Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circulating immune complexes (ICs), assayed by the L1210 enzyme-linked immunoassay, were detected in 48% of patients with hemophilia. A, 50% of patients with von Willebrand's disease, and in none of our patients with hemophilia B. Eighty-five % of the hemophilia A and B patients had mild to moderate disease with only one patient demonstrating a circulating inhibitor. No correlation was found between IC levels and hepatitis B infection, SGOT, disease severity, total quantity of factor VIII or IX infused, time interval from list infusion, or rheumatoid factor positivity. Although the nature of the ICs is not known, the similarity of IC levels between hemophilia A and von Willebrand's disease is discussed with regard to antibodies generated to non-procoagulant portions of the factor VIII molecule.
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PMID:Immune complexes in hemophilia. 679 22

Using immune electron microscopy (IEM), low-level cross-reactions could be demonstrated between the surface antigens of hepatitis B and woodchuck hepatitis. However, immune complex formation was greatly enhanced by pre-exposure of the antigens to 0.5% deoxycholate. Cross-reaction between the core antigens and e antigens of both viruses was also confirmed by IEM as well as radioimmunoassay. It appears that the woodchuck sera used in this study may well contain an anti-immunoglobulin akin to rheumatoid factor.
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PMID:Antigenic cross-reactions between woodchuck hepatitis virus and human hepatitis B virus shown by immune electron microscopy. 683 11

Inhibition assay of 125I-C1q binding to IgG-p-azobenzamidoethyl Sepharose 6B (IgG-Sepharose) by immune complexes was developed for the detection of circulating soluble immune complexes in the liver disease and was compared with polyclonal rheumatoid factor (pRF) binding inhibition assay and with C1q binding assay. The C1q inhibition assay was proved to be very sensitive, reproducible and rapid. Sucrose density gradient ultracentrifugal analysis showed that the assay could detect aggregates of human IgG (AHGG) larger than 19s. C1q inhibition activity (C1qIA) correlated with severity of the liver disease, defined by histological criteria. The highest C1qIA was observed in sera of patients with primary biliary cirrhosis, followed by liver cirrhosis, fulminant hepatitis, chronic aggressive hepatitis (2B), lupoid hepatitis and hepatocellular carcinoma in the order. There were correlations of C1qIA with serum gamma-globulin levels, sero-positivity for rheumatoid factor and hepatitis B surface antigen, and significant correlations existed also among pRFIA, C1qIA and C1qBA. Ultracentrifugal analysis of sera from patients with the liver disease showed that ClqIA demonstrated two sizes of immune complexes, 7s and larger than 19s, while complexes larger than 8s were seen in pRFIA.
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PMID:Studies on circulating soluble immune complexes of the liver disease. 6. Comparative studies of 125I-pRF inhibition assay, 125I-Clq inhibition assay and 125I-Clq binding assay. 697 71

The clinical course of 40 patients with significant quantities of mixed cryoglobulins, but without lymphoproliferative, collagen-vascular or chronic infectious diseases, is presented. These cases comprise 51.3 percent of all mixed and 31.7 percent of all types of cryoglobulins evaluated by us over the period 1960--1978. A characteristic clinical syndrome, consisting of recurrent palpable purpura (100 percent), polyarthralgias (72.5 percent) and renal disease (55 percent), was seen. Biopsy specimens of skin lesions showed cutaneous vasculitis, and half had immune reactants in vessel walls. Seventy percent of patients had evidence of hepatic dysfunction, often subclinical, and more than 60 percent of those tested had serologic evidence of prior infection with hepatitis B virus. Hepatic lesions ranged from minimal triaditis to chronic active hepatitis and/or cirrhosis. All 22 patients in whom clinical renal disease developed had significant proteinuria; 63.6 percent had diastolic hypertension, 77.3 percent edema, 45.5 percent renal failure and 22.7 percent were nephrotic. Glomerular disease associated with deposition of immunoglobulin G, immunoglobulin M and complement, often with coexistent renal arteritis, was confirmed pathologically in 15 cases. All cryoglobulins had rheumatoid factor activity and consisted of IgM and polyclonal IgG; five also contained IgA. Thirteen had a monoclonal IgM kappa component. Serum protein electrophoresis was unremarkable or showed diffuse hyperglobulinemia. Striking depression of early complement components was noted but did not correlate well with the cryoprotein concentration, renal involvement or clinical course. Follow-up for periods up to 21 years from onset of symptoms revealed that renal involvement has a deleterious effect on prognosis. Postmorten examinations of nine patients demonstrated widespread vasculitis in addition to renal involvement. Preterminal infection was found in eight.
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PMID:Mixed cryoglobulinemia: clinical aspects and long-term follow-up of 40 patients. 699 82

An improved enzyme-immunoassay (EIA) for the detection of hepatitis B 'e' antigen (HBeAg) and its corresponding antibody is described. The present test is as sensitive as the previous one but it is more specific as demonstrated by testing donor/recipient sera, donor plasmas and patients sera. Interference by antibody against hepatitis B surface antigen (HBsAg) did not occur due to the use of HBsAg-free reagents. Interference by rheumatoid factor could be avoided by using enzyme-labelled F(ab')2 rather than IgG conjugates. The application of an F(ab')2 conjugate, however, introduced other non-specific reactions, particularly in sera from patients with (autoimmune) liver disorder. Further study into the applicability of F(ab')2 conjugates is therefore indicated.
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PMID:Comparison of enzyme-labelled F(ab')2 and IgG conjugates in an enzyme-immunoassay for hepatitis B 'e' antigen. 701 83

A solid phase radio-immunoassay (SPRIA) was developed for the detection of anti-HBc IgM. The assay proved sensitive and easy to perform and rheumatoid factor did not affect the test results. Anti-HBc IgM titres were followed in consecutive samples from 15 patients after uncomplicated acute hepatitis B. In the acute phase anti-HBc IgM titres ranged from 10(-5) to 10(-7) (mean 10(-6.4)). One year after onset of disease ten of the 15 had titres below 10(-4) and between two and three years after onset most patients had titres 10(-3). Anti-HBc IgM titres were determined in six episodes of acute hepatitis B, all HBsAg negative but anti-HBc positive in the first samples obtained (within 8 days) and developing anti-HBs during convalescence. Acute phase anti-HBc IgM titres in these patients ranged between 10(-5.5) and 10(-7) (mean 10(-6.5)) and were thus identical with HBsAg positive cases. When acute phase sera from 168 episodes of acute hepatitis primarily classified as non-A, non-B, were tested for anti-HBc IgM titres above 10(-5), sera from 13 episodes were positive and in seven of these hepatitis B diagnosis could be confirmed by rising anti-HBs titres in convalescence. Sera from four of the 13 patients contained HBeAg, which was thus demonstrated in the absence of HBsAg. The results show that testing for anti-HBc IgM is important for a true non-A, non-B diagnosis.
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PMID:IgM antibody to the hepatitis B core antigen in acute hepatitis determined by SPRIA--diagnostic value. 708 Aug 27

Immune complexes of the hepatitis B e-antigen (HBeAg) could be labeled and thus visually identified in the electron microscope by using antibody to HBeAg (anti-HBe) tagged with colloidal gold particles. Circulating immune complexes of HBeAg were detected in sera from patients with acute hepatitis B infections as well as from asymptomatic carriers of hepatitis B surface antigens (HBsAg). Sera positive for rheumatoid factor frequently contained mixed aggregates in which immune complexes of HBsAg were closely bound to immune complexes of HBeAg.
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PMID:An electron microscopic demonstration of immune complexes of hepatitis B e-antigen using colloid gold as a marker. 709 54

An enzyme-linked immunosorbent assay for detection of specific immunoglobulin M (IgM) antibodies against the core antigen of the hepatitis B virus (anti-HBc IgM) is described. The interference of IgM rheumatoid factor was evaluated quantitatively. In the anti-HBc IgM test, the rheumatoid factor gave false-positive results when the concentration exceeded 20 IU/ml. The rheumatoid-positive sera were disclosed by a control and retested for anti-HBc IgM after absorption of rheumatoid factor with latex particles aggregated with human IgG. In five of seven selected patients with acute hepatitis B followed to biochemical and clinical recovery, anti-HBc IgM was present transiently until antibodies against hepatitis B surface antigen (anti-HBs) appeared. Two patients had persistent anti-HBc IgM during the follow-up period. Four patients with hepatitis B surface antigenemia and progression to chronic liver disease did not clear their anti-HBc IgM in the period of observation (11 to 24 months). Anti-HBc IgM could not be demonstrated in 223 of 225 Danish blood donors. The two donors found positive for anti-HBc IgM also had anti-HBs. Twenty patients with acute A or non-A non-B hepatitis were negative for anti-HBc IgM. The enzyme-linked immunosorbent assay for anti-HBc IgM described here has a high specificity and sensitivity. The diagnostic relevance needs further evaluation, including quantitation of anti-HBc IgM, but the results presented indicate that anti-HBc IgM may be helpful in differentiating between prior and recent or ongoing hepatitis B infection.
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PMID:Enzyme-linked immunosorbent assay for detection of immunoglobulin M antibody to hepatitis B core antigen. 724 Mar 84

A passive haemoagglutination method (rHA) was compared to a solid-phase radioimmunoassay (RIA) in detecting hepatitis B surface antigen (HBsAg) in order to evaluate their sensitivity and specificity. The test was performed on sera from 297 subjects with acute and chronic hepatitis, 23 asymptomatic HBsAg-RIA positive carriers, 20 patients with infectious mononucleosis, 110 HBsAg RIA negative healthy persons; 30 sera positive for rheumatoid factor and/or autoantibody were also tested. Our data confirm that RIA is highly specific and rarely shows false negative results, depending on antibody excess, rHA shows less sensitivity than RIA in detecting HBsAg especially in sera of patients with acute hepatitis.
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PMID:[Sensitivity and specificity of 2 methods of determining surface antigen (HBsAg) in various forms of hepatitis B pathology]. 734 32

Sera from 99 chronic hepatitis B surface antigen carriers, 12 individuals with acute type B hepatitis, 26 hepatitis B surface antibody-seropositive subjects, and 50 hepatitis B surface antigen, hepatitis B surface antibody-seronegative subjects were evaluated for the presence of serum imunoconglutinis (IKs). The mean serum IK titers of hepatitis B surface antibody-seropositive and hepatitis B virus-seronegative subjects wre 5.3 and 4.9, respectively. The IK titers of subjects with acute and chronic hepatitis B virus infections were 215.4 and 19.1, respectively. These groups also manifested IK titers greater than or equal to > 16 significantly (P < 0.005) more often than controls did. Among chronic hepatitis B surface antigen carriers, high IK titers were associated with low levels of hepatitis B surface antigen. IK titers of individuals chronically infected with hepatitis B virus and having the rheumatoid factor were similar to those of individuals without the rheumatoid factor. Elevated IK titers represent a physiological autoimmune response and may indicate the presence of immune complexes in acute and chronic hepatitis B virus infection.
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PMID:Serum immunoconglutinin titers during acute and chronic hepatitis B virus infection. 739 98


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