Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concentration of beta 2-microglobulin in serum was determined in seventy-one patients with various liver disorders. Elevated values were found in most patients with chronic active or chronic persistent hepatitis and in over 80% of patients with alcohol-induced liver cirrhosis. In contrast, patients with alcohol-induced fatty liver, the serum beta 2-microglobulin concentrations were mostly within the normal range. Significant correlation (P less than 0.001) was noted between the elimination rate of galactose from blood and the serum beta 2-microglobulin concentration in patients with alcoholic liver damage but not in patients with chronic hepatitis. The reasons for the increased S-beta 2-microglobulin concentrations in liver diseases are unknown. Several explanations including a release of beta 2-microglobulin from necrotic liver cells or an increased synthesis of beta 2-microglobulin consequent to inflammation in the liver are possible. Alternatively, raised beta 2-microglobulin levels may reflect the hepatic synthesis during reparative growth.
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PMID:Serum beta2-microglobulin in liver disease. 9 2

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

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

Recent studies have demonstrated aberrant expression and topographical heterogeneity of HLA Class I and Class II antigens in tissues of patients with certain immunologic or neoplastic diseases. Current information about the expression of HLA antigens by normal and diseased hepatocytes is controversial. We analyzed the HLA antigenic profile of 4 normal fetal livers, 5 normal adult livers, 7 cases of chronic hepatitis B virus (HBV) infection, 14 cases of cirrhosis of various etiologies, 11 hepatic neoplasms, and 5 continuous cell lines derived from hepatic tumors. The specimens were tested by the indirect fluorescent antibody method with a panel of monoclonal antibodies to distinct monomorphic determinants of HLA Class I and Class II antigens and to beta 2-microglobulin. HLA Cells I antigens were not detected on normal fetal and adult hepatocytes, but were displayed on the plasma membrane of hepatocytes in the majority of all hepatic diseases tested and of the 5 hepatic tumor cell lines. There was a significant correlation between the expression of HLA Class I antigens on hepatocytes and the intensity of intralobular inflammation. Double immunofluorescent staining of livers infected with hepatitis B virus demonstrated simultaneous expression of HLA Class I antigens and HBsAg or HBcAg only in a small percentage of hepatocytes, suggesting lack of a specific association between HLA Class I and these viral antigens. HLA Class II antigens were not detected on hepatocytes from any of the liver diseases tested but were expressed by one of the 5 liver carcinoma cell lines analyzed. These findings confirm that HLA Class I antigens are not detectable within the limits of several immunohistochemical methods on normal hepatocytes and suggest that injury by a variety of factors directly or indirectly leads to induction of these antigens on the plasma membrane of hepatocytes.
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PMID:Expression of HLA class I antigens on hepatocytes in liver disease. 242 44

Serum beta 2-microglobulin (beta 2 mu), a reliable marker of T-cell activation, was measured in 25 patients with chronic post-transfusion non A non B (NANB) liver disease and in 21 patients with HBsAg positive chronic liver disease. beta 2 mu levels were elevated in NANB patients when compared with controls but not in comparison with the HBsAg carriers. In NANB patients, beta 2 mu concentrations were significantly correlated with serum IgG (P less than 0.001) and with circulating immune complex activity, assessed by the 125IClq binding test (P less than 0.01). These findings suggest that, in addition to T-cells, the B-cells contributed also to the beta 2 mu production. Patients with "active disease" (chronic active hepatitis and active cirrhosis) had significantly higher beta 2 mu levels (P less than 0.001) than did those with "inactive disease" (chronic persistent hepatitis and inactive cirrhosis). This relation of serum beta 2 mu concentrations and histological activity was also observed in the HBsAg carriers and suggests that the course of post-transfusion NANB chronic hepatitis could be determined by host's immune response rather than by a direct effect of the virus.
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PMID:Serum beta 2-microglobulin levels in chronic post-transfusion non A non B liver disease. 313 11

Serum beta 2-microglobulin (beta 2m) concentration is increased in pathological processes associated with lymphocyte activation. beta 2m and anti-beta 2m autoantibody (anti-beta 2m) determinations were made in the sera of 41 patients with chronic hepatitis and cirrhosis, respectively, in 19 with systemic lupus erythematosus (SLE) as well as in 27 healthy controls. A pathologically high beta 2m value was found in one-third of inactive persistent hepatitis, and in more than two-thirds of active hepatitis and postnecrotic cirrhosis cases. In SLE it occurred in 16 out of 19 cases. The beta 2m level was elevated mainly in HBV-negative and circulating immune complex-positive hepatic patients. Anti-beta 2m antibody occurred in one-third of chronic hepatitis, but only in one out of 13 cases in cirrhosis and in 12 out of nineteen patients with SLE. The results suggest that beta 2m and anti-beta 2m as in SLE may be further laboratory indicators of immunological activity in inflammatory hepatic disease.
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PMID:Serum beta 2-microglobulin (beta 2m) and anti-beta 2m antibody in chronic hepatitis. 329 46

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

Using antibodies directed to beta 2-microglobulin (b2-m) and HLADR antigens, the expression of MHC products by normal and abnormal bile ducts in 90 paraffin-embedded biopsies showing various liver diseases, was studied. Normal and abnormal bile ducts constantly expressed b2-m. Increased b2-m expression was found in 17/19 PBC, and 4/7 chronic aggressive hepatitis or cirrhosis of viral etiology with hepatitic bile duct lesions. Normal bile ducts failed to express HLADR antigens. Aberrant HLADR display was found in 24/26 PBC and 10/16 chronic aggressive hepatitis or cirrhosis of viral etiology with hepatitic bile duct lesions. It is concluded that the pattern of the major histocompatibility complex (MHC) display does not discriminate between PBC and hepatitic bile duct lesions. Enhanced expression of class I MHC products at the surface of medium-sized bile ducts in PBC may render these structures more susceptible to lysis by cytotoxic T-cells, whereas its significance in chronic aggressive hepatitis or cirrhosis remains unknown. Aberrant expression of HLADR antigens by abnormal bile ducts in PBC and chronic aggressive hepatitis or cirrhosis of viral etiology is probably induced by gamma-interferon, liberated by intra-epithelial lymphocytes, and may serve to enhance the immune response, either by attracting HLADR-restricted cytotoxic T-cells or by the presentation of non-self antigens at the surface of bile duct epithelium.
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PMID:Expression of MHC products by normal and abnormal bile duct epithelium. 354 67

Serum levels of beta 2-microglobulin (beta 2-M) were found to be significantly elevated in acute viral hepatitis, chronic persistent or active hepatitis and liver cirrhosis. beta 2-M values were significantly lower in chronic persistent hepatitis than in the three other groups. Serum beta 2-M was normal in 75 asymptomatic carriers of HBsAg. Steroid therapy was followed by reduction of serum beta 2-M levels in 11 cases of chronic active hepatitis. Variations of beta 2-M were independent from that of transaminases, bilirubin and gamma-globulins.
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PMID:Significance of beta 2-microglobulin in liver diseases. 615 23

The levels of serum alpha 1-microglobulin in 60 normal persons and in 191 patients suffering from a variety of benign and malignant disorders were determined by an enzyme immunoassay, and these values were compared with the levels of beta 2-microglobulin. A discrepancy between the serum levels of these proteins was found in hepatobiliary disorders; that is, an increased serum level of beta 2-microglobulin was observed in 73.9%, while in only 4.3% was there an elevation of alpha 1-microglobulin. In particular, alpha 1-microglobulin levels in patients with liver cirrhosis were well below the normal range, while beta 2-microglobulin levels were elevated. Elevated levels of both proteins were noted in patients with some impairments of renal function, particularly in chronic renal failure, and in immunological diseases. In 81 patients with neoplastic diseases, a high alpha 1-microglobulin value was found in only 15 patients (16.4%), while a high beta 2-microglobulin value in 62 patients (76.5%). The serum levels of both alpha 1-microglobulin and beta 2-microglobulin were especially high in plasma cell dyscrasia with Bence Jones protein, but other neoplastic diseases were mostly associated with beta 2-microglobulin elevation alone.
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PMID:A comparative study of serum alpha 1-microglobulin and beta 2-microglobulin levels in cancerous and other diseases. 616 Sep 31


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