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)

Delta hepatitis is a defective virus dependent on hepatitis B virus for replication and transmission. Delta hepatitis infection is becoming more prevalent in the United States, especially in parenteral drug abusers; several outbreaks have occurred. Infection control procedures and the hepatitis B vaccine can protect the dental staff from infection and transmission.
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PMID:Delta hepatitis: another concern for dentistry. 345 94

Chronic evolution after acute hepatitis B virus infection. During a 13 months period 1977-1978 a total of 129 cases of acute viral hepatitis type B occurred among patients who were admitted with hepatitis to Roslagstull, Hospital, Stockholm, Sweden. Less than 1% progressed to chronicity. Prevalence of Delta superinfection was studied among 60 patients with chronic hepatitis B. Nineteen (32%) were anti-delta positive. The majority of the positive patients were either non-European immigrants or addicts, both 9/19 (47%). Infections with the delta agent was found to have occurred in Stockholm already in the early 1970s. Rate of HBeAg clearance during chronic HBV was studied among 36 HBeAg positive patients. Seroconversion to anti-HBe was noted in 17 patients (47%), whereas HBeAg persisted in 19 during a mean follow-up period of 53 months. The spontaneous annual HBeAg seroconversion rate was 11%. HBeAg clearance occurred as frequently among homosexual men as among patients in other categories. However, 12/14 homosexual men were HBeAg positive after 2 years follow-up, compared with 1/13 drug addicts. Thus, homosexual men seemed to require a longer time for HBeAg seroconversion than i.v. drug addicts. HBV-DNA in serum, a strong indicator of viral particles and infectivity was analysed among patients with HBeAg seroconversion, initial HBeAg negativity and/or delta superinfection. HBV-DNA was found in 75-80% of our HBeAg positive patients. A correlation between chronic liver disease and presence of HBV-DNA in serum was also found. Thus, HBV DNA was found in 63% of patients with CAH or CAH/CI as compared with only 39% of patients with CPH. Delta infected patients had HBV-DNA more often than those without hepatitis D infection. Seven delta infected, anti-HBe positive, patients were still HBV-DNA positive five to eight years later. Therefore delta infected anti-HBe positive patients can be infectious for prolonged periods. Histological outcome. 63% (12/19) anti-delta positive patients were classified as CAH with or without cirrhosis as against 39% (16/41) of the anti-delta negative patients. Eleven of 15 homosexual men (73%) had histological findings classified as CAH or CAH/CI. None of them were superinfected with HDV. Thus homosexual men developed severe hepatic lesions without being delta infected. In contrast 78% (7/9) i.v. drug addicts with CAH were delta infected. A numerical scoring system was applied and compared with conventional morphological classification of liver histology to assess the histological outcome of 42 patients with repetitive liver biopsies.
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PMID:Chronic hepatitis B. Impact of hepatitis D virus superinfection and the hepatitis B e-system on histological outcome, and correlation of the hepatitis B e-system to HBV-DNA in serum. 346 8

Trimethoprim-sulfamethoxazole (co-trimoxazole) is used extensively for treatment of pulmonary and urinary tract infections. Side effects may affect skin, blood, bone marrow, kidney and the liver. Although a number of sulfonamides have been reported to have produced hepatic lesions, hepatitis following therapy with trimethoprim-sulfamethoxazole is a rather rare event. While trimethoprim has not yet been reported as a cause of hepatic disorders, sulfamethoxazole has occasionally been described as inducing hepatic injury. In some cases, these reactions are accompanied by symptoms indicative for allergic reactions such as fever, rash and eosinophilia. Seven well documented cases are analyzed and discussed with respect to the nature of side effects caused by co-trimoxazole.
Infection 1987
PMID:Co-trimoxazole-induced hepatic injury--an analysis of cases with hypersensitivity-like reactions. 350 74

The murine hepatitis virus, JHM strain, causes a relapsing subacute demyelinating encephalomyelitis in Lewis rats after intracranial infection. The disease process involves both virus persistence within glial cells and the induction of autoimmunological attack of myelin, however, the relative importance of these features involved in chronic relapsing demyelination remains to be determined. In this report, we analyze the tropism of JHM virus to various neural cell types present within primary Lewis rat central nervous system cultures. Infection of primary cultures with JHM virus revealed that type I astrocytes and brain macrophages are the initial target cells of infection and that the myelin-forming oligodendrocytes are comparatively resistant, becoming infected only rarely through virus mediated cell fusion with previously infected cells. In addition, infection of cultures after removal of oligodendrocytes by various means had no effect on the tropism of JHM virus for the cultures. Cytopathic effects of JHM virus proceed rapidly by cell fusion within the astrocyte-macrophage monolayer, leaving the oligodendrocyte population largely unaffected. Therefore, the highly selective infection of type I astrocytes and macrophages appears to form the basis of JHM virus neurotropism in Lewis rats. These results indicate that JHM virus infection of astrocytes and brain macrophages may be more important in inducing chronic relapsing demyelinating processes than direct infection of the myelin-forming oligodendrocytes. Other possible pathways leading to chronic demyelination in rats involving type I astrocytes and brain macrophages are discussed.
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PMID:Analysis of murine hepatitis virus (JHM strain) tropism toward Lewis rat glial cells in vitro. Type I astrocytes and brain macrophages (microglia) as primary glial cell targets. 352 62

Infection with the hepatitis Delta virus results in a reduction in hepatitis B virus replication. To study the question as to whether expression of large surface (pre-S1) protein is changed in patients with previous and chronic hepatitis Delta virus infection, sera of 25 HBsAg- and anti-HD-positive patients were analyzed by the Western blot technique using an antibody directed against a pre-S1 fusion protein. Pre-S1 proteins were present only in 3 of the 25 sera. This finding suggests that the expression of pre-S1 proteins and HBsAg is regulated independently, and that pre-S1 proteins are not necessarily required for the envelope of hepatitis Delta virus.
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PMID:Pre-S1 proteins in sera of patients positive for HBsAg and antibodies to hepatitis delta virus. 359 56

During a prospective study of acute symptomatic viral hepatitis, started in 1978, 664 consecutive adult patients, including 223 drug abusers, fulfilled the diagnostic criteria (anti-HBc IgM positivity) for acute type B hepatitis. In order to evaluate the outcome of the disease, 443 patients were followed for up to 12 months after the onset. 2.4% of the infections became chronic; the rate did not significantly differ between drug addicts and non-drug abusers, suggesting that chronic hepatitis is a rare complication of acute symptomatic hepatitis type B. Ongoing liver damage after clearance of HBsAg from serum was observed in drug abusers only (14% of the cases). Clinical, biochemical and virological features of the acute phase in patients with ongoing infection were compared with those of uncomplicated cases. Anicteric hepatitis and lower transaminase values were significantly (p less than 0.05) associated to a chronic evolution of the disease, as well as a higher prevalence of HBV-DNA, DNA polymerase and HBcAg positivity in serum. Testing HBV-DNA and DNA polymerase early in the course of the infection appeared to be of high predictive value for the subsequent outcome of the illness.
Infection
PMID:Chronic evolution of acute hepatitis type B: prevalence and predictive markers. 371 May 94

A previously well young woman presented with an acute hepatitis resembling viral hepatitis and a liver biopsy after 5 weeks showed features of acute hepatitis. Infection with identifiable viruses or other organisms known to cause hepatitis was excluded. Evidence for autoimmune chronic active hepatitis ab initio included prolonged fever, lymphadenopathy, urticaria, arthralgia, Coombs' positive hemolytic anemia, lymphopenia, a markedly raised level of immunoglobulin G and a positive antinuclear antibody test. Liver biopsies after 4 and 28 months showed typical histologic features of autoimmune chronic active hepatitis and the subsequent clinical course was typical, being marked by relapses and remissions responsive to prednisolone. Thus, described here is a woman in whom an acute onset of autoimmune chronic active hepatitis was clinically and histologically identified.
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PMID:'Acute' autoimmune hepatitis. 375 17

The hepatitis D virus (or delta agent) is a defective virus whose replication has an absolute requirement for the hepatitis B virus. Type D hepatitis occurs exclusively in patients simultaneously or previously infected by the hepatitis B virus, often intravenous drug abusers or male homosexuals. Infection by the hepatitis D virus is often responsible for an increase in the severity of the hepatic lesions due to the hepatitis B virus. It can result in fulminant hepatitis. The best prevention is vaccination against hepatitis B.
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PMID:[Hepatitis D]. 381 55

Beta-interferon was administered by intravenous infusion to 16 patients affected with fulminant hepatitis B virus infection in third or fourth-grade coma. Ten patients presented a superinfection or a co-infection due to the delta (delta)-agent. None had detectable interferon (IFN) activity before therapy was begun. Besides fever, no significant side-effects were observed during treatment. Both the IFN-treated group as well as the "historical" control group, made up of 70 cases of fulminant virus hepatitis, not treated with IFN and observed during a previous ten year-period, received supportive therapy; survival rates were similar in both groups. Furthermore, the presence or absence of the delta-agent did not appear to affect survival rates significantly.
Infection
PMID:Attempted treatment of fulminant viral hepatitis with human fibroblast interferon. 389 68

A new antifungal agent, ketoconazole, has been added to the drugs available for the treatment of fungal infections. Ketoconazole has been shown to be effective in the treatment of mucocutaneous candidiasis with a reported 97% positive response rate. This drug may be administered orally to outpatients with a low risk of toxicity. Hepatitis has been reported as a possible complication of treatment. Infection relapse is the most significant posttherapeutic problem. Five patients suffering from mucocutaneous candidiasis after irradiation therapy are reported to have had favorable responses. The other available antifungal agents are reviewed and discussed.
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PMID:Ketoconazole and the antifungals. 392 Jun 12


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