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systemic vasculitis/protease
Veza se sprema u međuspremnik
Page 1 od 31 rezultati
Alpha-1-antitrypsin phenotyping in ANCA-associated diseases: one of several arguments for protease/antiprotease imbalance in systemic vasculitis.
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The vasculitic lesions observed in Wegener's granulomatosis may be partly the consequence of proteases released following activation of neutrophils by ANCA. The activity of these proteases, including proteinase 3 (PR3) and elastase, is normally closely restricted to the inflammation site by a large
Azurocidin is a novel antigen for anti-neutrophil cytoplasmic autoantibodies (ANCA) in systemic vasculitis.
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We isolated a 27-kD protein using cation exchange chromatography from an acid extract of neutrophil granules. N-terminal amino acid sequence analysis of the first 10 residues showed that this protein is azurocidin, a member of the family of neutral serine proteinase found in the neutrophil, which
Antineutrophil cytoplasmic antibodies (ANCA) and systemic vasculitis: update of assays, immunopathogenesis, controversies, and report of a novel de novo ANCA-associated vasculitis after kidney transplantation.
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OBJECTIVE
To characterize antineutrophil cytoplasmic antibodies (ANCA), their major autoantigens, disease associations, and pathophysiology in systemic vasculitides. To describe a patient with a novel de novo ANCA-associated vasculitis after kidney transplantation.
METHODS
We reviewed and compiled
Primary systemic vasculitis with severe α1-antitrypsin deficiency revisited.
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OBJECTIVE
To study the clinical characteristics and epidemiology of the combination of primary systemic vasculitis (PSV) and severe alpha-1 antitrypsin (α1-AT) deficiency.
METHODS
Patients with PSV [granulomatosis with polyangiitis (GPA) (Wegener's), microscopic polyangiitis, eosinophilic
Systemic vasculitis associated with alphal-antitrypsin deficiency.
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We describe a rare case of systemic vasculitis associated with alpha1-antitrypsin (alpha1-AT) deficiency. Mutational analysis of the alpha1-AT gene in this patient revealed a homozygous alpha1-AT Mnichinan variant. Alpha1-AT possesses broad-spectrum inhibitory activity against many serine proteases,
New developments in the treatment of systemic vasculitis.
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Although precise diagnosis of the systemic vasculitides can provide general prognostic information and help to guide initial therapy, recent studies on the long-term clinical course have revealed considerable variation in clinical severity. Therefore, anatomic distribution of involvement and speed
Mediation of endothelial cell damage by serine proteases, but not superoxide, released from antineutrophil cytoplasmic antibody-stimulated neutrophils.
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OBJECTIVE
To evaluate potential mediators of endothelial cell injury in systemic vasculitis associated with antineutrophil cytoplasmic antibodies (ANCAs), we investigated the factors controlling the neutrophil respiratory burst and endothelial release of von Willebrand factor (vWF) during
Alpha 1-antitrypsin genetic polymorphism in ANCA-positive systemic vasculitis.
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Alpha 1-antitrypsin (alpha 1-AT) is the major inhibitor of proteinase 3 (PR3), the main target antigen of antineutrophil cytoplasm antibodies (ANCA) in Wegener's granulomatosis. alpha 1-AT is encoded by a polymorphic gene, with over 75 alleles, defining severely, medium and non-deficient protease
Distinct differences in autoantigen specificity of anti-neutrophil cytoplasm antibodies in systemic vasculitides and other inflammatory diseases.
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BACKGROUND
Anti-neutrophil cytoplasm antibodies in necrotizing vasculitides need to be distinguished from ANCAs in other inflammatory conditions to avoid clinical misinterpretation.
OBJECTIVE
To help clinicians and laboratory scientists recognize and utilize vasculitis-related ANCAs as an aid in
The role of myeloperoxidase in the pathogenesis of systemic vasculitis.
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Wegener's granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome and idiopathic pauci-immune necrotizing crescentic glomerulonephritis are strongly associated with the presence of anti-neutrophil cytoplasmic antibodies (ANCA). These ANCA-associated vasculitides can serologically be
Detection of autoantibodies against myeloid lysosomal enzymes: a useful adjunct to classification of patients with biopsy-proven necrotizing arteritis.
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OBJECTIVE
Assessment of the value of determination of antineutrophil cytoplasmic antibodies (ANCA) and its specificities for classification of patients with biopsy-proven necrotizing arteritis.
METHODS
The serum samples of 28 consecutive patients with biopsy-proven vasculitis involving medium-
Intestinal Wegener's granulomatosis in a patient with severe alpha-1-antitrypsin deficiency resulting from a unique combination of two deficiency alleles (PiZ and PiMProcida).
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Alpha-1-antitripsyn neutralizes the tissue damaging effects of proteases. Alpha-1-antitripsyn deficiency manifests with necrotizing vasculitis. Wegener's granulomatosis is a systemic necrotizing vasculitis that uncommonly affects the gut. The molecular genetics of patients with Wegener's
Association of autoantibodies to myeloperoxidase with different forms of vasculitis.
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Antineutrophil cytoplasmic autoantibodies with specificity for myeloperoxidase (MPO) were found in 53 patient sera that were routinely submitted for antineutrophil cytoplasmic antibody determination. Based on clinical and histologic criteria, 15 of these 53 patients were classified as having
Treatment of hepatitis C virus infection in patients with mixed cryoglobulinemic syndrome and cryoglobulinemic glomerulonephritis.
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Cryoglobulinemia is a common extrahepatic manifestation of infection with hepatitis C virus (HCV). When signs and symptoms of systemic vasculitis or glomerulonephritis occur in the presence of circulating cryoglobulins, this syndrome is called "mixed cryoglobulinemia syndrome" (MCS). Historically,
Concomitant thrombotic thrombocytopenic purpura and ANCA-associated vasculitis in an adolescent.
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Thrombotic thrombocytopenic purpura (TTP) rarely occurs with systemic vasculitis. A 17-year-old girl presented with non-bloody diarrhea, menorrhagia, and syncope. She had severe anemia (hemoglobin = 3.8 g/dl), thrombocytopenia (platelet = 7,000/mm(3)), and acute kidney injury (serum creatinine, Cr =
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