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)

An overview of dermatological diseases which occur in conjunction with oral contraceptive (o.c.) use is presented. An increase in pigmentation during o.c. use is attributed to an increase in the binding of cortisol with transcortin caused by the estrogen component, which leads to an increase in melanin-stimulating hormone production. Sebum production is decreased during o.c. use, which has a beneficial effect in cases of acne and seborrhea oleosa. This effect is most pronounced with preparations containing chlormadinon acetate, which has an antiandrogenic effect. O.C. use can influence hair growth by disturbing the balance between anagenic and telogenic hairs. Androgenetic alopecia is most often caused by preparations containing nortestosterone. Peroral dermatitits, lupus erythmatodes visceralis and similar disorders, and allergic skin reactions have been observed among o.c. users. Porphyria cutanea tarda is generally found in young women in conjunction with o.c. use, which can be related to liver dysfunctions. Vaginal candidosis is also more frequently found among o.c. users, particularly in conjunction with combination preparations. Herpes gestationes can occur during o.c. use, mainly among women who developed it during pregnancy. Progesterone appears to be responsible for provoking the condition. 166 patients who developed dermatological disorders during o.c. use were studied according to the preparation each used. Acne vulgaris improved more frequently among Ovosiston users. A marked increase in vaginal fluor indicated an increase in trichomoniasis and candida mycosis. In all observed cases of porphyria cutanea tarda, liver damage (hepatitis, cyrrhosis, or fatty liver) could be ascertained.
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PMID:[Reactions and side effects of ovulation inhibitors on the skin]. 72 69

Ammonia toxicity and the protective effect of arginine thereon were investigated in rats after single and repeated doses of galactosamine. Urea cycle enzymes and ornithine-oxo-acid transaminase activities were measured in rat liver homogenates. Ammonium acetate proved to be less toxic in rats treated with single or repeated doses of galactosamine than in untreated animals. Urea cycle enzyme activities of galactosamine-treated rats were clearly lowered. The protective effect of arginine against lethal ammonia intoxication was found in animals that had been treated with galactosamine as well as in untreated rats. Since the toxicity of ammonium acetate is lower in rats with galactosamine hepatitis, in which the activities of the liver urea cycle enzymes are reduced, it seems likely that ammonia detoxication in galactosamine-poisoned rat liver partly bypasses the urea cycle.
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PMID:[Toxicity of ammonium acetate in rats with acute and subacute galactosamine-induced hepatitis (author's transl)]. 76 43

Adult human liver biopsies were cultured from normal, alcoholic hepatitis, chronic active hepatitis, fibrosis plus alcoholic hepatitis (active cirrhosis), inactive cirrhosis, and drug hepatitis. The synthesis of collagen was estimated in cultures from 58 livers by measuring the conversion of [(14)C]proline to the [(14)C]hydroxyproline of collagen; that of glycosaminoglycans in cultures from 57 livers by the incorporation of [(3)H]acetate and (35)SO(4) into glycosaminoglycans (GAG). The synthesis of procollagen was increased only in cultures from alcoholic hepatitis, both in the pulse medium (P < 0.05) and in the chase medium (P < 0.02). The synthesis of insoluble collagen was increased in cultures from chronic (active) hepatitis (P < 0.01), fibrosis plus alcoholic hepatitis (active cirrhosis) (P < 0.001), and inactive cirrhosis (P < 0.05). Essentially all radioactive GAG was soluble in culture media. The predominant GAG were chondroitin-4 or -6-SO(4). The synthesis of GAG was increased only in cultures from fibrosis plus alcoholic hepatitis (active cirrhosis) both in the pulse medium (P < 0.01) and chase medium (P < 0.001). The data indicate that in the absence of immuno-competent cells or their secretory products, tissue cultures from livers showing biopsy evidence of active fibrosis in vivo may demonstrate increased synthesis of collagen and GAG in vitro. Increased (soluble) procollagen synthesis in cultures from alcoholic hepatitis was not associated with histologically demonstrable overt hepatic fibrosis in vivo, nor was it associated with increased GAG synthesis in vitro. No significant difference was demonstrable in collagen or GAG synthesis in paired cultures which contained either 300 mg/dl ethanol or 3.75 mg/dl methylprednisolone compared to their respective controls.
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PMID:The rate of synthesis of glycosaminoglycans and collagen by fibroblasts cultured from adult human liver biopsies. 87 75

Hepatic insufficiency is generally caused by active liver cirrhosis with portal hypertension. The final stage is the exogenous hepatic coma. Much rarer is the endogenous hepatic coma caused by fulminant acute hepatitis or severe intoxications. In the treatment of hepatic insufficiency it is first necessary to eliminate all exacerbating factors such as too high protein-intake, gastrointestinal bleedings, abuse of alcohol and diuretics. Because hepatic encephalopathy is mainly produced by toxic intestinal protein metabolites no protein should be adminstered at the beginining of the disease. The production of toxic protein metabolites in the gut can be diminished as well by enemas with sodium acetate buffer (pH 4, 5) as by neomycin (6-8 gm daily). Because long-term treatment with neomycin reduces also the physiological intestinal bacteria combination with lactulose (70-100 gm daily) is better. Treatment with lactulose reduces not only significantly hyperammoniemia but also increases serum phenols. The same effect have so-called ammonia reducing amino acids such as arginine, ornithine and glutamic acid. In endogenous hepatic coma blood exchange transfusions, liver perfusions and charcoal perfusions are necessary. Nevertheless, the prognosis of hepatic insufficiency caused by fulminant hepatitis is very poor in the final stage of the disease. Therefore early diagnosis and treatment in special departments with intensive care is necessary.
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PMID:[Therapy of hepatic insufficiency]. 91 52

Glycylprolyl beta-naphthylamidase activities in sera from 40 normal subjects (18-81 years) were: 22.6 +/- 0.9 (S.E.) (11.8-38.2) I.U./1 serum at 37 degrees C. The enzyme activities did not differ significantly with age between the younger group under 40-years-old and the older group over 40-years-old. Males, especially under 40-years-old, had slight but significantly higher activities than females. The levels were decreased in patients with gastric cancer. The levels were elevated in patients with hepatobiliary diseases, and had significant correlations with the results of the serum tests in hepatic diseases such as glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, alkaline phosphatase and total bilirubin, but had no correlation with serum lactate dehydrogenase. In cellulose acetate electrophoresis, normal sera had a single peak at the beta-globulin region, but the sera in hepatitis or liver cirrhosis showed not only an increase in the normal peak at the beta-globulin region but also the appearance of the other one or two new peaks in the alpha1 and alpha2-globulin regions.
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PMID:Glycylprolyl beta-naphthylamidase activity in human serum. 114 81

Zinc acetate was used for the treatment and prophylaxis of hepatic copper toxicosis in 3 Bedlington Terriers and 3 West Highland White Terriers. Two dogs of each breed were treated for 2 years, and 1 of each breed for 1 year. A dosage of 200 mg of elemental zinc per day was required to achieve therapeutic objectives related to copper, which included a doubling of plasma zinc concentration to 200 micrograms/dl and a suppression of oral 64 copper absorption. The dosage was later reduced to 50 to 100 mg/day to avoid an excessive increase in plasma zinc concentration. The preliminary clinical results were good. Three dogs had mild to moderate active liver disease and high liver copper concentrations at the time of initiation of zinc administration. Biopsy of the liver 2 years later revealed a reduction in hepatitis and copper concentrations. One other dog without active hepatitis also had a reduction in hepatic copper concentrations over a 2-year period. All 6 dogs have done well clinically. On the basis of these findings, we believe zinc acetate to be an effective and nontoxic treatment for copper toxicosis in dogs.
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PMID:Use of zinc acetate to treat copper toxicosis in dogs. 151 30

Circular RNA replicons have been reported in plants and, in one case, in animal cells. We describe such an element in yeast. In certain yeast strains, a 20S RNA species appears on transfer of cells to acetate medium. This phenotype shows cytoplasmic (non-Mendelian) inheritance and the 20S RNA is associated with 23-kDa protein subunits as a 32S particle. We demonstrate that yeast 20S RNA is an independent replicon with no homology to host genomic, mitochondrial, or 2-microns plasmid DNA or to the L-A, L-BC, or M1 double-stranded RNA viruses of yeast. The circularity of the 20S RNA is shown by the apparent absence of 3' and 5' ends, by two-dimensional gel electrophoresis, and by electron microscopy. Replication of yeast 20S RNA proceeds through an RNA-RNA pathway, and a 10,000-fold amplification occurs on shift to acetate medium. The copy number of 20S RNA is also reduced severalfold by the SKI gene products, a host antiviral system that also lowers the copy numbers of yeast double-stranded RNA viruses. Yeast 20S RNA and the hepatitis delta virus show some similarities.
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PMID:Circular single-stranded RNA replicon in Saccharomyces cerevisiae. 169 30

Regarding a case of little-differentiated adenocarcinoma of prostate in a 79-year old male patient undergoing antiandrogenic corticosteroid therapy (cyproterone acetate), the authors describe a rare complication related to treatment with the drug. Cytolytic icterus, without cholestasis, occurred eleven weeks after starting the treatment without metastasis of the primary cancerous lesion, and regressed when administration of the antiandrogenic agent was interrupted. This description is compatible with toxic hepatitis. This is a rare complication, which should be differentiated from stasis icterus consecutive to treatment with progestogens. Its diagnosis precludes also primary or drug-induced secondary tumors or degenerative hepatic lesions. A knowledge of this complication by the urologist is important, so the latter might not conclude too hastily to metastatic extension of primary cancer of prostate. Withdrawal of the patient from antiandrogenic therapy is mandatory, and management should incorporate complete biological investigation of liver function, CT scans and, depending upon the case, liver biopsy as the only means of studying this exceptionally rare complication.
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PMID:[Hepatitis after treatment with cyproterone acetate. Apropos of a case]. 214 71

The duration of mouse hepatitis virus (MHV) infection was examined in mice inoculated intranasally with selected strains of MHV. Following inoculation with virulent MHV-JHM, genetically susceptible BALB/c mice and resistant CD1 mice had detectable virus in the brain at 1 month, but not later intervals up to 12 months. BALB/c mice infected with avirulent MHV-S or MHV-1 had no detectable virus in brains at 1 month or thereafter. Immunosuppression of BALB/c mice with treatment regimens of hydrocortisone acetate or cyclophosphamide at 1 and 2 months after infection with MHV-JHM did not activate detectable virus in liver or increase the prevalence or degree of brain infection. Immunosuppression with these drugs during the acute phase of MHV-JHM infection influenced MHV infection, based on virus quantification in livers, but timing of drug treatment relative to MHV infection was critical. Mice infected with MHV developed IgG serum antibody titers that persisted without decline for up to 1 year after infection. Antibody titers varied with mouse genotype and infecting virus. These studies, using intranasal inoculation, support the conclusions of others, using other routes of inoculation, that MHV infection is not persistent in adult, immunocompetent mice.
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PMID:Duration of mouse hepatitis virus infection: studies in immunocompetent and chemically immunosuppressed mice. 215 90

Intravenous administration of soybean phosphatidylcholine liposomes containing different amounts of tocopherol acetate leads to a dose and time dependent increase of mouse liver tocopherol content, which was not observed when the preparation was given orally. When benzo[a]pyrene pretreated mice intoxicated with 400 mg/kg AAP were pretreated 2 h before with 1 g/kg phosphatidylcholine liposomes containing 4 mg/kg vitamin E acetate, these animals were protected against liver damage. Vitamin E alone or liposomes lacking vitamin E showed no protection. In an inflammatory liver disease model, i.e. fulminant hepatitis induced by intraperitoneal administration of 700 mg/kg galactosamine and 1 microgram/kg lipopolysaccharide phosphatidylcholine liposomes protected at a dose of 1 g/kg i.v. In this case, however, the protection was not due to the presence of vitamin E. These findings demonstrate the usefulness of phosphatidylcholine for liver protection and show that the protective spectrum is improved when they contain vitamin E. The data suggest that phosphatidylcholine is an excellent carrier for delivery of vitamin E to the liver.
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PMID:Hepatic uptake and antihepatotoxic properties of vitamin E and liposomes in the mouse. 236 59


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