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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunoglobulin M antibody to hepatitis A virus (IgM anti-HAV) is found in most patients with acute type A hepatitis. To determine the duration of this IgM response as well as to confirm that IgM anti-HAV is a specific marker for acute infection, we developed a solid-phase radioimmunoassay for IgM anti-HAV. This new assay is 25-fold more sensitive than a conventional blocking radioimmunoassay for anti-HAV, and interference due to rheumatoid factor was eliminated by simultaneously testing sera against virus-free control antigen. Maximum IgM anti-HAV titers (1:6,400 to greater than or equal to 1:51,200) were detected during the first 30 days after the onset of illness. Although the IgM anti-HAV titer subsequently declined 64-fold over the ensuing 90 days, low-titer IgM anti-HAV (1:100 to 1:400) persisted in many sera for 90 to 150 days. Acute sera having an IgM anti-HAV titer of greater than or equal to 1:25,600 possessed a significantly higher mean IgM concentration (492 mg/dl) than acute sera with an IgM anti-HAV titer of less than or equal to 1:12,800 (344 mg/dl; P < 0.05). IgM anti-HAV titers did not correlate with other clinical or laboratory measures of disease severity. Detection of IgM anti-HAV proved to be both a highly specific (>99%) and a sensitive (>99%) method for the diagnosis of type A hepatitis.
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PMID:Specific immunoglobulin M response to hepatitis A virus determined by solid-phase radioimmunoassay. 624 50

A three-step solid-phase radioimmunoassay, HAVAB-M, was developed for use in clinical labs as an aid to diagnosing hepatitis A. Polystyrene beads were coated with anti-human IgM (mu-chain specific) and were incubated successively with serum specimen, HAV, and anti-HAV 125I. HAVAB-M was used to assay sera from patients with hepatitis A and was found to have high sensitivity for the IgM antibody to HAV. The antibody was detectable within a few days of onset of symptoms of hepatitis, and it reached maximum concentrations within one to three weeks. The test was designed so that most patients' sera would become negative approximately three months after onset. HAVAB-M was shown to be specific for IgM antibody, with virtually no detection of IgG anti-HAV. The test showed no interference fro rheumatoid factor and no cross-reactivity with sera from patients with hepatitis B or other infectious diseases.
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PMID:Diagnosis of acute hepatitis A by HAVAB-M, a direct radioimmunoassay for IgM anti-HAV. 626 29

Serum specimens from 12 patients with type A hepatitis were analyzed for immunoglobulin M-type antibody to hepatitis A virus (IgM anti-HA). A recently developed solid-phase radioimmunoassay kit for IgM anti-HA (HAVAB-M, Abbott Laboratories) and a competitive binding radioimmunoassay kit (HAVAB, Abbott Laboratories) with or without 2-mercaptoethanol treatment, as modified by Yano et al. (Acta Hepatol. Jpn. 21, 704-712, 1980) were used to obtain an M-index. All specimens obtained within 60 days of the onset of illness and specimens from 2 of 4 patients later than 60 days after the onset were positive with the HAVAB-M test. This test gave negative results to sera which were positive for anti-HA by a standard HAVAB test in the following: 3 patients with type B hepatitis; 5 with non-A, non-B hepatitis; 11 healthy adults; and 10 sera strongly positive for rheumatoid factor. The M-index for type A hepatitis in sera within 30 days of the onset (mean value of the M-index, m, = 1.52; standard deviation, SD, = 0.25) was significantly higher than that for non-A hepatitis (m = 1.05; SD = 0.15) and for healthy adults (m = 1.02; SD = 0.10). The simplicity and usefulness of the HAVAB-M test in diagnosis of acute type A hepatitis over those measuring the M-index by HAVAB tests were shown by direct comparison of the results.
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PMID:Serodiagnosis of type A hepatitis by detection of immunoglobulin M-type antibody to hepatitis A virus. 626 62

Infants born to HBsAg-positive mothers are at high risk of contracting perinatal hepatitis B infection. The prevention is based on active as well as passive immunoprophylaxis. We have used hepatitis vaccine in 18 newborns of as many HBsAg-positive mothers. Some haematologic and immunologic parameters are here reported. No alterations were observed as to liver function. Immunoglobulin values were normal for age. Auto-antibodies and rheumatoid factor were constantly absent. Immunecomplexes were present in the serum of some infants. The study of T cell subsets and of natural killer cells activity did not reveal any important changes, whereas minor modifications were present in polymorphonuclear leucocyte function. In all infants submitted to vaccination serum conversion was observed a with different antibody levels.
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PMID:[Active and passive immunoprevention of hepatitis B in newborn infants with HBsAg-positive mothers]. 633 50

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

Serological parameters were compared in 15 cases of Coxiella burnetii infection comprising 5 cases each of primary Q fever, chronic granulomatous hepatitis, and endocarditis. The diagnosis was made on the basis of clinical history and serology and on the isolation of C. burnetii phase I from biopsy specimens of liver and bone marrow from two patients with granulomatous hepatitis and from the aortic valve vegetations of five patients with endocarditis. The temporal sequences of immunoglobulin levels, rheumatoid factor, and specific antibody responses to phase II and phase I antigens of C. burnetii were evaluated as predictive correlates of the three Q fever entities. Serum levels of immunoglobulin classes G, M, and A were variable in all the entities of Q fever. Increased mean levels (in milligrams per deciliter) of immunoglobulin G (IgG) and IgA were noted with chronic disease in the sera of some patients, whereas IgM levels were not significantly different from normal values. Rheumatoid factor was significantly elevated in chronic disease but not in primary Q fever. The temporal sequence of C. burnetii phase II and phase I antibodies were compared by microagglutination, complement fixation, and indirect microimmunofluorescence tests. All of these serological tests were useful in distinguishing primary from chronic disease. Thus, the ratio of anti-phase II to anti-phase I antibodies was greater than 1, greater than or equal to 1, and less than or equal to 1 for primary Q fever, granulomatous hepatitis, and Q fever endocarditis, respectively. Moreover, the high phase-specific IgA antibody titers in the indirect microimmunofluorescence test were diagnostic for endocarditis.
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PMID:Serological evaluation of O fever in humans: enhanced phase I titers of immunoglobulins G and A are diagnostic for Q fever endocarditis. 688 55

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

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

Anti-dsDNA and anti-ssDNA antibodies, rheumatoid factors, HBsAg and C1q binding activity were determined in sera of patients with various liver diseases. Anti-dsDNA were only slightly increased in chronic aggressive hepatitis, activity severe and liver cirrhosis. A moderate elevation of anti-dsDNA was detected in possible lupoid hepatitis and it was highly increased in lupoid hepatitis as well as systemic lupus erythematosus. Non-specific elevation of anti-ssDNA titers were observed in all of the liver disease groups. In patients with increased anti-dsDNA titers, C1q binding activity and titers for rheumatoid factor and HBsAg tended to increase. According to reactivity of their sera to DNA, patients with liver disease could be divided in 4 groups: 1. high responders to dsDNA (lupoid hepatitis), 2. moderate responders to dsDNA (possible lupoid hepatitis or lupoid-like liver disease), 3. low responders (only positive for ssDNA), and 4. non-responders.
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PMID:Studies on circulating immune complexes of the liver diseases. 5. Anti-DNA antibodies and C1q binding activity. 738 Jan 68

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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