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 presence of antibodies toward hepatitis C virus (HCV) was examined in 78 polytransfused beta-thalassaemic children. The anti-HCV status was correlated with acute and chronic non-A non-B (NANB) hepatitis that developed during a follow up of about 13 years. Anti-HCV was present in 83.3% of children with acute NANB hepatitis and in 82.9% of those with chronic NANB hepatitis. The percentage of chronic evolution was 56.7% for acute anti-HCV positive NANB hepatitis and 50.0% for anti-HCV negative NANB hepatitis. The long-term persistence of anti-HCV antibodies did not correlate with chronic evolution of liver infection in thalassaemic patients. Histological features of chronic hepatitis showed little or no difference between HCV associated or non-associated liver disease. The multifactorial liver injury in beta-thalassaemic children explains the high prevalence of cirrhosis (about 30%) observed in these patients with NANB hepatitis. On the other hand, independent of liver disease, some patients never seroconverted during the follow up in spite of the high number of transfusions suggesting the existence of "non-responders".
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PMID:Hepatitis C virus antibodies in a long-term follow-up of beta-thalassaemic children with acute and chronic non-A non-B hepatitis. 768 47

A gene region encoding a segment of the major surface protein, HBsAg, of hepatitis B virus was analyzed from serum samples after orthotopic liver transplantation of three hepatitis B virus chronic carrier patients treated with a human anti-hepatitis B virus monoclonal antibody (SDZ OST 577). Each of these three patients became HBsAg negative after transplantation and therapy with the human anti-hepatitis B virus monoclonal antibody but returned to HBsAg positivity (first detected 143,251 and 252 days after the transplantation). Polymerase chain reaction DNA amplification was performed on DNA from serum samples showing low levels of recurrent HBsAg and reduced antigen reactivity with SDZ OST 577 antibody. Polymerase chain reaction DNA included a 230-bp highly conserved, major S gene region that was cloned into M13 bacteriophage; analysis of this DNA segment provided a consensus of DNA sequences for the serum samples exhibiting altered reactivity with the therapeutic monoclonal. Analysis of independent DNA clones from serum samples of patients exhibiting low but detectable recurrent serum levels of posttherapy HBsAg revealed the presence of S protein variant sequences when compared with polymerase chain reaction DNA derived from the original infected liver or pretherapy serum HBsAg. Genetic variation was predominant in a highly conserved peptide domain that has previously been implicated in antibody binding and neutralizing antibody epitopes. In independent patients infected with either adw or ayw hepatitis B virus subtypes, single nucleotide changes resulted in one to two amino acid differences for each variant allele (residues 124, 129, 131, 137, 140 and/or 145) when compared with pretherapy viral DNA. Administration of serum containing one of these variant viruses to a single hepatitis B-naive chimpanzee resulted in subclinical hepatitis and detectable levels of circulating anti-HBs and anti-HBc antibodies 49 and 70 days after virus administration, respectively. Hepatitis B virus DNA was recovered on liver biopsy between 6 and 8 wk after inoculation, although the animal remained persistently seronegative for HBsAg. DNA sequence analysis of both primate and patient liver hepatitis B virus confirmed the presence of the DNA encoding the S protein variant and associates this DNA with the predominant hepatotropic virus in liver infection.
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PMID:Genetic alterations in the gene encoding the major HBsAg: DNA and immunological analysis of recurrent HBsAg derived from monoclonal antibody-treated liver transplant patients. 156 15

During the period 1974-1983, Yersinia enterocolitica infection was diagnosed in 458 hospitalized patients by antibody response or isolation of the micro-organism. A total of 54 (11.9%) patients had acute liver infection, with significantly elevated serum levels (greater than or equal to 2-fold) of bilirubin and/or enzyme levels. Serious liver disease with cellular necrosis was observed in biopsy specimens from two of 12 patients examined; six had unspecific changes. The patients were followed up for 4-14 years (until 1987). A total of 22 (4.9%) patients were readmitted with chronic liver disease; in one case non-specific microscopic changes developed into granulomatous hepatitis over a period of 3 years. In both the acute and chronic stages of disease, liver involvement was associated with involvement of other organ systems, and some patients developed multi-organ disease. Chronic liver disease was associated with positive tests for antinuclear antibody and rheumatoid factor, and with a high mortality.
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PMID:Acute and chronic liver disease associated with Yersinia enterocolitica infection: a Norwegian 10-year follow-up study of 458 hospitalized patients. 160 89

The abuse by injection of heroin or other drugs has long been associated with liver disease caused by hepatitis B virus (HBV) and other viruses. Increasingly severe hepatic and virological complications of parenteral drug abuse have been reported due to infection with new viruses or concomitant alcohol abuse. The hepatitis delta virus (HDV) can replicate and cause liver infection only in the presence of HBV; such infection in HBV carriers may cause rapidly progressive and clinically significant liver disease. Liver cirrhosis is frequently detected in parenteral drug abusers who have chronic infection with both HBV and HDV or who also abuse alcohol. More than one quarter of those persons with acquired immunodeficiency syndrome (AIDS) in the United States of America are homosexual or heterosexual males who are parenteral drug abusers. Existing evidence implicates parenteral drug abusers in the spread of hepatitis viruses and the retrovirus associated with AIDS to the general population. To cope with these serious problems the authors suggest that more intensive international co-operation is needed, particularly with a view to promoting data collection, research and the exchange of knowledge and experience on measures that have been effective in dealing with parenteral drug abuse and its complications.
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PMID:Acquired immunodeficiency syndrome and infection with hepatitis viruses in individuals abusing drugs by injection. 377 78

A case of granulomatous hepatitis induced by cytomegalovirus in a 34-year-old immunocompetent male with no other history of interest is presented. The clinical severity of the picture with progressive cholestasis, evening fever peaks and the development of echographic signs of portal hypertension led to treatment with high doses of intravenous ganciclovir. Rapid clinical improvement was observed with normalization of the analytical parameters after 15 days of treatment. The pathologic, clinical and therapeutic aspects of the liver infection by cytomegalovirus in an immunocompetent patient are discussed.
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PMID:[Cytomegalovirus granulomatous hepatitis in an immunocompetent patient]. 1039 4

To evaluate the occurrence of hepatotoxicity in patients during antiretroviral therapy (ART) that contains protease inhibitors and the role of hepatitis viruses in its development, we performed a retrospective study including 1325 HIV-infected patients treated with ART for at least 6 months. Presence or absence of hepatitis viruses, alanine aminotransferase (ALT), total bilirubin, CD4 cell count, and plasma HIV RNA levels were evaluated. Hepatotoxicity developed in a few study subjects without coinfection, whereas it was significantly higher in coinfected patients. Univariate logistic regression analysis showed that viral hepatitis coinfections are independent risk factors for hepatotoxicity. After 6 months of treatment, ritonavir was associated with higher rates of severe hepatotoxicity in the coinfected group; in fact, ritonavir seems to be the most strongly hepatotoxic agent among coinfected patients. After 12 months of therapy, hepatotoxicity occurred more frequently in patients with hepatitis C virus who did not respond to antiretroviral therapy (ART), whereas patients who did respond to ART showed decreased ALT levels. Hepatotoxicity is not exclusively an effect of drug toxicity, and the presence of hepatitis coinfection is an independent risk factor. Moreover, chronic hepatotoxicity mainly occurs in patients who did not respond to therapy. Conversely, patients who did respond to ART seemed to show improvement of chronic liver infection.
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PMID:Hepatotoxicity development during antiretroviral therapy containing protease inhibitors in patients with HIV: the role of hepatitis B and C virus infection. 1178 88

This study aimed at identifying the prevalence of hepatitis A virus (HAV) infection in children with biliary atresia (BA). Blood samples were collected from children with BA whom had undergone portoenterostomy and attended the pediatric liver clinic, King Chulalongkorn Memorial Hospital between May 2002 and May 2003. Seventy-seven patients, 45 females and 32 males, ages ranging from 0.2-19 years (mean +/- SD = 5.9 +/- 4.6 years) were enrolled in the study. The HAV seropositivity rate of patients aged <10 years and > or =10 years were 13.1% and 25%, respectively. The seropositivity rate of patients with favorable outcomes (total bilirubin level < or =2 mg/dl) and unfavorable outcome (total bilirubin level >2 mg/dl) were 17.5% and 13.5%, respectively, which were not statistically different (p = 0.6). Children suffering from BA with failed portoenterostomy are at risk of developing severe liver damage at an early age. In these patients a superimposed acute liver infection due to a hepatitis virus, including HAV, may affect liver function and lead to particularly severe disease. The effectiveness of HAV immunization in this particular group of children merits further study.
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PMID:Prevalence of hepatitis A virus infection in children with biliary atresia. 1591 98

Yellow fever (YF) is a life-threatening mosquito-borne flaviviral hemorrhagic fever (VHF) characterized by severe hepatitis, renal failure, hemorrhage, and rapid terminal events with shock and multi-organ failure. A live, attenuated vaccine (YF 17D), in wide use for over 60 years, causes a disease identical to wild-type virus at an incidence of 2.5x10(-6). Our current understanding of the pathogenesis and treatment of YF (described in this brief review) is derived from studies of animal models (macaques, hamsters) that reproduce the features of human YF and from descriptive studies of human cases of naturally acquired and vaccine-associated VHF. The least understood, but potentially most important terminal events appear to be due to 'cytokine storm' and represent a potential target for therapeutic interventions. Areas for future study include dissection of cytokine-mediated events in animal models, the pathogenic role of the profound neutrophilia that occurs pre-terminally, the (pathological) role of adaptive immune clearance in pathogenesis, and treatments directed at cytokine storm. Antibody, interferon-alpha, polyICLC and other immune modulators are highly effective when administered before or within a narrow time window after infection, but are ineffective when given after the infection is established. A few antivirals have been evaluated (ribavirin, tiazofurin, carboxamide, pyrazoline compounds). Ribavirin has been used successfully to treat hamsters when the drug is given at high doses up to 2 days after virus infection (shortly before liver infection), but has not shown promise in nonhuman primate models. Future work should focus on evaluating higher doses of ribavirin alone or in combinations with potentially synergistic drugs, including interferons. Also specific inhibitors against other flaviviruses such as dengue virus should be investigated for potential pan-flavivirus activity since recent studies have shown that specific targets such as the flavivirus proteases and helicases are very similar in structure.
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PMID:Treatment of yellow fever. 1806 88

The causes of death from intranasal cowpox virus infections in mice remain unclear. Hypotheses include severe pneumonitis, hepatitis and/or hyperproduction of cytokines and chemokines. This work explores these hypotheses by studying the influence of low- and high-volume virus inocula on viral pathogenesis. BALB/c mice were infected intranasally with a syncytium-forming variant of cowpox virus in 5 microL or 50 microL volumes containing the same infectious virus challenge dose. The 50 microL infection produced a more rapidly lethal disease associated with severe pneumonitis, high lung and nasal virus titres and increased cytokine and chemokine levels in the lungs and nasal tissue, whilst liver infection was minimal. The 5 microL inoculum infection was also lethal, but the infection was primarily confined to the upper respiratory tract and included elevated nasal cytokine and chemokine levels. Levels of the pro-inflammatory cytokine interleukin-6 were particularly high in both infections. Treatment of the infections with cidofovir (100mg/kg/day for 2 days starting 24h after virus exposure) led to survival and suppression of tissue virus titres. Treatment reduced pneumonitis in the 50 microL infection and lessened cytokine hyperproduction in both infections. We conclude that a 5 microL volume inoculum of cowpox virus causes a lethal upper respiratory tract infection, whilst the 50 microL inoculum targets both upper and lower respiratory tracts, with excessive release of systemic pro-inflammatory factors. Cidofovir effectively treated both infections and slowed viral replication sufficiently to subdue the exaggerated release of pro-inflammatory mediators.
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PMID:Differential pathogenesis of cowpox virus intranasal infections in mice induced by low and high inoculum volumes and effects of cidofovir treatment. 1820 53

The NF-kappaB signaling pathway has particular relevance to several liver diseases including hepatitis (liver infection by Helicobacter, viral hepatitis induced by HBV and HCV), liver fibrosis and cirrhosis and hepatocellular carcinoma. Furthermore, the NF-kappaB signaling pathway is a potential target for development of hepatoprotective agents. Several types of drugs including: selective estrogen receptor modulators (SERMs), antioxidants, proteasome inhibitors, IKK inhibitors and nucleic acid-based decoys have been shown to interfere with NF-kappaB activity at different levels and may be useful for the treatment of liver diseases. However, NF-kappaB also plays an important hepatoprotective function that needs to be taken into consideration during development of new therapeutic regimens.
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PMID:NF-kappaB signaling, liver disease and hepatoprotective agents. 1893 90


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