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)

We examined the association of three serum immune markers with CD4 cell counts in a large cohort of i.v. drug users with and without human immunodeficiency virus (HIV) infection. Levels of beta 2-microglobulin and neopterin were significantly elevated in HIV-infected subjects and increased in association with decline in CD4 cell counts (all p less than 0.001). Serum IgA levels in HIV-seropositive individuals were significantly elevated only when the CD4 cell count was less than 200/microliters (p less than 0.001). After controlling for HIV status and CD4 count, recent history of hepatitis was associated with significantly higher beta 2-microglobulin (p = 0.028) and marginally higher neopterin (p = 0.052) levels. There was no association of race, gender, or drug use patterns with levels of serum immune markers after controlling for HIV status and CD4 count. These data indicate that immune activation is coupled with immunosuppression in HIV-infected i.v. drug users. In addition, beta 2-microglobulin and neopterin levels are elevated in persons with a recent history of hepatitis but not in those with recent non-AIDS-defining bacterial infections. Markers of immune activation do not vary by race, gender, or drug use patterns among i.v. drug users.
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PMID:Immune serum markers and CD4 cell counts in HIV-infected intravenous drug users. 136 May 38

To identify the target antigen during hepatocyte damage in hepatitis type B virus (HBV) infections, the expression of HBc and HBs antigens, and beta 2-microglobulin (BMG) were studied in liver tissue. Serial changes of serum DNA-polymerase (DNA-P) activity and HBV DNA were also measured. After the onset of acute hepatitis, HBs antigen in liver tissues was observed from many patients; but HBc antigen was rarely detected. In liver tissues of patients with chronic hepatitis, HBs antigen was consistently positive, irrespective of the changes in sGPT. On the other hand, HBc antigen was frequently positive both preceding and during the culmination period for sGPT. The distribution of HBc antigen in the hepatocyte was mostly cytoplasmic. During the same period the serum DNA-P and HBV DNA were frequently positive. Immunoelectron microscopy showed that reaction products with HBc antigen existed in the cytoplasm and the cell membrane. These results indicate that HBc antigens become the target, when HBV infected hepatocytes are eliminated.
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PMID:Immunological study of the association between hepatocyte damage and HBc antigen. 140 34

Thirty-three patients with chronic hepatitis C/non-A, non-B were included in a randomized controlled study of interferon-alpha 2b (IFN-alpha 2b) treatment, 3 x 10(6) U three times weekly for 36 weeks. Using an immunoperoxidase technique, frozen liver biopsy specimens were examined with MoAbs for the presence of T helper cells (CD4), T suppressor/cytotoxic cells (CD8), total T cells (CD2) and B cells (CD22) before and after treatment. beta 2-microglobulin (beta 2-MG) expression on hepatocytes was semiquantified using a scoring system on sections from paraffin-embedded biopsy specimens. Serum levels of beta 2-MG were analysed with a radioimmunoassay technique. Intralobular T helper and T suppressor/cytotoxic cells declined significantly in the treated patients but not in the controls. The portal CD4/CD8 ratio did not change. Before treatment, serum beta 2-MG levels and hepatocyte beta 2-MG expression were significantly higher in patients with chronic active hepatitis compared to patients with chronic persistent hepatitis. Serum beta 2-MG levels increased significantly in responders during IFN treatment, with a maximum after 12 weeks. However, in the liver, the hepatocyte beta 2-MG expression was significantly decreased after treatment. Thus, IFN-alpha treatment does not seem to induce an increased HLA class I antigen hepatocyte expression in chronic non-A, non-B hepatitis, which favours the hypothesis that its anti-viral effects are more important in modulating the disease activity.
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PMID:Lymphocyte subsets and beta 2-microglobulin expression in chronic hepatitis C/non-A, non-B. Effects of interferon-alpha treatment. 154 20

Intrahepatic infiltrate from 18 patients who died of fulminant hepatitis, was analyzed by an immunohistochemical method using formalin-fixed, paraffin-embedded liver sections and monoclonal antibodies. Inflammatory cells were characteristically located in the portal and periportal areas adjoining resting hepatocytes, but were infrequently found in the perivenular areas where hemorrhagic hepatocyte necrosis predominated. In the inflammatory infiltrate, T cells were the most predominant cell type, composing about two-thirds of the total hepatic infiltrate, followed by lysozyme-positive macrophages which composed about one-third of the total hepatic infiltrate, irrespective of the etiology of the fulminant hepatitis. On the other hand, B cells made up less than 2% in all cases, and plasma cells were also few, less than 2% in 12 of 18 cases. Furthermore, an enhanced display of beta 2-microglobulin on hepatocyte membranes was demonstrated in all cases with remaining hepatocytes, indicating an increased expression of class I MHC antigens on these cells. These results suggest that T cells may play an important role in the pathogenesis of the portal and periportal lesions of fulminant hepatitis, probably with a help of MHC class I antigens on hepatocytes, while hemorrhagic necrosis of hepatocytes around the central veins may be caused by a different mechanism, most likely a circulatory disturbance secondary to cell-mediated immune reactions in the periportal areas.
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PMID:The cellular infiltrate in the liver of patients with fulminant hepatitis: analysis of paraffin-embedded tissue sections. 160 Feb 59

Nineteen patients with chronic non-A, non-B hepatitis (CH-NANB) and 24 patients with chronic hepatitis B (CH-B) were treated with interferons, and the therapeutic and biological responses of the two groups (CH-NANB and CH-B) were compared. All patients had had sustained elevations in serum glutamic pyruvic transaminase (sGPT) levels for more than 6 months and were proven to have chronic hepatitis by liver biopsy. alpha-Interferon (IFN-alpha) or beta-interferon (IFN-beta) was administered in low doses of 3 to 6 mega international units (MIU) daily for 4 wk. Liver biopsies were taken from 13 CH-NANB and 14 CH-B subjects just before and immediately after treatment, and histological findings were assessed by the histology activity index (HAI) score. SGPT levels decreased much more rapidly and markedly in CH-NANB than in CH-B during IFN therapy (p less than 0.01). The HAI score decreased 3.5 points in CH-NANB and 1.0 point in CH-B between pretreatment and posttreatment. Serum beta 2-microglobulin (beta 2-MG) increased in both types of chronic hepatitis during treatment, but the rate of elevation was significantly less in CH-NANB than in CH-B (p less than 0.001). beta 2-MG expression on hepatocytes stained by the PAP method was almost identical in CH-NANB before and after treatment, whereas it increased steadily in CH-B. The serum 2',5'-oligoadenylate synthetase level increased in both types of hepatitis on IFN administration. These results suggest that, in IFN treatment for CH-NANB, the antiviral actions of IFNs may play a very important role in reducing the activity of chronic hepatitis.
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PMID:Comparative study of clinical, histological, and immunological responses to interferon therapy in type non-A, non-B, and type B chronic hepatitis. 168 84

We investigated the effects of interferon therapy on hepatocyte human leukocyte antigen class I and class II antigen expression and intrahepatic lymphocyte subsets in patients with chronic viral hepatitis B (n = 11) and C (n = 10). Interferon-alpha was administered intramuscularly in doses ranging from 3 to 18 million international units daily for 4 wk. Liver biopsy specimens were obtained just before and immediately after treatment, and the specimens were stained by the indirect immunoperoxidase method for evaluation of human leukocyte antigen expression and lymphocyte subsets. Before therapy, no significant difference was noted between hepatitis B and C in human leukocyte antigen class I antigen expression on hepatocytes or in the lymphocyte subsets in the intralobular and portal areas. After interferon-alpha treatment, hepatocyte expression of human leukocyte antigen class I antigens and serum beta 2-microglobulin levels were virtually unchanged in chronic viral hepatitis C patients, but both were increased in chronic viral hepatitis B patients. Human leukocyte antigen class II antigens were not expressed during treatment. The mean number of intralobular CD3+ and CD8+ cells and the mean serum ALT level decreased significantly in chronic viral hepatitis C patients (p less than 0.05) but not in chronic viral hepatitis B patients. The mean number of intralobular CD4+ cells was unaffected by interferon therapy in both groups. In all 21 patients, the changes in CD8+ cell numbers paralleled the changes in serum ALT levels. Our findings suggest that T-cell cytotoxicity may play an important role in hepatocyte damage in both chronic viral hepatitis C and chronic viral hepatitis B and that the response to interferon-alpha differs in these two types of hepatitis.
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PMID:Effects of interferon on intrahepatic human leukocyte antigens and lymphocyte subsets in patients with chronic hepatitis B and C. 171 Oct

Twenty-seven patients suffering from congenital coagulation defects of the prothrombin complex factors were investigated: six had haemophilia B; 14, factor VII defect; four, factor X defect; and three, factor II defect. Nineteen patients (70.3%) had previously received plasma and/or clotting factors concentrates. Among these, markers of hepatitis B infection (HBV) were present in five cases (26.3%) and hepatitis C (HCV) antibodies were found in seven cases (36.8%). The HIV1 prevalence was similarly high. In fact, five patients (26.3%), previously infused with factor IX or prothrombin complex factors concentrates, developed HIV1 infection. No patient with factor VII deficiency became HIV1 positive, despite the administration of unheated factor VII concentrates and the consequent HBV and HCV contamination. In the HIV1 positive group, three patients showed a false positivity for HIV2 antibodies. Five years after seroconversion, three patients developed AIDS (stage IV) and died, one had persistent generalized lymphadenopathy (stage III), and one with post-hepatitis liver cirrhosis was asymptomatic (stage II) for HIV infection. The significant decrease in total white cells, T4 lymphocytes and platelet counts and increase of beta 2-microglobulin and neopterin levels confirmed the prognostic value of these markers for the progression of HIV1 disease. Only one HIV1 negative transfused patient developed anti-HTLV-I p19 antibodies.
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PMID:Prevalence of HIV infection in a cohort of patients with congenital coagulation defects of the prothrombin complex factors. 178 37

The levels of beta 2-microglobulin (beta 2m) in peripheral blood mononuclear cells (PBMC) and livers from patients with chronic liver diseases type B were measured. Beta 2m of liver and PBMC in chronic active hepatitis was higher than those of controls (p less than 0.01, p less than 0.01). beta 2m of PBMC are directly proportional to those of livers (r = 0.746), beta 2m levels of PBMC in patients with chronic active hepatitis during the exacerbation of hepatitis was higher than those of remission of hepatitis. The levels of beta 2m in PBMC in vivo, was significantly increased during either interferon alpha or beta administration. Interferon-gamma positive cells in the liver were exacted in the beta 2m increased group of chronic hepatitis type B. INF-gamma production in the lymphocyte of livers, may play an important role in the occurrence of liver injury in patients with chronic hepatitis type B.
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PMID:[Increased levels of beta 2-microglobulin in peripheral blood mononuclear cells and hepatocytes in patients with chronic hepatitis type B]. 190 79

Beta 2-Microglobulin expression on hepatocyte membrane was studied in 117 liver biopsies from patients with acute and chronic hepatitis B and in 11 subjects with normal liver function, using immunohistochemical PAP method. In normal liver beta 2-microglobulin could not be detected on hepatocyte membrane, compared with that in subjects with normal liver, in asymptomatic HBsAg carrier and in patients with chronic persistent hepatitis, there is significant enhancement of beta 2-microglobulin expression in patients with acute mild hepatitis and chronic mild active hepatitis. Beta 2-Microglobulin expression in patients with chronic active hepatitis with moderate to severe activity and cirrhosis has a significant enhancement, when compared with acute mild hepatitis and chronic mild active hepatitis. Moreover, location of beta 2-microglobulin expression on hepatocyte membrane was associated with lesion of hepatocytes. Enhanced expression of beta 2-microglobulin on hepatocyte membrane in acute and chronic hepatitis B probably reflects enhanced display of HLA-ABC antigens and may influence the course of hepatitis B virus infection by increasing susceptibility of T cell-mediated hepatocytelysis.
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PMID:[A study of the relation of the expression of beta-microglobulin and hepatocytic lesions in hepatitis B]. 220 29

In a chimpanzee model of acute type B hepatitis, at the time of onset of hepatitis B virus replication and before the development of immunity to hepatitis B virus, interferon is present in the plasma. This is followed by an increase in the display of HLA class I, but not class II proteins, on the hepatocyte membrane. In chronic hepatitis B virus infection, there is a low density of HLA class I protein display on the infected hepatocyte. Administration of alpha-interferon enhances HLA display and in many cases is followed by a transaminase elevation, seroconversion of HBe antigen to antibody and disappearance of hepatitis B virus DNA from serum, changes implying clearance of infected hepatocytes. Successful response to interferon therapy may be predicted by a rapidly rising serum beta 2-microglobulin, a component of the HLA class I molecule, during the first 2 weeks of therapy, before the rise in transaminases.
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PMID:HLA class I antigens on the hepatocyte membrane during recovery from acute hepatitis B virus infection and during interferon therapy in chronic hepatitis B virus infection. 242 27


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