Cases reported "Hepatitis C"

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1/12. interferon-alpha may exacerbate cryoblobulinemia-related ischemic manifestations: an adverse effect potentially related to its anti-angiogenic activity.

    The discovery of the strong association between hepatitis c virus (HCV) infection and the development of mixed cryoglobulinemia has motivated active testing of antiviral-directed alternative therapies. Several trials have demonstrated that classic cryoglobulinemia-associated manifestations improve with interferon-alpha (IFNalpha) treatment. Herein we report on 3 HCV-infected patients with severe cryoglobulinemia-related ischemic manifestations who were closely followed up during IFNalpha therapy. Clinical evaluations with special attention to ischemic lesions, liver function tests, and cryocrit determinations were serially performed. In addition to prednisone and immunosuppressive agents, the patients received IFNalpha at 3 x 10(6) units, 3 times per week for 2 months, 3 months, and 4 months, respectively. In all 3 patients, systemic features improved, liver function results returned to normal, and cryocrit values decreased. However, ischemic lesions became less vascularized and ischemia progressed, leading to transmetatarsal and subcondylar amputation, respectively, in 2 of the patients and fingertip necrosis and ulcer enlargement in the third. skin biopsies performed before IFNalpha therapy and after 2 months of IFNalpha therapy in the third patient showed a significant decrease in subepidermal microvessels. When IFNalpha was discontinued, the lesions finally healed. cryoglobulinemia-related ischemic lesions may worsen during IFNalpha treatment, presumably through a decrease in inflammation-induced angiogenesis. The anti-angiogenic activity of IFNalpha may delay the appropriate healing of ischemic lesions.
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2/12. Isolated central nervous system vasculitis associated with hepatitis c infection.

    Since its identification in 1989, hepatitis c has been implicated in the pathogenesis of an increasing number of diseases previously believed to be primary or idiopathic. We report 2 rarely seen cases of isolated central nervous system (CNS) vasculitis in patients with hepatitis c infection. Patient 1. A 43-year-old man with 4 day right temporal headache developed a left hemiparesis. Weakness was his only physical finding. Computed tomography (CT) scan demonstrated a large right frontotemporal hemorrhage, and angiography revealed focal dilatations and irregularities of multiple branches of the right middle and anterior cerebral arteries. Cerebral decompression was performed and leptomeningeal biopsies showed granulomatous angiitis. Laboratory results were normal except for elevated liver biochemical tests. Later testing for hepatitis c was positive. His neurological symptoms improved with corticosteroids and cyclophosphamide. Patient 2. A 39 yr old male developed 3 days of left sided weakness, slurred speech and difficulty swallowing fluids. Physical findings were limited to his weakness. magnetic resonance imaging demonstrated a right superior pontine subacute infarct with a small left internal capsule lacunar infarct. angiography revealed multiple areas of focal narrowing with no areas of abrupt vessel cut off. Cerebral spinal fluid showed 71 PMN, 29 RBC, normal glucose, elevated protein (64 mg/dl), no oligoclonal bands, and low myelin basic protein. Other laboratory analyses were normal including liver biochemical tests. However, hepatitis c serology was positive and mixed cryoglobulins were detected. CNS vasculitis was diagnosed and nearly full recovery was achieved with corticosteroids, cyclophosphamide and warfarin.
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3/12. Cerebral vasculitis in a patient with HCV-related type II mixed cryoglobulinemia.

    The peripheral nervous system is often involved in patients with mixed cryoglobulinemia (MC), while there are few reports of central nervous system involvement. We describe a case of HCV-related type II MC with peripheral and central nervous system involvement. A 61-year-old woman, suffering from flaccid tetraparesis, was referred to our department because of an increasing disability. The presence of delirium prompted us to also investigate the central nervous system. MMSE, EEG, EMG, brain CT-scan, color-Doppler of neck vessels, retinal fluorangiography and brain MRI were performed. These investigations suggested a cerebral vasculitis. The finding of very low C4 serum levels, together with high rheumatoid factor serum levels, suggested the search for cryoglobulins. The laboratory findings showed a HCV-related type II (IgMk) MC. A marked improvement of symptoms and of laboratory data was obtained by treatment with methylprednisolone cyclophosphamide.
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4/12. Acquired intestinal lymphangiectasia successfully treated with a low-fat and medium-chain triacylglycerol-enriched diet in a patient with liver transplantation.

    Intestinal lymphangiectasia is defined as a dilatation of small bowel lymphatic capillaries and a loss of lymph into the bowel lumen. Clinically it is characterized by hypoproteinaemia and oedema. We present here a case of protein-losing enteropathy due to intestinal lymphangiectasia after liver transplantation in a 57-year-old man who was transplanted for hepatitis c virus. Four years after liver transplantation, the patient developed hypoalbuminaemia and ascites associated with recurrence of cirrhosis. The sudden fall in serum albumin led us to look for a cause of reduction other than or in addition to cirrhosis. Duodenal biopsies showed tall villi with dilated lymphatic vessels and widening of the villi caused by oedema, demonstrating intestinal lymphangiectasia. In this case a low-fat diet supplemented with medium-chain triacylglycerols achieved an early clinical improvement with increased serum albumin levels and ascites disappearance. Intestinal lymphangiectasia should be suspected in liver-transplanted patients developing hypoproteinaemia and hypoalbuminaemia after the recurrence of cirrhosis.
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5/12. hepatitis c infection, cryoglobulinemia, and vasculitic neuropathy. Treatment with interferon alfa: case report and literature review.

    A patient with mononeuropathy multiplex, hepatitis c viral infection, and mixed cryoglobulinemia had axonal degeneration by EMG and vasculitis of the epineurial vessels on sural nerve biopsy. There was no evidence of viral particles in the nerve by immunofluorescence. Treatment with interferon alfa improved the patient's symptoms and cleared the hepatitis c viral RNA and cryoglobulins from the serum.
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6/12. 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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7/12. Leucocytoclastic vasculitis associated with hepatitis c virus antibodies.

    The actiopathogenesis of leucocytoclastic vasculitis is still unknown, but recently hepatitis c virus (HCV) has been suggested as trigger of autoimmunity. We report a case of a 26-yr-old patient with purpura due to leucocytoclastic vasculitis associated with hepatitis c virus infection. Laboratory findings showed AST, ALT, gamma GT within normal limits, positive antibodies to HCV (IIF and Riba II) and polymerase chain reaction for HCV RNA. Anti-nuclear antibodies, IgG and IgM anti-cardiolipin antibodies, anti-platelet antibodies and anti-neutrophil cytoplasmic antibodies with perinuclear pattern were also present. A skin biopsy specimen of a purpuric lesion showed leucocytoclastic vasculitis with small vessel thrombosis and perivascular deposition of IgM and fibrinogen on immunofluorescence study. This case shows a role of HCV in leucocytoclastic vasculitis; it is possible that this HCV can induce autoimmunity independently of cryoglobulins and liver involvement.
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8/12. Temporal arteritis symptoms in a patient with hepatitis c virus associated type II cryoglobulinemia and small vessel vasculitis.

    We describe temporal artery localization of hepatitic C virus related cryoglobulin induced vasculitis in a 66-year-old woman. The patient had features of both cryoglobulin induced vasculitis (palpable purpura, arthralgia, hypocomplementemia, no inflammatory syndrome) and temporal arteritis (recent onset of headaches, jaw claudication). In the temporal artery biopsy, the vasculitis was localized to a small adventitial artery and did not involve the superficial temporal artery. Thus temporal arteritis and jaw claudication can be signs of cryoglobulin induced vasculitis.
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9/12. Successful treatment of severe hepatitis c-associated pulmonary vasculitis in a liver transplant recipient.

    BACKGROUND: We report the clinical course of a patient who developed fever, hypoxia, and bilateral pulmonary infiltrates two and a half years after orthotopic liver transplantation (OLT) for cirrhosis due to hepatitis c. The patient had a history of hepatitis c-associated vasculitis manifested by purpuric skin rashes, renal abnormalities, and elevated cryoglobulins, and was receiving interferon-alpha at the time of presentation. RESULTS: The results of bronchoscopy with bronchoalveolar lavage were unrevealing, and open lung biopsy revealed active small vessel vasculitis. The patient responded dramatically to plasmapheresis and the addition of high-dose corticosteroids with resolution of hypoxia, pulmonary infiltrates, and glomerulonephritis. This is, to our knowledge, the first report of the successful treatment of hepatitis c-associated pulmonary vasculitis after OLT. CONCLUSIONS: We conclude that hepatitis c-associated pulmonary vasculitis should be included in the differential diagnosis of a patient presenting with fever, hypoxia, and pulmonary infiltrates after OLT for hepatitis c. Treatment with plasmapheresis and high-dose corticosteroids may be effective in patients with this disorder.
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10/12. Scarring alopecia and sclerodermatous changes of the scalp in a patient with hepatitis c infection.

    hepatitis c virus (HCV) is a common cause of chronic hepatitis and is frequently associated with extrahepatic disease. Recently, cutaneous disorders have been a presenting manifestation of HCV infection. porphyria cutanea tarda (PCT) is one of the cutaneous diseases associated with hepatitis c. PCT manifests in an acute form with tense bullae and erosions and in a chronic form with milia, scarring, and sclerodermatous changes. HCV has also been implicated as a cause of vasculitis through immune complex deposition. We report a patient in whom HCV was associated with sclerodermoid PCT and a medium vessel vasculitis. This case underscores the importance of HCV and its potential cutaneous manifestations, as well as the importance of recognizing cutaneous manifestations of internal disease that may be the first clue to diagnosis of HCV.
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