Cases reported "Vasculitis"

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1/22. A Japanese case of dengue fever with lymphocytic vasculitis: diagnosis by polymerase chain reaction.

    A 37-year-old Japanese male was admitted to Nagasaki University Hospital with abrupt onset of biphasic fever, general malaise and myalgia 9 days after coming back to japan from Manila. He developed a rubella like erythematous rash 3 days after admission and purpuric eruption one week after admission. A biopsied specimen from the purpura revealed lymphocytic vasculitis with T cell dominance and without immunoglobulin or complement deposition around the blood vessels. RT-PCR analysis on peripheral blood mononuclear cells using dengue virus specific primers confirmed the diagnosis of type 3 dengue fever. PCR analysis using virus specific primers is a rapid and valuable method for making a correct diagnosis of dengue fever.
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keywords = lyme
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2/22. Acute respiratory distress syndrome associated with scrub typhus: diffuse alveolar damage without pulmonary vasculitis.

    Pathologic findings of scrub typhus have been characterized by vasculitis of the microvasculature of the involved organ resulting from a direct invasion by orientia tsutsugamushi. We experienced a case of acute respiratory distress syndrome (ARDS) associated with scrub typhus. The case was proven by eschar and high titer of serum IgM antibody (positive at 1:1280). Open lung biopsy showed diffuse alveolar damage (DAD) in the organizing stage without evidence of vasculitis. Immunofluorescent antibody staining and polymerase chain reaction for O. tsutsugamushi failed to demonstrate the organism in the lung tissue. The patient expired due to progressive respiratory failure despite doxycycline therapy. Immunologic mechanism, without direct invasion of the organism, may participate in the pathogenesis of ARDS associated with scrub typhus.
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keywords = lyme
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3/22. Lymphocytic vasculitis in X-linked lymphoproliferative disease.

    systemic vasculitis is an uncommon manifestation of X-linked lymphoproliferative disease (XLP), a disorder in which there is a selective immune deficiency to Epstein-Barr virus (EBV). The molecular basis for XLP has recently been ascribed to mutations within SLAM-associated protein (SAP), an SH2 domain-containing protein expressed primarily in T cells. The authors describe a patient who died as a result of chronic systemic vasculitis and fulfilled clinical criteria for the diagnosis of XLP. Sequencing of this patient's SAP gene uncovered a novel point mutation affecting the SH2 domain. The patient presented with virus-associated hemophagocytic syndrome (VAHS) and later had chorioretinitis, bronchiectasis, and hypogammaglobulinemia develop. He further developed mononeuritis and fatal respiratory failure. Evidence of widespread small and medium vessel vasculitis was noted at autopsy with involvement of retinal, cerebral, and coronary arteries as well as the segmental vessels of the kidneys, testes, and pancreas. Immunohistochemical analysis using antibodies to CD20, CD45RO, and CD8 revealed that the vessel wall infiltrates consisted primarily of CD8( ) T cells, implying a cytotoxic T-lymphocyte response to antigen. EBV dna was detected by polymerase chain reaction (PCR) in arterial wall tissue microdissected from infiltrated vessels further suggesting that the CD8( ) T cells were targeting EBV antigens within the endothelium. The authors propose that functional inactivation of the SAP protein can impair the immunologic response to EBV, resulting in systemic vasculitis.
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4/22. cytomegalovirus infection in systemic necrotizing vasculitis: causative agent or opportunistic infection?

    We report on a 69-year-old woman who presented with myalgia, hearing impairment, fever, night sweats, weight loss, muscular weakness, paresthesia, hypesthesia, and hypalgesia. sural nerve biopsy showed demyelinative and axonal polyneuropathy due to necrotizing vasculitis with fibrinoid necrosis. A positive test for antineutrophil cytoplasmic antibodies (ANCA) with a perinuclear immunofluorescence pattern directed against myeloperoxidase was more suggestive of microscopic polyangiitis (MPA) than of polyarteritis nodosa (PAN), the possible differential diagnoses. In addition, positive tests for cytomegalovirus (CMV) antibodies (immunoglobulin (Ig)M and IgG) and the detection of CMV-dna in sputum specimens by polymerase chain reaction (PCR) were indicative of active CMV infection. Treatment with ganciclovir and anti-CMV immunoglobulin in addition to prednisolone medication for 6 months resulted in rapid improvement of the clinical symptoms without relapse. CMV infection has been described to be related to ANCA-associated vasculitis in non-immunocompromized patients and may be either a causative agent or an opportunistic infection. Identification of a viral etiology in patients with atypical ANCA-associated vasculitides may lead to different, less aggressive treatment approaches, including antiviral therapy.
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5/22. Molecular genetic diagnosis of a primary central nervous system T cell lymphoma.

    Primary central nervous system T cell lymphomas are rare tumors. Histologically, they may be indistinguishable from other entities like inflammatory processes. In such cases, molecular genetic verification of clonal T cell receptor (TCR) gene rearrangements is an indispensable diagnostic tool. Here we present a case where identification of TCR beta and gamma gene rearrangements by polymerase chain reaction was used to differentiate between a vasculitis and a primary CNS T cell lymphoma, which has profound consequences for therapy management and outcome.
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6/22. Small-bowel hemorrhage caused by cytomegalovirus vasculitis following fulminant hepatitis.

    We describe life-threatening vasculitis of the small bowel following fulminant hepatitis. A 35-year-old man was admitted to our hospital due to consciousness disturbance and jaundice. He was diagnosed with fulminant hepatitis, and recovered after intensive medical care that included corticosteroid administration and artificial liver support. During reduction of the dosage of steroid, massive gastrointestinal hemorrhage occurred from the upper jejunum, revealed by arteriography. The hemorrhage could not be stopped, so a portion of the ileum, including the bleeding point, was excised. However, the intestinal hemorrhage continued from several small ulcers remaining outside the resected area. Pathological findings revealed an ulcerative region that was diagnosed as cytomegalovirus (CMV) vasculitis. His serum level of CMV (measured by real-time-detection polymerase chain reaction [PCR]) was high. ganciclovir therapy was started, and manifestations of the CMV infection improved. In addition to CMV, PCR assay for hepatitis a virus (HAV), HBV, HCV, Epstein-Barr virus (EBV), human herpes virus-6 (HHV-6), and herpes simplex virus (HSV) was performed, but no viruses other than CMV were detected. We are the first to report such a case. We conclude that the possibility of CMV enteritis should be considered when patients present with unexplained fever and gastrointestinal hemorrhage following fulminant hepatitis, and we conclude that the early administration of ganciclovir should be considered.
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7/22. Immunology of cutaneous vasculitis associated with both etanercept and infliximab.

    Targeted inhibition of tumour necrosis factor-alpha (TNF-alpha) is an effective therapy in rheumatoid arthritis and Crohn's disease (CD). Infliximab, a monoclonal murine-human chimeric antibody to TNF-alpha, and etanercept, a fusion protein of two p75 chains of the TNF receptor II and the Fc portion of IgG1, are generally well tolerated. Rarely does clinically significant autoimmunity, including drug-induced lupus and vasculitis occur. Immunologic mechanisms underlying the development of autoimmunity in the presence of such powerful immunosuppressants are unknown. We describe a patient with CD, who developed cutaneous vasculitis on etanercept, which worsened significantly with switch to infliximab. Investigation of the associated systemic and local immune response demonstrated the absence of human antichimera antibodies, but mRNA for T-helper 1 cytokines, chemokines and defensins in the skin and elevated angiogenesis factors in the serum, as determined by reverse-transcriptase polymerase chain reaction and enzyme-linked immunosorbent assay. Histopathology revealed a lymphocytic vasculitis composed of T cells. A permanent B-cell line (MD-B) producing extremely high amounts of chemokines and interleukin-6 was established from this patient's peripheral blood. Lesions progressed despite discontinuation of the drugs and (40 mg/day) prednisone but almost completely resolved with single dose of (0.1 mg/kg) intravenous dexamethasone, which may be therapy of choice for this reaction. A few lesions (<10) have recurred intermittently over 4 years of follow-up, suggesting possible persistence of this TNF-inhibitor-triggered autoimmune disease.
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8/22. Granulomatous vasculitis occurring after cutaneous herpes zoster despite absence of viral genome.

    granuloma annulare, sarcoidal and other granulomatous dermatitides, pseudolymphoma, lymphoplasmacytoid lymphoma, and Kaposi's sarcoma have been described as sequelae of herpes zoster. We report a new postzoster reaction, granulomatous vasculitis, that caused flat-topped papules restricted to the affected dermatome. polymerase chain reaction failed to detect varicella-zoster virus in a biopsy specimen. These results suggest that granulomatous vasculitis occurs without persistence of the viral genome and, perhaps, is a reaction to minute amounts of viral proteins.
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9/22. subarachnoid hemorrhage due to borrelia burgdorferi-associated vasculitis.

    We report the case history of a patient who suffered a subarachnoid hemorrhage (SAH) in association with early lyme neuroborreliosis. After a tick bite, this patient developed erythema chronicum migrans and complained of stinging radicular pain in both legs. A computed tomography (CT) scan was performed because of acute headache and nuchal rigidity, which revealed an occipital SAH. cerebrospinal fluid analysis provided further evidence of acute neuroborreliosis. Digital substraction angiography showed irregularities in the right posterior cerebral artery, which might be due to vasculitis, but no aneurysms.
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ranking = 23.570194654789
keywords = borreliosis
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10/22. Successful treatment with adefovir of one patient whose cryoglobulinemic vasculitis relapsed under lamivudine therapy and who was diagnosed to have HBV virologic breakthrough with YMDD mutations.

    We report a patient whose cryoglobulinemic vasculitis recurred due to reactivation of lamivudine-resistant HBV. Our patient with hepatitis b-related cryoglobulinemic vasculitis was administered lamivudine. Her vasculitis regressed, ALT normalized, HBV-dna became negative. Under lamivudine therapy, her cryoglobulinemic cutaneous vasculitis recurred. ALT increased significantly; it was found that tyrosine-methionine-aspartate-aspartate (YMDD) motif in the dna polymerase gene had been replaced by YIDD. Adefovir was added to lamivudine. During follow-up, her purpura disappeared, ALT normalized, HBV-dna became negative. Our patient is the first whose cryoglobulinemic vasculitis recurred under lamivudine, who had a HBV virologic breakthrough with YMDD mutation, and was successfully treated with adefovir.
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