Cases reported "Hepatitis B"

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1/9. Large artery vasculitis following recombinant hepatitis B vaccination: 2 cases.

    We describe 2 women who developed large artery vasculitis shortly after receiving recombinant hepatitis B vaccination. One patient developed Takayasu's arteritis, the other a vasculitis involving subclavian and renal arteries. Both developed renal failure. Whether the vasculitis was caused by the vaccination is not known. Although small vessel vasculitis following hepatitis B vaccination has been reported a number of times, large vessel vasculitis associated with hepatitis B vaccination has been reported only once. These cases suggest that large artery vasculitis should be added to the list of possible side effects of hepatitis B vaccination.
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2/9. Waldenstrom's macroglobulinaemia presenting as reticulate purpura and bullae in a patient with hepatitis b virus infection.

    Cutaneous manifestations of Waldenstrom's macroglobulinaemia (WM) include purpura, ulcers, urticaria, leukocytoclastic vasculitis, and immunobullous dermatoses. No association has been reported previously of WM and hepatitis b virus (HBV) infection. A 40-year-old female HBV carrier was admitted to hospital because of generalized oedema, oliguria, haematuria, hypertension, fever and blood-tinged sputum. Cutaneous manifestations included generalized petechiae, palpable purpura mainly on the legs, multiple necrotic ulcerations and gangrenous changes on the toes, and necrotic, giant confluent reticulate purpura on the trunk surmounted by several tense bullae. Laboratory investigations revealed monoclonal gammopathy of IgM kappa type (6.7 g/L), membranoproliferative glomerulonephritis associated with HBV infection, Bence Jones proteinuria, and an increased number of abnormal plasmacytoid cells in the bone marrow. Pathologic examination demonstrated immune complex-mediated vasculitis with deposits of IgM in the walls of dermal vessels and secondary subepidermal bulla formation. HBV infection may have caused WM or modified the clinical course in this fatal case.
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3/9. Cryoprotein complexes and peripheral neuropathy in a patient with chronic active hepatitis.

    A cryoprotein complex was isolated and characterized from a patient with chronic active hepatitis and a severe peripheral neuropathy. This cryoprotein was composed of IgM, IgG, and hepatitis B surface antigen (HBsAg) and had a concentration of approximately 36 mg per 100 ml of serum. Electron microscopic examination of the cryoprotein demonstrated aggregates of Dane particles in close association with the antigenically related tubular and spherical forms of HBsAg. HBsAg, IgM, and IgG were detected by immunofluorescent staining in the intima of small arteries and veins. The association of a high serum level of cryoprotein and deposition of the cryoprotein components in small blood vessels suggests a role for the cryoprotein in the pathogenesis of peripheral neuropathy in this patient with chronic active hepatitis.
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4/9. Multiple vasculopathies and hepatitis B in a family.

    A unique kindred with an unusual high incidence of serological markers of past or present hepatitis B infection was studied. None of eight relatives had clinical or chemical evidence of hepatitis and all were negative for IgM anti-hepatitis A, but four sisters, each with at least one hepatitis B marker, had features of rheumatic disorders. The index patient had polyarteritis nodosa, two sisters had Raynaud's disease, and the fourth and unclassifiable non-inflammatory polyarthralgia. A daughter of one sister with Raynaud's developed the aortic arch syndrome. There was no segregation of HLA-A, -B and -C alleles with hepatitis B infection. The intrafamilial occurrence of B virus infection and multiple vasculopathies suggests a wider role of this virus in inflammatory vessel diseases.
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5/9. urticaria associated with acute viral hepatitis type B: studies of pathogenesis.

    To determine whether skin deposition of circulating immune complexes contributes to prodromal urticaria of acute hepatitis B, we studied two patients with hepatitis B who presented with urticaria and fever. During the urticarial prodrome but not thereafter, we found activation of both classic and alternative complement pathways. Hepatitis B surface antigen (HBsAg)-antibody complexes were identified (by electron microscopy) in cryoprecipitates from both patients and IgG (by immunodiffusion) in cryoprecipitates of one patient during urticaria. light and electron microscopy of involved urticarial skin revealed necrotizing venulitis in both patients. Immunofluorescence microscopy showed fibrin within involved cutaneous vessel walls in one patient and C3, IgM, and HBsAg, which were not detected in simultaneously obtained uninvolved skin, in both patients. Our findings suggest that deposition of circulating immune complexes containing HBsAg is important in the pathogenesis of urticaria associated with acute hepatitis b virus infection.
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6/9. hepatitis b virus and myocarditis.

    myocarditis may be a serious extrahepatic complication of hepatitis. In this fatal case of serologically documented hepatitis B viral hepatitis, acute myocarditis was present, with histologic features consistent with a viral pathogenesis. Hepatitis B surface antigen was demonstrated by immunoperoxidase methods in small intramyocardial vessels, suggesting that hepatitis b virus infected the heart. The resulting inflammatory heart disease may have been caused either directly, by virus infecting the myocardium, or indirectly, by an immune-mediated mechanism.
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7/9. Cutaneous vasculitis associated with acute and chronic hepatitis.

    We encountered 11 patients who had rashes associated with hepatitis. Five of six acute hepatitis cases, but only one of five chronic hepatitis cases, were related to hepatitis B. Nine of the 11 patients had rash in the absence of clinically overt liver disease. skin biopsy specimens showed histologic evidence of cutaneous vascular injury; specimens of urticarial and maculopapular rashes, which were seen in this series only with acute hepatitis, showed a primarily lymphocytic venulitis with focal necrosis, while palpable purpura, which was seen in this series only in chronic hepatitis, showed a primarily neutrophilic necrotizing vasculitis involving small vessels. One patient had lichen planus-like lesions. Demonstration of vascular deposits of immunoglobulins, complement, and fibrin in skin, as well as hypocomplementemia, circulating immune complexes, and mixed cryoglobulinemia, in these patients suggests that cutaneous lesions associated with liver disease resulted from immune complex-mediated vascular injury.
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8/9. Hepatitis B surface antigen deposition in the blood vessel walls of urticarial lesions in acute hepatitis B.

    urticaria is known to occur in the pre-icteric phase of acute viral hepatitis. Often such urticaria is a symptom of a serum sickness-like syndrome which can be a prodrome of viral hepatis. Immune complexes are thought to be pathogenetic in this condition. In this paper we present two patients with a serum sickness-like syndrome, urticaria and hepatitis B. By immunofluorescence techniques Hepatitis B surface antigen, CIq and C3 could be demonstrated in the blood vessels of the superficial dermis. These findings are consistent with the immune complex hypothesis.
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9/9. Immune complex mediated vasculitis in hepatitis B and C infections and the effect of antiviral therapy.

    case reports of seven patients with vasculitis and past or present viral hepatitis infection are presented, including studies on circulating immune complexes (CICs) and cryoglobulins by sucrose density gradient centrifugation or gel filtration, before and after antiviral therapy. Three patients had unusual vasculitic manifestations: coronary, large vessel, and muscle vasculitis, respectively. All the patients had high levels of CICs by the above methods, but only two had CICs by the C1q binding and conglutinin methods. The CICs/ cryoglobulins contained HBV and/or HCV antibodies, antigens, and genome. The concentration of hepatitis antibodies in immune complex form was severalfold higher than in the free form in serum. In one patient, the HBs antigen was present only in the CICs and in another, only hepatitis antibodies (no antigen/genome) were present in the serum or the cryoglobulins. With antiviral therapy, six patients went into long-lasting remissions. There was a temporal relationship between the regression of the vasculitic lesions and the decline in the levels of CICs/cryoglobulins.
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