Acute HBsAg-positive Hepatitis Research Articles

Differential diagnosis of acute HBsAg positive hepatitis using IgM anti-HBc by a rapid, fully automated microparticle enzyme immunoassay

Background/Aims: We determined the diagnostic significance of IgM anti-HBc by a rapid, fully automated microparticle enzyme immunoassay (IMx CORE-M) in acute HBsAg positive hepatitis. Methods: We studied prospectively for at least 6 months 100 patients with acute self-limited hepatitis B (group A) and 40 patients with acute hepatitis superimposed on histologically confirmed chronic hepatitis B (group B). On admission, all patients in group A were positive and those in group B were negative for IgM anti-HBc by a commercially available enzyme immunoassay. Results: Based on the assay criteria, the rates of IMx CORE-M ( > 1.2) positive serum samples on admission, 4, 12 and 24 weeks later were: in group A: 100%, 95%, 72%, 44% and in group B: 20%, 27.5%, 17.5%, and 15%, respectively. Misclassification was observed in 20-27.5% of the acute on chronic hepatitis B cases. However, the mean IMx CORE-M index value was found to be significantly higher in group A during the whole follow-up. In particular, on admission the mean IMx CORE-M index value weas 2.504±0.435 (range: 1.508–3.482)_ in group A and 0.747±0.346 (range: 0.062–1.384) in group B ( p<0.001). Discriminant function analysis showed that the cutoff level between the two groups for IMxCORE-M index on admission was 1.5. Four to 12 weeks from admission, in the group with acute on chronic hepatitis B cases, 13 patients with HDV and/or HCV superinfection had significantly lower IMx-CORE M index values compared with 27 patients with acute hepatitis due to exacerbation of chronic hepatitis B. Conclusions: IMx CORE-M appears to be an accurate diagnostic test to differentiate acute from acute on chronic HBsAg positive hepatitis, but the cut-off level seems to be higher (1.5 instead of 1.2).

Significance of anti-HBc IgM by a microparticle enzyme immunoassay in the differential diagnosis of acute HBsAg-positive hepatitis

Significance of anti-HBc IgM by a microparticle enzyme immunoassay in the differential diagnosis of acute HBsAg-positive hepatitis

Seroepidemiology of hepatitis C virus in Beijing, China

To investigate the seroprevalence of hepatitis C virus (HCV) in China we tested sera from healthy individuals without hepatitis and no history of parenteral blood exposure and from patients admitted to a hepatitis hospital in Beijing. Sera were tested for anti-HCV by first-generation enzyme immunoassay; selected positives were tested with two second-generation EIAs, one utilizing recombinant antigens and the other synthetic peptides. We found anti-HCV with the following frequencies: 10 of 164 (6%) individuals with no disease; 2 of 36 (5.5%) patients with acute non-A non-B hepatitis (NANBH); 26 of 39 (67%) patients with post-transfusion NANBH; 10 of 34 (29%) patients with chronic hepatitis negative for hepatitis B surface antigen (HBsAg); 3 of 30 (10%) patients with chronic HBsAg-positive hepatitis; 0 of 19 patients with acute HBsAg-positive hepatitis. Of 24 repeat-positive sera, 19 were positive by both and 4 by one second-generation tests. We conclude that hepatitis C infection is common in China, that it contributes substantially to the incidence of post-transfusion hepatitis, and that HCV plays a significant role in both acute and chronic hepatitis. Further studies are needed to extend these observations and to define the predominant routes of transmission of HCV in China.

Epidemiology and clinical outcome of hepatitis D virus infection in Turkey

The prevalence, the epidemiology, the clinical and biochemical characteristics of hepatitis delta virus (HDV) infection were studied in patients with HBsAg-positive acute hepatitis, in those with chronic liver disease, and in apparently healthy carriers in Turkey. Fifty-eight of the 242 carriers of HBsAg (23.9%) and 31 of the 237 (13.1%) patients with acute HBsAg-positive hepatitis had serological evidence of HDV infection. Eleven of these individuals were HBsAg carriers with acute HDV superinfection. The prevalence of HDV infection was significantly (p less than 0.001) higher in patients with chronic liver disease (54/165; 32.7%) than in asymptomatic carriers of HBsAg (4/77; 5.2%). The highest prevalence (26/57; 45.6%) of HDV infection was found in patients at high risk of acquiring hepatitis virus infection (health care workers, hemodialysis patients, polytransfused patients) with chronic liver disease. Whereas the frequency of "severe" or fulminant hepatitis was similar in HBV infected patients (7.8%) and in HBV/HDV coinfected individuals (10%), the frequency of biphasic hepatitis was significantly (p less than 0.005) higher in the latter patients (30%) than in those with classical hepatitis B (7.8%). Chronic evolution of the disease was observed in 3.9% of the patients with classical hepatitis B and in 5% of those who had evidence of simultaneous HBV/HDV infection. The 10 carriers of HBsAg who survived the acute HDV superinfection developed chronic delta hepatitis. These findings indicate that HDV is endemic in Turkey and that its prevalence is highest among chronic HBsAg-positive hepatitis patients, implicating HDV as a major cause of liver disease among urban Turkis.

Changes in the epidemiology of acute HBsAg positive hepatitis in an urban area

Changes in the epidemiology of acute HBsAg positive hepatitis in an urban area

Anti-Hepatitis B Core Immunoglobulin M in the Serologic Evaluation of Hepatitis B Virus Infection and Simultaneous Infection With Type B, Delta Agent, and Non-A, Non-B Viruses

The clinical value of an enzyme-linked immunosorbent assay for the detection of immunoglobulin M (IgM) antibody to hepatitis B core antigen (anti-HBc IgM) was evaluated by testing serum samples from the following groups of patients: (a) 27 individuals who had been diagnosed as having acute hepatitis B virus (HBV) infection, (b) 29 hepatitis B surface antigen (HBsAg) carriers, (c) 6 subjects with acute non-B hepatitis, and (d) 10 HBsAg-negative but anti-HBc-positive subjects who were suspected of being index cases for the intimate transmission of HBV. Whereas 24 of the 27 individuals with presumed acute HBV infection exhibited anti-HBc IgM, only 2 of 29 HBsAg carriers were found to be positive. Hepatitis B surface antigen persisted during an 8-mo observation period in 3 anti-HBc IgM-negative subjects with acute HBsAg-positive hepatitis. Before anti-HBc IgM testing, it was considered that these cases had evolved to the HBsAg carrier state. However, the regular demonstration of anti-HBc IgM in acute type B hepatitis, as well as the failure to detect this antibody in the majority of HBsAg carriers, led to reclassification of these cases as probable instances of acute non-A, non-B or delta-agent hepatitis superimposed on the HBsAg carrier state. Through additional testing, the diagnosis of non-A, non-B (NANB) infection was confirmed in 2 of these cases, and delta-agent infection was identified in the third. None of the non-B hepatitis cases exhibited anti-HBc IgM. However, 5 of the 10 suspected type B index cases were anti-HBc IgM-positive, indicating that they were very recently infected and most likely had infected their cohabiting sexual partners. The results from this study indicate that testing for anti-HBc IgM may improve serodiagnostic accuracy when acute NANB and delta-agent hepatitis occur in previously unrecognized HBsAg carriers. Moreover, it may be a useful test in defining potential high risk sources of exposure to HBV.

Complexes between hbsag and igm in serum of patients with acute hepatitis

HBsAg bound to IgM was measured in the serum of HBsAg carriers with acute hepatitis using a radioimmunoassay based on selective absorption of IgM on solid phase coated with antiserum to human IgM. HBsAg/IgM was detected in 94 (100%) patients with acute type B hepatitis during the acute phase of infection and persisted after the fourth week only in 13 of them, who developed chronic liver disease. HBsAg/IgM was detected only in 1 patient out of 15 carriers of the HBsAg with superimposed non-B hepatitis. No activity was found in serum of 20 patients with acute HBsAg-negative hepatitis. The nature of the IgM component of the complex is uncertain, however, blocking experiments of the HBsAg/IgM reaction with polymerized human albumin suggest that the IgM component of the complex might represent antibody to the denatured protein. Persistent HBsAg/IgM complex detection in patients with acute type B hepatitis provides a useful tool to predict transition of HBV infection to chronicity. Its absence in patients with acute HBsAg-positive hepatitis is indicative of non-B hepatitis in chronic carriers of the HBsAg.

Preprothrombin in acute viral hepatitis B

In vitamin K deficiency or treatment with vitamin K antagonists, a precoagulant of prothrombin (Factor II) called preprothrombin has been established. We measured preprothrombin with Clarke-Freeman electrophoresis in 26 patients with acute viral hepatitis (21 HBS-AG positive) who did not suffer from vitamin K deficiency. Prothrombin and the vitamin-K dependent Factors VII, IX, and X were determined by standard coagulometric methods. Prothrombin was additionally estimated by immunoelectrophoresis according to Laurell. Three patients with acute HBS-AG positive hepatitis showed preprothrombin in their plasma. The activity of Factors II, VII, IX, and X was slightly below normal with normal concentration of Factor II in the immunoelectrophoresis. Liver parenchymal damage and cholestasis were slight; the pseudocholinesterase showed subnormal levels in all three patients. Possible causes for the appearance of preprothrombin in the peripheral blood in acute viral hepatitis and the possible connections with liver cell damage are discussed.

Anti‐HBc of IgM‐class, HBeAg and anti‐HBe in acute and chronic hepatitis B

The presence and persistence of IgM antibody against hepatitis B core antigen (anti-HBc IgM) and the correlation with other HBV markers were studied in 42 patients, all of whom had acute HBsAg-positive hepatitis but whose subsequent diseases differed. All patients initially had anti-HBc IgM. In 13 out of 15 patients with uncomplicated acute hepatitis, anti-HBc IgM disappeared within 6 months after onset of the disease. In five out of 12 patients, who in spite of transient HBsAg developed chronic liver disease, the anti-HBc IgM persisted for more than 2 years. Among 15 patients with persistent HBsAg, anti-HBc IgM was present from 7 months to more than 8 years. Seroconversion from HBeAg to anti-HBe was observed in seven patients and in five of these anti-HBc IgM disappeared during the follow-up period. These results indicate that anti-HBc IgM can be used as a serological marker of recent or ongoing HBV infection.

Hepatitis B virus infection among household contacts of patients with acute HBsAg-positive hepatitis

Sixty-seven household contacts of 31 index cases with acute HBsAg-positive hepatitis were investigated forHepatitis B virus (HBV) markers. Follow-up findings in 50 household contacts revealed that six spouses and/or sexual partners had developed acute clinical hepatitis B. Three of these six contacts were drug addicts. A further seven contacts showed serological changes compatible with exposure to HBV, but had no signs of acute clinical hepatitis. Six of these seven contacts were spouses and/or sexual partners of their index case. Possible prophylactic or post-exposure measures only seem to be necessary in the spouses and/or sexual partners of patients with acute hepatitis B.

K-lymphocytes (killer-cells) in Crohn's disease and acute virus B-hepatitis.

Total lymphocyte counts, B-, T-, C'3 receptor-bearing lymphocytes, and K-cell activity were studied in peripheral blood in patients with Crohn's disease and inflammatory liver disease. Patients with active untreated Crohn's disease and acute virus B hepatitis exhibited a markedly increased K-cell activity measured in a plaque assay when compared with normal controls (P less than 0.01). Patients with immunosuppressive treated Crohn's disease, HBsAg-positive chronic active hepatitis, and cirrhosis of the liver showed only a slight increase of K-cell activity (P less than 0.01). In the postacute phase of hepatitis (four to 12 weeks from onset) K-cell activity fell to normal levels. The number of B-lymphocytes showed a relative and absolute decrease in all groups of patients. With the exception of patients with acute HBsAg-positive hepatitis and the post-acute phase of hepatitis all the other groups showed statistically decreased absolute numbers for C'3 receptor-bearing lymphocytes. The significant decrease in K-cell activity and the number of T-lymphocytes in Crohn's disease treated with immunosuppressive drugs was interpreted as an effect of azathioprine and prednisone on these lymphocyte subpopulations.

Ground-Glass Hepatocytes in Unselected Liver Biopsies. Ultrastructure and Relationship to Hepatitis B Surface Antigen

400 unselected liver biopsies were stained with aldehyde-thionin (AT) and examined for ground-glass hepatocytes (GGH). 1) AT-positive GGH were found in about half of all HBSAg-positive patients but were never seen in HBSAg-negative patients. 2) AT-positive GGH were observed in healthy HBSAg carriers and in all forms of chronic hepatitis but never in acute HBSAg-positive hepatitis. 3) AT-negative GGH were occasionally seen in HBSAg-negative patients under drug treatment. 4) Ultrastructurally GGH showed proliferation of smooth endoplasmic reticulum which only in AT-positive GGH contained filaments, 20-25 nm in diameter, within its cisternae.

The Nature and Incidence of Cryoproteins in Hepatitis B Antigen (Hb&lt;sub&gt;s&lt;/sub&gt;Ag) Positive Patients

Hepatitis B (HbsAg) surface antigen has been detected in the serum of patients with a variety of diseases and immune complexes of this antigen and antibody have been implicated in tissue damage to various organs. Previously we have demonstrated that serum cryoproteins occur in a variety of immune complex disorders and represent pathogenic complexes of antigen and specific antibody. Sera from patients with acute HbsAg positive hepatitis, chronic hepatitis B antigenemia, acute and chronic HbsAg negative hepatitis, as well as a variety HbsAg negative miscellaneous liver diseases and normals were studied for the presence and nature of cryoproteins. Cryoproteins were detected in a large number of patients with acute and chronic HbsAg positive hepatitis and chronic HbsAg carriers. The quantity of these cold insoluble precipitates was highest in acute hepatitis. Cryoproteins were detected with much less frequency in HbsAg negative patients and were not found in normals. The precipitates in HbsAg patients contained either HbsAg, anti-HBsAg or both, along with immunoglobulins and occasionally complement and rheumatoid factor. The cryoproteins in these patients had biological properties attributable to immune complexes and several of the patients had clinical manifestations of acute or chronic serum sickness. Cryoproteins from HbsAg negative patients did not contain HbsAg or antibody to HbsAg and did not have biologic properties of immune complexes. In HbsAg positive patients HbsAg and antibody to HbsAg were concentrated in the cryoprecipitate. The preliminary studies suggest that investigation on cryoproteins in hepatitis may be of clinical and immunopathogenic value.

Health-care workers positive for hepatitis B surface antigen. Are their contacts at risk?

To assess the hepatitis risk to patients exposed to HBs AG-positive health-care workers, 228 contacts were followed prospectively for six to nine months. Health workers included two physicians with chronic hepatitis, a chronic asymptomatic carrier nurse, a food handler with acute HBs Ag-positive hepatitis and a physician who was HBs Ag-positive for 25 days before the onset of acute hepatitis. Controls (167) consisted of identically followed patients who had not been exposed to an HBs Ag-positive health worker. No exposed or control patient acquired clinical hepatitis or HBs Ag. Isolated elevations in serum glutamic pyruvic transaminase occurred equally in both groups and did not correlate with serologic evidence for hepatitis B infection. One exposed patient demonstrated antibody seroconversion (anti-HBs), as did two of the controls. These data do not demonstrate hepatitis B transmission from HBs Ag-positive health workers to their patients. Restriction of such carriers is not warranted at present.