Immune complexes of hepatitis B surface antigen in the pathogenesis of periarteritis nodosa. A study of seven necropsy cases.
In 7 unselected necropsy cases of clinically diagnosed periarteritis nodosa, the detection of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg) in the cytoplasm and nuclei of hepatocytes indicated an ongoing infection with hepititis B virus (HBV). In all these cases histologic changes found in the liver varied from "minimal" to chronic aggressive hepatitis. In all the cases, deposits of HBsAg, immunoglobulins, beta1C-globulin and C1q were detected in vascular lesions. That these deposits could represent HBsAg-anti-HBs immune complexes was supported by demonstrating their strong binding of guinea pig complement and by the successful elution of all HBsAg and part of the immunoglobulin from these deposits by treatment with buffers known to dissociate antigen-antibody bonds but not with phosphate-buffered saline, pH 7.6 (PBS). Glomerulonephritis associated with these immune complexes was found in 6 cases. The presence of larger masses of HBsAg immune complexes, chiefly in recent insudative and fibrinoid vascular lesions, their lesser amounts in lesions undergoing involution, and their absence from healed lesions strongly suggest that these complexes play a primary role in the pathogenesis of acute vascular damage in periarteritis nodosa.
Immune complexes of hepatitis B surface antigen in the pathogenesis of periarteritis nodosa. A study of seven necropsy cases. In 7 unselected necropsy cases of clinically diagnosed periarteritis nodosa, the detection of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg) in the cytoplasm and nuclei of hepatocytes indicated an ongoing infection with hepititis B virus (HBV). In all these cases histologic changes found in the liver varied from "minimal" to chronic aggressive hepatitis. In all the cases, deposits of HBsAg, immunoglobulins, beta1C-globulin and C1q were detected in vascular lesions. That these deposits could represent HBsAg-anti-HBs immune complexes was supported by demonstrating their strong binding of guinea pig complement and by the successful elution of all HBsAg and part of the immunoglobulin from these deposits by treatment with buffers known to dissociate antigen-antibody bonds but not with phosphate-buffered saline, pH 7.6 (PBS). Glomerulonephritis associated with these immune complexes was found in 6 cases. The presence of larger masses of HBsAg immune complexes, chiefly in recent insudative and fibrinoid vascular lesions, their lesser amounts in lesions undergoing involution, and their absence from healed lesions strongly suggest that these complexes play a primary role in the pathogenesis of acute vascular damage in periarteritis nodosa.