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)

Management of the pediatric renal-transplant recipient requires careful pretransplant evaluation including psychosocial assessment and cautious donor/recipient selection. Early transplantation is preferable in infants less than 1 year of age if a suitable live-related donor is available. However, cadaveric-allograft transplantation is best reserved for patients older than 3 years with donors older than 5 years. Pre-emptive transplantation is suitable for approximately one fifth of the population. Medical preparation includes careful HLA-A, -B, and -DR loci matching, interferon treatment for positive hepatitis antigenemia, and acyclovir prophylaxis for a cytomegalovirus (CMV) antibody-negative patient to a seropositive donor. Postoperative management requires close monitoring of the patient's volume status with careful fluid replacement in the form of colloid and crystalloid. Immunosuppression involves multiple drug regimens that include corticosteroids, ciclosporin, azathioprine, antilymphocyte (or -thymocyte) globulin (ALG/ATG), monoclonal antibodies (OKT3), and a ciclosporin alternative: FK-506. Long-term complications dictate management and are divided into medical, surgical, immune, and infectious categories. These are predominated by treatment of acute and chronic rejection, hypertension, and CMV infection.
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PMID:Clinical management of the pediatric renal-allograft recipient. 166 34

HLA-A,B,DR antigens of two groups, one of normal individuals (N- = 31) and another of CRF (Chronic Renal Failure) patients (K- = 37), who did not develop anti-HBs protective antibodies after Hepatitis B (HB) vaccination, were compared, respectively, to the HLA antigens of two corresponding control groups (N+ = 52, K+ = 49), who responded to the vaccine. A statistically significant difference (Pc less than 0.02) in the frequency of HLA-DR3 was observed between responders and non-responders. An increased frequency of HLA-A1 and HLA-B8 in N- as well as of HLA-A1 and HLA-B35 in K- was also noticed, but this was not of statistical significance. As these antigens have been associated to both HBs antigenemia as well as chronic active hepatitis, we suggest that these genes or other genes in linkage to those may suppress the response to HBV vaccination while, in parallel, they may predispose to an autoimmune course of Hepatitis.
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PMID:HLA-associated non-responsiveness to hepatitis B vaccine. 234 53

HLA antigens, hepatitis B virus (HBV)-associated antigens and lymphocyte subsets in liver tissue from 35 patients with HBs antigenemia were studied using an immunoperoxidase double staining method and immunoelectron microscopy in order to clarify the immune mechanism of hepatocyte lysis in type B hepatitis. Immune light and electron microscopy using monoclonal antibodies to lymphocyte subsets revealed that infiltrating lymphocytes in the areas of piecemeal necrosis and focal necrosis were predominantly CD8-positive, showing direct contact with hepatocytes. In contrast, CD4(+) cells were infrequently observed in necrotizing inflammatory lesions. HLA-A,B,C antigens were mainly found on hepatocytes in areas of piecemeal necrosis and focal necrosis, in association with CD8(+) lymphocyte infiltration. HLA-DR antigens were demonstrated on a few hepatocytes in the same lesions. In cases of CAH with serum HBeAg positive, HLA-A,B,C, antigens and HBV antigens simultaneously demonstrated on the same hepatocytes. Especially, hepatocytes expressing both HLA-A,B,C antigen and HBsAg on the plasma membrane showed direct contact with CD8(+)lymphocytes. This finding fulfilled the morphological requirements for HBsAg as a target antigen. On the other hand, HBcAg was hardly demonstrated in the liver cell membrane but was demonstrated mainly in the cytoplasm. Compared with the nuclear localization of HBcAg in cases of NSR, cytoplasmic localization of this antigen may be associated with membranous expression of new antigens induced by HBV infection.
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PMID:Immunohistochemical investigation of hepatitis B virus associated antigens, HLA antigens and lymphocyte subsets in type B chronic hepatitis. 240 98

Our study was undertaken to determine whether human recombinant interferon alpha(rIFN alpha), gamma(rIFN gamma), and tumor necrosis factor alpha(rTNF alpha) exert an effect on the HLA-A, B, C expression of human liver cell lines. The HLA-A, B, C expression was assayed by immunoperoxidase staining and enzyme-linked immunosorbent assay. rIFN alpha and gamma enhanced the HLA-A, B, C expression of the three cell lines tested, Chang cells, SK-Hep-1, and PLC/PRF/5. The activity of rIFN gamma proved more than 8000 times more potent than that of rIFN alpha in Chang cells, 30 times in SK-Hep-1, and 20 times in PLC/PRF/5, respectively. rTNF alpha also enhanced the HLA-A, B, C expression of the three cell lines. The enhancement of HLA-A, B, C expression by rIFN alpha and gamma reached a peak on day 3, and that by rTNF alpha on day 5. These findings suggest that IFN alpha, IFN gamma, and TNF alpha may play similar roles in enhancement of HLA-A, B, C expression of hepatocytes in hepatitis and hepatoma cells.
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PMID:Effect of interferon alpha, gamma, and tumor necrosis factor alpha on the HLA-A, B, C expression of cell lines derived from human liver. 249 41

A unique kindred with an unusual high incidence of serological markers of past or present hepatitis B infection was studied. None of eight relatives had clinical or chemical evidence of hepatitis and all were negative for IgM anti-hepatitis A, but four sisters, each with at least one hepatitis B marker, had features of rheumatic disorders. The index patient had polyarteritis nodosa, two sisters had Raynaud's disease, and the fourth and unclassifiable non-inflammatory polyarthralgia. A daughter of one sister with Raynaud's developed the aortic arch syndrome. There was no segregation of HLA-A, -B and -C alleles with hepatitis B infection. The intrafamilial occurrence of B virus infection and multiple vasculopathies suggests a wider role of this virus in inflammatory vessel diseases.
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PMID:Multiple vasculopathies and hepatitis B in a family. 285 41

The variation in immune responses to standard inoculation of the hepatitis-B virus vaccine suggest that host factors influence response in ways that are not presently understood. We studied 25 low/nonresponding health care workers (anti-HBs titer less than 50 IU/l) after the third inoculation of an experimental hepatitis-B vaccine to determine their immune status (through lymphocyte phenotypes) and HLA type. After application of a fourth inoculation, the seroconverting subjects showed only low anti-HBs levels; three male subjects remained anti-HBs negative. Twelve months after the fourth inoculation only 9 of 25 subjects (36%) maintained anti-HBs titer greater than 10 IU/l. Almost all subjects had normal B-cell and CD-4 and CD-8 counts and ratios. Relative to other European populations HLA-A-10 (P less than 0.05), B-12 (P less than 0.025), CW-5 (P less than 0.05), DR-3 (P less than 0.025), and DR-5 (P less than 0.025) were increased, whereas DR-2 (P less than 0.05) was decreased. However, after correction of the P-values for the number of HLA antigens determined, these differences were no longer significant. Furthermore, these HLA types were not the same as those reported in other studies (except for DR-3). We suggest that larger sample sizes or even not yet available immunogenetic markers will be required to prove an "immunogenetic background" in low/nonresponders, if it exists.
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PMID:Non-responsiveness to hepatitis-B vaccination: revaccination and immunogenetic typing. 297 38

beta 2-Microglobulin display was examined in 131 liver biopsies from patients with acute and chronic type B hepatitis, using an indirect immunoperoxidase method. Enhanced expression of beta 2-microglobulin on hepatocyte membranes was observed in patients with acute hepatitis, chronic active hepatitis with moderate to severe activity and cirrhosis, when compared with normal liver. In acute hepatitis, beta 2-microglobulin-positive hepatocytes were mainly observed in perivenular areas in association with bridging necrosis. In chronic hepatitis, beta 2-microglobulin-positive hepatocytes were observed mainly in periportal zones and in some areas of lobular activity. Diffuse-enhanced display of beta 2-microglobulin on hepatocytes was observed in 5 of 6 patients treated with lymphoblastoid interferon as part of a trial of antiviral therapy. The mechanism by which beta 2-microglobulin display is enhanced on hepatocytes in patients not treated with interferon is uncertain. However, display of beta 2-microglobulin on hepatocytes probably reflects display of HLA-A, B and C antigens and may influence the course of hepatitis B virus infection by increasing susceptibility of the affected cells to T cell-mediated immune attack.
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PMID:Expression of beta 2-microglobulin on hepatocytes in acute and chronic type B hepatitis. 351 Sep 50

We examined HLA-A,B,C and DR locus antigens in 38 Japanese patients who had recovered from halothane hepatitis. The patients were divided into two subgroups, i.e. jaundice and non-jaundice groups, because the clinical features were quite different in each. DR2 was positive in 14 (58.3%) of 24 patients with jaundice, compared with 281 (33.6%) of the 837 Japanese healthy controls (chi-square with Yates' correction = 5.30, relative risk = 2.77, P less than 0.025). Conversely, Bw44 was increased in non-jaundice patients (50.0%), compared with 157 (12.7%) of the 1234 Japanese healthy controls (chi-square with Yates' correction = 13.75, relative risk = 6.86, P less than 0.001). The haplotype frequency (Hf) of Aw24-Bw52-DR2 was high in the patients with jaundice (Hf = 0.2362), while it was zero in the patients without jaundice (P less than 0.0042). These data suggest that the two groups of halothane hepatitis have different genetic backgrounds.
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PMID:HLA antigens in patients with unexplained hepatitis following halothane anesthesia. 386 24

Susceptibility to autoimmune hepatitis is associated with the HLA-DR3 and DR4 haplotypes, but which genes are directly involved in the pathogenesis, has not been established. Low levels of complement component C4 and elevated frequencies of C4 null allotypes have been described in patients, suggesting that the C4 genes, which are closely linked with the HLA loci, may play a role. We therefore examined restriction fragment length polymorphisms in the C4 and 21-hydroxylase genes, and determined HLA-A and B phenotypes, and HLA-DR, DQ and DP genotypes in a large series of Caucasoid patients with autoimmune hepatitis and matched controls. A DNA deletion of the C4A gene and the 21-hydroxylase A pseudogene was found to be present in 50% of patients compared to 23% of controls (Pc < 0.005, relative risk = 3.3). This increase, however, appears to be due to linkage disequilibrium with HLA-DR52a which was most strongly associated with the disease. Complete C4A deficiency, determined by homozygosity for the deletion increased the risk to 18.1 (16% versus 1%, Pc < 0.005), suggesting an additional role for C4 in disease susceptibility. C4 deletions were associated with an increased mortality and tendency to relapse whilst on treatment but did not correlate with age of onset of disease. Our data suggest that MHC-encoded susceptibility to autoimmune hepatitis is polygenic, involving the HLA-DR genes plus other loci, and C4 deficiency may be a marker of disease susceptibility and/or severity.
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PMID:Polymorphism in the human complement C4 genes and genetic susceptibility to autoimmune hepatitis. 785 9

HLA-A, B, C and DR locus specificities studied in 168 patients (71 Chronic active Hepatitis, 97 Chronic Persistent Hepatitis) serologically and histopathologically proven Chronic Hepatitis B Virus infection. There were 113 men and 55 women with a mean age of 23.2 (21-52) years. Hundred and seventy four healthy subjects (107 men, 67 women) included in control group with a mean age of 26.4 (20-54) years. The frequency of HLA A3 (p < 0.01), HLA A11 (p < 0.01), HLA B35 (p < 0.05) and HLA B51 (p < 0.01) were significantly higher in patients than in healthy control subjects. Comparisons among the other HLA-A, B, C and DR locus were found to be statistically non-significant.
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PMID:[Relationship of histocompatibility groups to chronic HBV infections]. 836 14


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