The significance of IgM antibodies to hepatitis B core antigen in hepatitis B carriers and hepatitis B-associated chronic liver disease.

Abstract

IgM antibody to hepatitis B core antigen (IgM anti–HBc) was determined in 60 patients whose serum was positive for hepatitis B surface antigen (HBsAg) and 18 patients whose serum was negative for HBsAg, but positive for antibody to hepatitis B core antigen (anti–HBc). Two radioimmunoassays were done utilizing either anti–u antibody to capture IgM or Staphylococcus A protein to separate IgG and IgM. Both methods failed to detect IgM anti–HBc in 30 healthy carriers, 5 HBsAg–positive cirrhotics, 2 patients with HBsAg–positive hepatocellular carcinoma, and 18 HBsAg–negative anti–HBc–positive patients. IgM anti–HBc was present in all 4 patients with acute hepatitis B and in 4 of 8 patients with HBsAg–positive chronic active hepatitis. In patients with chronic active hepatitis, IgM anti–HBc was positive in those with the most intense infiltrate of mononuclear cells on liver biopsy. There was no correlation with the presence of hepatitis B e antigen or anti–HBe. Three of 11 patients with HBsAg–positive chronic persistent hepatitis were intermittently positive by the Staphylococcus A method but all were negative by the u–capture method when a low sensitivity cutoff was employed. The sensitivity of the test can be adjusted at will by the manufacturers and, therefore, introduction of interchangeable controls and standards will enable clinical application of this testing system with meaningful results. Testing for IgM anti–HBc may help the clinician in differentiating healthy HBsAg carriers from patients with HBsAg–positive acute and chronic hepatitis. It is also of value in differentiating patients with acute hepatitis B from HBsAg carriers who develop acute hepatitis of different etiology. Accumulation of more data and correlations with the intensity and nature of the mononuclear infiltrates in chronic hepatitis will increase understanding of the mechanism of switchover from IgM to IgG anti–HBc response and factors favoring chronicity in hepatitis B.