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)

An association between viral hepatitis and two rheumatic disease syndromes has been observed. Twenty-nine patients manifested a transient polyarthritis, sometimes associated with a rash (Group I). Ten patients were seen with a multisystem disease (Group II). Histologic evidence of arteritis or glomerulonephritis was present in seven of ten patients with multisystem disease. Liver tissue from 18 patients showed morphologic evidence of hepatitis with viral features in 9 of 10 patients in Group I and in 6 of 8 patients in Group II. Hepatitis B surface antigen (HBsAg) and/or antibody to HBsAg were detected in sera of all 39 patients. Abnormal liver functions were present in 36. Twelve Group I patients and 2 Group II patients became jaundiced. Rheumatoid factor was present in sera of seven patients in each group. The third component of complement (C3) was depressed in 13 patients in Group I and 7 patients in Group II. The fourth component of complement (C4) was decreased in 8 of 21 Group I and 3 of 7 Group II patients. Synovial fluid C3 was decreased in 2 of 11 Group I and 1 of 4 Group II patient's fluids. Articular inflammation in patients with transient polyarthritis responded in three to seven days to aspirin, acetominophen and/or bedrest alone and rashes disappeared spontaneously. Patients with multisystem disease generally had a prolonged illness and responded somewhat unpredictably to prednisone or a combination of prednisone and cyclophosphamide.
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PMID:Polyarthritis, polyarteritis and hepatitis B. 0 29

An immune Indian ink micro-agglutination method has been evolved for the detection of an antigen present in the blood associated with infectious hepatitis (called IHxAg). In previous studies 86% of serum samples taken from children with hepatitis A proved to be positive by this technique. Present studies were related to 239 adult in-patients with a clinical diagnosis of hepatitis A (123 cases) or hepatitis B (116 cases). Blood samples taken serially during the illness were tested for IHxAg, HBsAg and anti-HBsAg. The results were in accordance with the clinical diagnosis in 60% in contradiction in 30%, whilst all tests brought negative results in 10%. The clinical laboratory findings (SGPT, thymol turbidity) were more in harmony with our laboratory results than with the clinical diagnoses. Rheumatoid factor did not disturb the immune Indian ink reaction, labile serum proteins caused, however, non-specific reaction in 30% of serum samples. When durocytes were used instead of Indian ink the rate of false positive results dropped to 10%. Sera taken in convalescent phase from patients with IHx antigenemia in the acute phase of illness contained an antibody against IHxAg. A crude gammaglobulin preparation from a pool of convalescent sera gave a precipitation line in agarose gel with an antigen present in the fecal extract of children with hepatitis A. This precipitation line proved to contain virus-like particles with an approximate diameter of 25 nm when tested by electronmicroscopy. No precipitation could be seen when sera of the same patients were tested against the same gammaglobulin preparation.
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PMID:Attempts to differential hepatitis B from hepatitis A infection by newly developed serological tests. 17 4

A sandwich ELISA for hepatitis B virus surface antigen (HBsAg) was developed using monoclonal anti-HBs for the solid phase and horse-radish peroxidase labelled sheep anti-HBs. The sensitivity was approx. 0.3 U/ml HBsAg, in the standard test procedure, comprising two incubation steps of 1 h at 37 degrees C, or in a shortened procedure comprising two incubation steps of 30 min at 50 degrees C. A slightly reduced sensitivity (approx. 0.5 U/ml) was obtained when the two incubations were combined in a one-step incubation for 1 h at 37 degrees C. All three procedures were completed by an incubation for 30 min at room temperature with peroxide and tetra-methylbenzidine. The number of false positives obtained when donor sera were screened was below 0.5%. False positive reactions occurred more frequently, but still to a limited extent, when previously selected sera containing rheumatoid factor or other possibly interfering factors were tested with the standard procedure. Most sera containing factors that interfere with a commercial ELISA for HBsAg using sheep anti-HBs coated plates, were negative. Rheumatoid factor positive sera seldom gave false positive results. The lower detection limit became approx. 0.1 U/ml when the cut-off was reduced, while the number of false positives in a donor population only increased to 1.5%. The results obtained with reagents from four different batches indicate a stability of up to 4 wk at 37 degrees C and for at least 26 wk at 4 degrees C.
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PMID:Improved ELISA for the detection of HBsAg. 399 41

Current techniques for the measurement of BK papovavirus (BKV) specific IgM include sucrose density gradient centrifugation followed by hemagglutination inhibition (HAI) or indirect immunofluorescent (IF) staining of BKV infected cells using a fluorescein conjugated anti-human IgM antibody. These techniques are cumbersome and labor intensive and do not lend themselves to testing large numbers of sera. A solid phase radioimmunoassay (RIA) was developed to facilitate the measurement of BKV IgG and IgM in large numbers of sera. Solid phase antigen was prepared by adsorbing CsCl purified BKV antigen to polyvinyl chloride microtiter plates. Following reaction with serum, bound immunoglobulin was detected with iodinated goat anti-human IgG or IgM. RIA for the measurement of BKV IgG was sensitive with titers approaching 10(-6). Determination of IgG titers by RIA and HAI showed good agreement (P less than 0.01, correlation coefficient = 0.74). Measurement of BKV IgM was not affected by the presence of BKV IgG as evidenced by sucrose density gradient fractionation of IgM positive sera, removal of IgG by treatment with S. aureus protein A, and addition of BKV IgG to BKV IgM. Rheumatoid factor (RF) gave false positive IgM titers in the presence of BKV IgG when RF titers were greater than or equal to 1:640 by latex agglutination testing and BKV IgG levels exceed 1:256 by HAI. False positives due to RF could be eliminated by treatment of sera with sheep anti-human IgG antisera. RIA for BKV IgM was specific as sera containing JCV-, cytomegalovirus (CMV)-, rubella-, or hepatitis B core antibody (anti HBc)-IgM were negative by RIA. RIA detected BKV IgM in several sera from renal dialysis or allograft patients with titers ranging from 1:400 to 1:128,000 and demonstrated that BKV IgM persisted in sera of renal allograft patients for as long as 343 days post transplantation.
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PMID:Measurement of BK papovavirus IgG and IgM by radioimmunoassay (RIA). 609 27

The prevalence of circulating immune complexes (CIC) was investigated using the C1q binding assay (C1q BA) and the conglutinin binding assay (Kg BA) in 200 patients undergoing maintenance hemodialysis. Increased C1q binding was found in 45% (87 of 194) of the patients, and the modified Kg BA gave elevated values in 31% (20 of 65). The prevalence of CIC was similar in American and Swiss patients, and in patients undergoing hemodialysis, self-dialysis or peritoneal dialysis. In patients with 'nonimmunological' renal diseases, CIC were detected with similar frequency. No change in CIC was noted during hemodialysis in 6 additional patients tested. The abnormality was not related to age, sex, duration of dialysis, hepatitis B antigenemia, bacterial infections, or transfusions. Anti-DNA antibodies were absent in all subjects tested and the results of the C1q BA were not changed by DNase digestion of eight sera with high C1q binding. Rheumatoid factor activity (RF) was detected in approximately one-fifth of the patients, and there was a direct correlation between positive C1q binding and RF. There was no correlation between CIC and lymphocytotoxic antibodies. This study demonstrated a high prevalence of CIC in dialyzed uremic patients and established its relationship to other immunological abnormalities.
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PMID:Circulating immune complexes in regularly dialyzed patients with chronic renal failure. 623 93

The specificity and sensitivity of the IgM-capture immunoassay (IgM-CI) were evaluated for detection of rubella specific IgM and hepatitis B core (HBc) specific IgM. For rubella specific IgM, antibodies bound to the solid phase were detected by haemadsorption and for HBc specific IgM, by using HBc antigen (HBcAg) and radiolabelled IgG anti-HBc. Rheumatoid factor (RF) was found to interfere in the test for HBc specific IgM because IgM-RF bound to the solid phase reacted with aggregated radiolabelled HBc specific IgG. This false positive reaction did not occur when radiolabelled F(ab')2 was used instead of the whole IgG molecule. HBcAg purified from biological fluids might be coated with host IgG and under these conditions, HBcAg could react with RF. It was also demonstrated that high levels of IgG antibodies could interfere with IgG anti-mu coated-surface by means of non-immunological protein-protein interactions. In fact, IgG did not interfere in the rubella assay, whereas it did in the very sensitive anti-HBc test. To prevent this false-positive reaction, different dilution media were tested. Only the addition of non-specific IgG and fetal calf serum (FCS), to the dilution medium, seems to improve the specificity of the test. Furthermore, in order to decrease this non-specific IgG-IgG interaction and an occasional prozoning phenomenon, the dilution of serum to be tested was taken into account. Parameters considered to decrease sensitivity were also studied. RF, anti-F(ab')2 antibodies and non-specific IgM did not decrease significantly the sensitivity of the assay.
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PMID:Specificity and sensitivity of the IgM capture immunoassay: studies of possible factors inducing false positive or false negative results. 650 34

Sera from 200 volunteer donors and 200 paid blood donors, all positive for hepatitis B surface antigen (HBsAg), were tested for the presence of hepatitis B e antigen (HBeAg).HBeAg was detected in 31 HBsAg-positive paid donors (15%), and in 11 HBsAg-positive volunteer donors (5%) by agar gel diffusion. The presence of HBsAg was associated with higher titers of HBsAg. No significant difference was found in the prevalence of antibody to HBeAg (anti-HBe) in the two donor groups. Rheumatoid factor was not associated with the presence or absence of HBeAg or anti-HBe, indicating that HBeAg is probably not an anti-IgG. These data support the epidemiological evidence that paid blood donors appear to be more likely than volunteer donors to transmit hepatitis B virus infection to recipients of their blood.
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PMID:Hepatitis B e antigen in volunteer and paid blood donors. 696 88

Complement activation at a low temperature in vitro and cryoglobulinaemia are associated with hepatitis C virus (HCV) infection. The frequency of HCV antibody positivity determined in serum specimens that showed the cold-dependent activation of complement was 100%, whereas it was 48% among sera with cryoglobulin. On the other hand, the frequency of cold activation among HCV-infected sera was 41%, and that of cryoglobulin 48%. Cold activation was not found in any HCV- sera studied, whereas cryoglobulin was found at a frequency of 14% in HCV- sera. Cold activation was also absent among hepatitis B virus (HBV) S antigen or antibody-positive sera, except a few that were both HBV+ and HCV+. Rheumatoid factor was also frequently detected in sera with cold activation or cryoglobulin. Cold activation and cryoglobulin may be generated by common mechanisms in which a low avidity, low temperature-preferring antibody may function. In sera with cold activation, fine particles of immune complexes, which do not form precipitates, may activate the complement system. HCV is a unique virus that coexists with antibody in the serum, therefore the avidity of the antibody for the virus antigen may be low, and occasionally react only at a low temperature. This may be why the in vitro phenomenon related to immune complexes occurs specifically in HCV-infected sera.
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PMID:The association of complement activation at a low temperature with hepatitis C virus infection in comparison with cryoglobulin. 764 11

Rheumatoid factor is of limited value in the diagnosis of rheumatoid arthritis (RA) in West Africa. Consequent upon previous findings, we have studied the role of the absence of antibodies to malaria and human immunodeficiency virus (HIV) as well as the presence of the hepatitis B surface antigen (HBsAg) as diagnostic markers of rheumatoid arthritis in West Africa. We have found a significant association (p < 0.001) between RA and titre of HBsAg, but only between RA and malaria (p < 0.05) when sera with low malaria antibodies were studied. No correlation between either HBsAg or malaria and rheumatoid factor was found and no RA patient was either HIV-1 or HIV-2 positive.
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PMID:The absence of antibodies to malaria and human immunodeficiency virus, and the presence of hepatitis B surface antigen as diagnostic markers of rheumatoid arthritis. 812 6

We presented a case of acute inflammatory demyelinating polyneuropathy associated with autoimmune chronic active hepatitis (AI-CAH). This is the third case report of neuropathy in AI-CAH. A 64-year-old male with chronic liver dysfunction was admitted to the hospital because of high fever, distal weakness and sensory disturbance of all extremities, bilateral facial weakness and dysphagia. On neurologic examination, there was bilateral weakness of the upper and lower facial muscles, bulbar palsy and severe distal weakness of all extremities. The deep tendon reflexes were absent and the sensation of touch, pinprick, temperature, and vibration was impaired bilaterally symmetrically in all extremities. Serum biochemistry revealed hyperproteinemia, hypergammaglobulinemia and elevated liver enzymes. Rheumatoid factor, antinuclear antibody anti-smooth muscle antibody were positive. Serological tests for hepatitis B surface antigen and its antibody hepatitis B core antibody, and hepatitis C antibody were all negative. Serum anti-GM1, anti-GD1b, anti-GQ1b and anti-MAG antibodies were negative. Liver biopsy findings were consistent with AI-CAH with marked lymphocytic infiltration in the portal tracts. Albuminocytologic dissociation was noted in CSF. Motorconduction velocity of the median, ulnar and facial nerves were markedly reduced with temporal dispersion. No motor response was evoked in the lower extremities. Needle electromyography revealed denervation and reinnervation potentials in the arm and leg. The sural nerve biopsy showed segmental de- and re-myelination and deposition of IgG components in endoneurium. Neurological symptoms and liver dysfunction improved with corticosteroid treatment. In this case, hypergammaglobulinemia associated with an exacerbation of AI-CAH may be responsible for the acute inflammatory demyelinating neuropathy through an unknown autoimmune mechanism.
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PMID:[A case of acute inflammatory demyelinating neuropathy associated with autoimmune-type chronic active hepatitis]. 950 66


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