of endometriosis drugs with hipogonadotrofic and hypoestrogenic effects, as the danazol and gestrinona has been used. At present, there are analogies of GnRH factor where leuprolide acetate allow a continue liberation in a monthly administration. This is a case of a woman with extensive endometriosis that has hepatitis due to danazol and subsequently was treated with leuprolide acetate. The effectiveness of leuprolide acetate is analyzed in relation with the relief of pain and the laparoscopic evaluation of the endometriosis focus.
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PMID:[Advanced endometriosis treatment with leuprolide acetate]. 799 63

Elevation of the serum angiotensin-converting enzyme (sACE) level and hepatic granulomas were found during a clinical relapse in a 22 year old patient with acute viral hepatitis type A (AVH-A). The serum transaminase level and sACE level remained high for more than 6 months. In the biopsied specimen of the liver, fibrous rings of granulomas composed of collagen types I, III, and V were observed. Furthermore, the localization of ACE was visible in the rough endoplasmic reticulum of epithelioid cells of granulomas in the liver under electron microscopy using the indirect immunoperoxidase method. These results suggest that granuloma cells in the liver caused by hepatitis A may be involved in ACE production. In addition, other diseases associated with the presence of granulomas in the liver, such as lymphoma, cytomegalovirus infection, visceral leishmaniasis, and lupoid hepatitis, were ruled out. However, the hepatic granulomas disappeared with the healing of AVH-A. In this regard, the present case is considered to be one of the very few cases of hepatic sarcoidosis.
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PMID:A patient with hepatic granuloma formation and angiotensin-converting enzyme production by granuloma cells during clinical relapse of hepatitis A. 804 9


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