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)

Sera from 30 patients with community-acquired, biopsy-proven chronic non-a,non-B hepatitis (NANBH) were tested for antibodies to the C100 protein of hepatitis C virus (HCV). The 20 patients who showed reactivity in this assay were followed prospectively for 6 months, during which time seven were treated with recombinant alpha-interferon. HCV RNA was detected by "nested" polymerase chain reaction (PCR) in 19 of the 20 anti-C100-positive sera taken at the onset of the study and also in five of the ten anti-C100-negative sera. Pretreatment viraemia levels ranged from 2 x 10(3) to 2 x 10(8) HCV genomes/ml. After 6 months of interferon, elevated serum alanine aminotransferase (ALT) levels had fallen to normal in four of the seven treated patients. In each case the response to interferon was accompanied by either a disappearance of or a decline (1 log to 8 log reduction) in viraemia. HCV genome titres in the three nonresponders and in the 13 untreated anti-C100-positive patients did not change significantly over this 6 month period. These findings confirm the aetiological role of HCV in community-acquired NANBH and suggest that quantitative PCR will become a valuable technique for monitoring the antiviral effect of interferon and other experimental treatments.
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PMID:Effect of alpha-interferon therapy on hepatitis C viraemia in community-acquired chronic non-A, non-B hepatitis: a quantitative polymerase chain reaction study. 171 96

An acute or fulminant adenovirus hepatitis developed in 5 of 224 pediatric patients who were recipients of orthotopic liver transplants. All had received prednisolone, azathioprine, and cyclosporine as basal immunosuppression, and four received monoclonal (OKT3) or polyclonal (antithymocyte globulin) antibodies for steroid-resistant rejection episodes. These patients initially had high fever and a worsening condition for a mean of 73 days after transplantation (range 44 to 140 days). Results of biochemical tests showed very high serum levels of lactate dehydrogenase. Aspartate aminotransferase values were always markedly more elevated than those of alanine aminotransferase. Two patients had severe leukopenia. Results of histologic studies of the liver showed extensive areas of confluent necrosis and targetlike hepatocyte nuclei. Typical intranuclear viral inclusions were observed on electron microscopy. Adenovirus was cultured in all patients and in two relatives. Two patients died of liver failure; others recovered after cessation of immunosuppression. We conclude that adenovirus hepatitis can be fatal in liver transplant recipients. There is no specific treatment, and immunosuppression must be discontinued.
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PMID:Acute adenovirus hepatitis in liver transplant recipients. 173 Oct 21

Herpes simplex virus (HSV) hepatitis is rare in adults, usually occurring in immunocompromised individuals and in otherwise healthy women in the third trimester of pregnancy. Three cases of HSV hepatitis occurring in pregnant women were diagnosed at our institution between 1981 and 1990. This diagnosis was not suspected clinically, and in each case was made on the basis of histology, immunoperoxidase studies, and viral cultures of liver tissue. Clinically, the patients had severe anicteric liver failure with markedly elevated serum aspartate aminotransferase and alanine aminotransferase levels; two of the three patients died. None had mucocutaneous lesions at the time of diagnosis. Histologically, two distinct patterns of necrosis and inflammation were seen. Two of the cases had well-demarcated foci of necrosis scattered randomly throughout the lobules with neutrophilic infiltration, giving the impression of abscess formation. Hepatocytes at the periphery of these areas of necrosis had enlarged nuclei with "ground-glass" inclusions; however, no Cowdry type A inclusions were seen. Rare multinucleated cells were present. Immunoperoxidase staining using antibodies to HSV was positive primarily in the hepatocytes with inclusions. The third case had diffuse, almost total hepatic necrosis with no viral inclusions and virtually no inflammatory response. This histologic pattern is similar to that seen in neonates with HSV infection. Immunoperoxidase studies in this case were negative; however, viral cultures were positive. While HSV hepatitis may be suspected or diagnosed on the basis of histology alone, viral cultures are an important adjunct since viral inclusions may be absent. Prompt diagnosis is important since antiviral therapy is now available.
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PMID:Herpes simplex virus hepatitis in pregnancy: a clinicopathologic study of three cases. 174 Mar 3

Blood donor screening for hepatitis B core antibody and elevation of serum alanine aminotransferase level, surrogate markers of hepatitis C/non-A, non-B (NANB) infection, was implemented in 1986. Reported cases of posttransfusion hepatitis (PTH) from 1985 to 1988 were reviewed to ascertain the effect of surrogate testing on the number and character of cases and to compare any changes with those in the incidence of hepatitis in the general population. The reports of all PTH, NANB PTH, and type B PTH decreased 61.5%, 75.4%, and 84.5%, respectively. The rates of reported cases of NANB hepatitis and hepatitis B in the general community also fell during the period of review. The decrease in PTH and background hepatitis was similar between 1985 and 1986. In 1987, the first complete year of surrogate testing, the incidence of PTH decreased at a greater rate, to levels 50% below what would have been projected on the basis of background changes alone for NANB PTH, and to 35% below projected for type B PTH. There appears to have been a substantial decrease in the risk of both type B PTH and NANB PTH in the northeastern United States between 1985 and 1988 due to a combined effect of donor surrogate testing and a decrease in the background rates of hepatitis in the donor population.
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PMID:Decrease in reported posttransfusion hepatitis. Contributions of donor screening for alanine aminotransferase and antibodies to hepatitis B core antigen and changes in the general population. 174 1

The serum kinetics of preS1 and preS2 antigens has been evaluated in 38 serial samples from eight patients with chronic active (CAH) or chronic persistent (CPH) hepatitis, followed for 2-7 years (mean 4.4 years) in whom liver biopsy was performed at intervals, and in 46 samples from ten asymptomatic HBsAg carriers followed for 4-5 years (mean 4.6 years). Four patterns of preS behaviour have been observed: (1) persistently positive preS1 and preS2; (2) disappearance of preS2; (3) disappearance of both preS1 and preS2; and (4) persistently negative preS1 and preS2. Pattern 4 has been observed exclusively among healthy carriers, while seven out of eight chronic patients exhibited either pattern 1 or 2. Among the chronic patients, preS2 disappearance was accompanied or followed by alanine aminotransferase (ALT) normalization. The correlation of preS antigens with conventional viral replication markers showed that 100% of hepatitis B virus (HBV)-DNA-positive and 86.6% of HBeAg-positive sera were preS1/preS2 positive, while 61% of HBV-DNA-negative and 64% of HBeAg-negative sera were preS1/preS2 negative. Our data suggest that continuous monitoring of preS antigens in follow-up sera will allow for an improved prognostic evaluation of chronic HBV infection.
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PMID:Correlation of preS antigens and clinical status during chronic hepatitis B virus infection. 176 4

To investigate the role of neutrophils (PMNs) and PMN-dependent adhesion molecules in the pathogenesis of liver injury in a model of endotoxin shock, male ICR mice received a dose of 700 mg/kg galactosamine and 100 micrograms/kg Salmonella abortus equi endotoxin. PMNs accumulated continuously in the liver, reaching values of 446 +/- 71 PMNs/50 high-power fields at 9 h (basal value 18 +/- 7). Plasma alanine aminotransferase activities as index of parenchymal cell injury did not change up to 5 h posttreatment (basal value 35 +/- 5 U/l) but increased to 1,950 +/- 460 U/l at 9 h. The formation of glutathione disulfide (GSSG) in plasma as an index of an extracellular oxidant stress also increased only at 9 h. Pretreatment of animals with monoclonal antibodies against the CD11b and CD18 subunits of the CD11/CD18 integrin family on the surface of the PMN reduced the number of PMNs in the liver by 50% and significantly attenuated liver injury and GSSG formation. An anti-CD11a and a nonbinding control antibody were ineffective. It is concluded that PMNs are actively involved in the pathogenesis of galactosamine and endotoxin shock and that at least in part the accumulation of PMNs, the subsequent oxidant stress, and the tissue injury in this model of experimental hepatitis are CD11b/CD18 (Mac-1) dependent.
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PMID:Neutrophil-induced liver cell injury in endotoxin shock is a CD11b/CD18-dependent mechanism. 176 46

The risk of non-A, non-B hepatitis transmission by an intravenous immunoglobulin (IVIG) preparation was assessed in a prospective multicenter trial in 68 patients with primary immunodeficiency disorders (40 children or adolescents and 28 adults). During the 4-week prestudy evaluation period the clinical examinations and liver function tests including alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transpeptidase, alkaline phosphatase, and bilirubin were normal in all patients. The treatment consisted of three infusions of 200 mg IVIG (pH 4; pepsin procedure) per kilogram body weight at 2-week intervals. During the observation period of 24 weeks following the first infusion of the study IVIG, the patients were monitored at regular time intervals. No clinical and laboratory signs of hepatitis or liver dysfunction were noticed. All patients completed the study. In 5 patients, one isolated alanine aminotransferase value and in another patient one gamma-glutamyl transpeptidase value were moderately elevated, but always below 2.5 times the upper limit of the reference range. Similar isolated and transient elevations were observed for aspartate aminotransferase and alkaline phosphatase. It was concluded that the IVIG preparation did not transmit non-A, non-B hepatitis or other viral liver diseases.
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PMID:Safety of intravenous immunoglobulin preparations: a prospective multicenter study to exclude the risk of non-A, non-B hepatitis. 177 40

To assess the efficacy of therapy with alfa Interferon in chronic hepatitis C (NANB), 18 patients were enrolled in an open trial. Eleven were males and 7 females with a mean age of 43 years. Interferon alfa 2b was used in titrated doses for 9 months and the treatment was started with 5 m.U./Ti. During therapy, the patients were evaluated clinically and biochemically. A liver biopsy was done within 3 months after the completion of treatment. The serum alanine aminotransferase (ALT) level 1 became completely normal in 11 patients (61%) at 3 months of therapy and a partial response was seen in 3 (16%). At the 6 months the ALT sustained normal in 10 patients (55%) and a partial response was seen in 5 (27.7%). Four out of 7 patients (57%) who completed the therapy had complete response and 2 (28.5%) a partial response. From 5 patients who completed the follow-up, 3 (60%) had a relapse of ALT levels. A low level of ALT at the beginning of treatment had a predictive value of response to the therapy (P less than 0.05). The side effects of interferon therapy were usually mild. Fever, myalgias and headaches were seen in 72% of patients in the first two weeks of therapy. No haematological alterations were seen. We conclude that a 9 month course of interferon therapy is effective in controlling disease activity in many patients with chronic NANB hepatitis. However, the high relapse rate suggest that future studies should establish the optimal dose and duration of treatment to induce a complete resolution of the disease.
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PMID:[Therapy of chronic non-A, non-B hepatitis with recombinant interferon alfa and factors that influence the response to the treatment]. 180 97

Non-A, non-B hepatitis is a significant cause of liver disease among renal allograft recipients. In order to assess the impact and prevalence of hepatitis C in a series of renal allograft recipients, we retrospectively screened 621 consecutive patients transplanted between 1979 and 1989 and 484 cadaver organ donors retrieved in the same interval for serologic evidence of hepatitis C viral (HCV) infection using the enzyme-linked assay for anti-HCV antibody. Of 596 HBsAg negative patients, 180 (30%) were anti-HCV positive at the time of transplant. One-year posttransplant, 117 (22%) had detectable levels of anti-HCV antibody. Chemically significant hepatitis developed in 52/234 (22%) anti-HCV positive patients, and 26 of these followed a clinical course consistent with chronic hepatitis. Significantly more males and patients with antibody to HCV detectable at 1 year posttransplant were in the group experiencing an increase in liver enzymes. Ten-year patient and graft survival was 78% and 50%, respectively, for the anti-HCV positive patients who had an elevation of alanine aminotransferase, and 76% and 57% for the cohort maintaining normal liver function (P = NS). There were also no differences in patient and graft survival among the anti-HCV positive group and the consistently sero-negative patients. Of 484 cadaver organ donors with serum available for analysis (out of 1200 retrieved), 67 (14%) were anti-HCV positive at the time of organ donation. Among 23 anti-HCV negative kidney recipients who received a kidney from an HCV antibody positive donor, only one had seroconverted at 1 year posttransplant. Antibody to HCV appears to be widespread among renal transplant recipients and cadaver organ donors. We were unable to demonstrate any evidence of long-term adverse effects on patient and graft survival among anti-HCV positive patients employing the first generation anti-HCV assay.
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PMID:Detection of antibody to hepatitis C virus in renal transplant recipients. 184 50

Blood samples from 2000 accepted blood donors and 343 deferred donors with antibody to hepatitis B core antigen (anti-HBc) and/or an alanine aminotransferase (ALT) elevation were evaluated for antibody to hepatitis C virus (anti-HCV). Sixteen (0.8%) of the 2000 sera initially reacted on enzyme-linked immunosorbent assay (ELISA); 12 (0.6%) were repeatably reactive. One repeatably reactive sample had an elevated ALT; two reacted on anti-HBc testing and had ALT elevations. When the repeatably reactive ELISA samples were tested by an immunoblot assay, four reacted, three were indeterminate, and five did not react. Among the 343 deferred donors, HCV antibodies were detected in 8 (3.8%) of 210 anti-HBc-reactive samples, 12 (11.8%) of 104 elevated-ALT samples, and 15 (52%) of 29 combined elevated-ALT and anti-HBc-reactive samples; 25 of 28 reacted on immunoblot. The anti-HBc-reactive sera were subdivided into groups according to strength of anti-HBc reactivity (weak or strong) and antibody to hepatitis B surface antigen status and then were compared for anti-HCV reactivity rates. The group of samples showing the greatest frequency of anti-HCV had strong anti-HBc reactivity. For blood donors, the anti-HCV test correlates with the surrogate tests for non-A, non-B hepatitis (anti-HBc and ALT); however, most anti-HCV-reactive units remain undetected by surrogate tests, so that implementation of anti-HCV screening should further reduce the transmission of HCV via transfusion.
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PMID:Prevalence of antibody to hepatitis C virus in a blood donor population. 165 55


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