1/64. Neurological manifestations of chronic hepatitis c.hepatitis c virus (HCV) infection is often associated with abnormal immunological responses. We describe four patients with vasculitic neurological signs and symptoms following HCV infection. A 56-year-old woman with HCV infection developed peripheral neuropathy characterized by asymmetric distal painful hypesthesia, dysesthesia and moderate motor weakness of the lower limbs. Serological examinations revealed cryoglobulinemia and low levels of complement c4. A biopsy of the sural nerve revealed vasculitic neuropathy. HCV infection associated immunomediated vasculitis was diagnosed. While steroid therapy was ineffective, treatment with interferon-alpha improved the neuropathy considerably without, however, eliminating HCV infection. A 62-year-old man with HCV infection developed peripheral sensory neuropathy. complement c3 was slightly diminished. Nerve biopsy revealed vasculitic neuropathy. A 71-year-old woman developed chronic symmetric sensomotor polyneuropathy. HCV hepatitis followed blood transfusions. cryoglobulins tested positive, consistent with type II cryoglobulinemia. Complements C3 and C4 were diminished. Inflammatory infiltrates in the sural nerve biopsy specimen led to the diagnosis of chronic vasculitic disorder. A 55-year-old woman with HCV infection developed vasculitis of the skin, connective tissue, visceral organs, and kidney, leading to hemodialysis. Neurologically she developed severe apathy and drowsiness, myoclonic jerks, exaggerated deep tendon reflexes, and positive pyramidal signs. magnetic resonance imaging of the brain showed diffuse increased signal abnormalities involving supra- and infratentorial white matter suggesting cerebral vasculitis. cryoglobulins were positive, complements C3 and C4 slightly diminished (54 mg/dl, 4.3 mg/dl). Supportive therapy resulted in neurological improvement. Treatment with interferon-alpha was discontinued because of agranulocytosis. In patients with peripheral neuropathy or signs of leucencephalopathy, a hepatitis c associated vasculitis should be considered in the differential diagnosis.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
2/64. Mixed cryoglobulinemia secondary to visceral leishmaniasis.We describe a case of type II mixed cryoglobulinemia, with monoclonal IgMkappa rheumatoid factor, associated with visceral leishmaniasis caused by leishmania infantum. Involvement of Leishmania antigen(s) in the formation of cryoprecipitable immune complexes was suggested by the fact that cryoglobulinemic vasculitis subsided after antiparasite therapy and that anti-Leishmania antibodies, as well as rheumatoid factor, were enriched in the cryoprecipitate. We observed 2 additional patients with visceral leishmaniasis and cryoglobulinemic vasculitis. All 3 patients had seemingly contracted leishmaniasis in italy, were hepatitis c virus negative, and were initially diagnosed as having autoimmune disorders. These findings indicate that Leishmania can be an etiologic agent of type II mixed cryoglobulinemia. This parasitosis should be taken into consideration in the differential diagnosis of vasculitides in endemic areas.- - - - - - - - - - ranking = 0.16666666666667keywords = hepatitis (Clic here for more details about this article) |
3/64. Cryoglobulinemic vasculitis resistant to intermittent intravenous pulse cyclophosphamide therapy.We report on a 78-year-old patient with severe disease manifestations including polyneuropathy and clinically suspected secondary temporal arteritis due to hepatitis c virus-associated cryoglobulinemic vasculitis (CV). Despite intermittent intravenous pulse cyclophosphamide therapy and oral corticosteroid therapy her condition further deteriorated. Only oral cyclophosphamide therapy with high-dose corticosteroid and plasmapheresis was efficient in inducing a remission of her CV. This case report demonstrates that pulse cyclophosphamide therapy may not be sufficient to control severe manifestations of cryoglobulinemic vasculitis.- - - - - - - - - - ranking = 0.16666666666667keywords = hepatitis (Clic here for more details about this article) |
4/64. Capillaritis associated with interferon-alfa treatment of chronic hepatitis c infection.We report the case of a 36-year-old man who was referred with an asymptomatic eruption that started on both lower legs. This started shortly after being commenced on interferon-alfa for chronic hepatitis secondary to hepatitis c. Clinically, the eruption was consistent with a capillaritis (pigmented purpuric dermatosis). histology confirmed this to be lymphocytic vasculitis. Lymphocytic vasculitis is frequently identified in the salivary glands of patients who are hepatitis c positive. Although leukocytoclastic vasculitis confined to the skin is frequently reported with hepatitis c, lymphocytic vasculitis is rarely reported. We consider that the lymphocytic vasculitis in our patient occurred as a result of interferon-alfa treatment because of the strong temporal relationship between the onset of the skin eruption and drug therapy.- - - - - - - - - - ranking = 1.3333333333333keywords = hepatitis (Clic here for more details about this article) |
5/64. Central venulitis in pediatric liver allografts.Central venulitis (CV), a distinct histologic lesion described in adult liver transplants, can occur with acute portal tract rejection or in isolation (ICV). Possible etiologies include immunosuppressive drug toxicity, acute cellular rejection, viral hepatitis, ischemic injury, and recurrent disease. This study was designed to characterize ICV and to assess its potential etiology in pediatric liver recipients because this population generally does not develop recurrent disease or viral hepatitis. All posttransplantation liver biopsy specimens that were obtained from children who received liver allografts over a 4-year period were reviewed. ICV was identified in 12 of 127 posttransplantation biopsies and in 7 of 45 allograft recipients. Only 4 liver transplantations were performed for potentially recurrent diseases (primary sclerosing cholangitis). ICV first appeared in posttransplantation biopsy specimens significantly later than did portal rejection alone. The finding of CV was not significantly correlated with elevation of tacrolimus levels, reason for transplantation, donor/recipient cytomegalovirus (CMV) status or blood type, cold ischemic times, or the incidence of outflow obstruction. The responses of CV to therapy were variable and, although the majority of cases resolved, several episodes persisted or recurred. In conclusion, ICV occurs in 16% of pediatric liver allograft recipients and does not appear to be related to recurrent disease, viral hepatitis, drug toxicity, or graft ischemia. CV may be a variant of acute rejection, but longer follow-up is required to determine the most adequate therapy for this entity.- - - - - - - - - - ranking = 0.5keywords = hepatitis (Clic here for more details about this article) |
6/64. The benefit of long-term interferon alfa therapy for symptomatic mixed cryoglobulinemia (cutaneous vasculitis/membranoproliferative glomerulonephritis) associated with chronic hepatitis c infection.The efficacy of long-term interferon therapy for chronic hepatitis c infection with symptomatic mixed cryoglobulinemia has not clearly been defined. We describe a patient with chronic hepatitis c, symptomatic mixed cryoglobulinemia (cutaneous vasculitis), and membranoproliferative glomerulonephritis (MPGN) who responded clinically, biochemically, and virologically to a 1-year course of interferon therapy. Interferon side effects were minimal. Relapse occurred when interferon was discontinued, and suppressive maintenance interferon therapy was required for clinical, biochemical, and virologic remission. During the 5th year of maintenance therapy, she developed potential side effects that necessitated discontinuation of interferon treatment. After treatment stoppage, a clinical, biochemical, and virologic remission was maintained for more than 1 year. However, the potential side effects, which included eye irritation, arthralgias, myalgias, fatigue, insomnia, memory loss, and depression, persisted. Ophthalmologic, rheumatologic, and neurologic evaluations were nondiagnostic. Psychometric testing revealed dementia and mood disorder. Because the disabling symptoms persisted after 9 months, a health-related quality of life assessment was carried out with the SF-36 survey. Compared with healthy individuals and patients with chronic hepatitis c, our case had a lower health-related quality of life assessment on six out of seven scales and on four out of seven scales of the SF-36 survey, respectively. This case report indicates that long-term maintenance interferon therapy was effective in the treatment of symptomatic mixed cryoglobulinemia and its renal complications and resulted in a clinical, biochemical, and virologic sustained response. It is postulated that the side effects of long-term interferon therapy in this setting may be problematic.- - - - - - - - - - ranking = 1.1666666666667keywords = hepatitis (Clic here for more details about this article) |
7/64. hepatitis c, cryoglobulinemia, and cutaneous vasculitis associated with unusual and serious manifestations.hepatitis c viral infection is currently the leading cause of chronic hepatitis and cirrhosis. It also is a major predisposing factor for the development of hepatocellular carcinoma. It is estimated that approximately 1-2% of patients with hepatitis c infection have nonhepatic manifestations that are protean in nature. In this report, we describe six unusual cases of nonhepatic manifestations: abdominal vasculitis in two, peripheral neuropathy in two, and one patient each with central nervous system vasculitis and necrotizing cutaneous vasculitis. All patients had cutaneous vasculitis and cryoglobulinemia. None of our patients had cirrhosis, yet three of the six patients died. Because of the severe manifestations, aggressive therapy was instituted with interferon, immunosuppressive medications, i.v. immunoglobulin, and plasmapheresis. Our report underscores the importance of recognizing nonhepatic manifestations in patients with hepatitis c infection that may be associated with high morbidity and mortality.- - - - - - - - - - ranking = 0.5keywords = hepatitis (Clic here for more details about this article) |
8/64. 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.- - - - - - - - - - ranking = 0.83333333333333keywords = hepatitis (Clic here for more details about this article) |
9/64. Regression of lymphoproliferative disorder after treatment for hepatitis c virus infection in a patient with partial trisomy 3, Bcl-2 overexpression, and type II cryoglobulinemia.A patient with type II cryoglobulinemic vasculitis and hepatitis c virus (HCV) infection presented with a leukemiclike proliferation of B cells bearing marginal zone B-cell phenotypic markers. A partial trisomy 3 (bands 3q11-29) and overexpression of Bcl-2 without t(14;18) translocation was detected in the monoclonal B cells that were classic rheumatoid factor-producing B cells bearing the WA cross-idiotype. Treatment with interferon-alpha produced a complete clinical remission and synchronous marked decreases in viremia and monoclonal B-cell prevalence. This is the first report of partial trisomy 3 and Bcl-2 overexpression in type II cryoglobulinemic vasculitis associated with HCV infection. Further studies of HCV-infected patients with and without type II cryoglobulinemia are required to determine the prevalence and possible physiologic and/or pathophysiologic significance of these findings.- - - - - - - - - - ranking = 0.83333333333333keywords = hepatitis (Clic here for more details about this article) |
10/64. allopurinol hypersensitivity syndrome and acute myocardial infarction--two case reports.INTRODUCTION: allopurinol hypersensitivity syndrome is an idiosyncratic drug reaction characterised by an acute and severe multiorgan disease. It usually begins 2 to 6 weeks after starting allopurinol. The most important and critical characteristics are the presence of visceral involvement and haematological abnormalities; hepatitis, interstitial nephritis and eosinophilia are most frequently seen. However, cardiac involvement has not been previously reported. CLINICAL PICTURE: Two previously well young Chinese men presented with fever, rash and hepatitis 3 weeks after taking allopurinol. The clinicopathological presentation was typical of allopurinol hypersensitivity syndrome. TREATMENT AND OUTCOME: Both men received systemic corticosteroid therapy and had full recovery. A few months later, they each had an acute myocardial infarction with a fatal outcome, despite minimal cardiac risk factors and no family history of coronary artery disease. CONCLUSION: The immunologic process in allopurinol hypersensitivity syndrome may have caused coronary vasculitis and subsequent myocardial infarct. Alternatively, the idiosyncratic reaction may have damaged myocardium, with the resultant myocarditis masquerading as coronary artery disease. patients with allopurinol hypersensitivity syndrome should be followed up for cardiac involvement.- - - - - - - - - - ranking = 0.33333333333333keywords = hepatitis (Clic here for more details about this article) |
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