microscopic polyangiitis/protease

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Propylthiouracil-induced microscopic polyangiitis.

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The use of propylthiouracil (PTU) has been associated with various forms of vasculitis. We herein describe the case of a patient with Grave's disease who, after years of PTU therapy, developed a necrotizing vasculitis with anti-serine protease-3 antibodies. Despite treatment with corticosteroids and

Gabexate mesylate as treatment in the course of ANCA-negative microscopic polyangiitis.

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Patients with small vessel vasculitis present fluctuating antineutrophil cytoplasmic antibodies (ANCA) levels to the point that positive ANCA may be missed even if only up to 10% of patients with microscopic polyangiitis (MPA) are ANCA-negative. The first-line treatment of MPA is the association of

Three wavelength substrate system of neutrophil serine proteinases.

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Neutrophil serine proteases, including elastase, proteinase 3, and cathepsin G, are closely related enzymes stored in similar amounts in azurophil granules and released at the same time from triggered neutrophils at inflammatory sites. We have synthesized new fluorescence resonance energy transfer

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

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 =

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

Genetics of ANCA-associated vasculitides: HLA and beyond.

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The pathogenesis of ANCA-associated vasculitis (AAV) is multifactorial and most likely involves the interaction of environmental and genetic factors. During the past few years, a number of studies have investigated genetic associations with AAV; earlier studies explored associations with single

The diagnostic and prognostic significance of ANCA.

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Antineutrophil cytoplasmic antibodies (ANCA) constitute a family of auto-antibodies directed against various components of the neutrophil cytoplasm. Their identification and association with vasculitis and rapidly progressive glomerulonephritis has led to considering these diseases as possible

Thrombotic thrombocytopenic purpura associated with polyarteritis nodosa.

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We present a case of classical polyarteritis nodosa (PN) overlapping thrombotic thrombocytopenic purpura (TTP). A 70-year-old woman was transferred to our hospital because of general fatigue and fever. On admission, laboratory findings revealed leukocytosis, normochromic normocytic anemia and renal

Antineutrophil cytoplasmic antibodies: major autoantigens, pathophysiology, and disease associations.

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Antineutrophil cytoplasmic antibodies (ANCA) are important serological markers for the primary systemic vasculitides, including microscopic polyarteritis and necrotizing crescentic glomerulonephritis. Numerous reports have established the clinical utility of ANCA titer in monitoring disease

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

Antineutrophil cytoplasmic antibodies: a still-growing class of autoantibodies in inflammatory disorders.

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Antineutrophil cytoplasmic antibodies (ANCA) have been described as sensitive and specific markers for active Wegener's granulomatosis (WG). ANCA in WG produce a characteristic cytoplasmic staining pattern of neutrophils (c-ANCA) and are directed against proteinase 3 (Pr3), a serine protease from

Epitope mapping of anti-proteinase 3 and anti-myeloperoxidase antibodies.

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Anti-proteinase 3 (PR3) and anti-myeloperoxidase (MPO) autoantibodies are present in many patients with Wegener's granulomatosis (WG) and microscopic polyarteritis. The aim of this study was to determine whether these antibodies bound to linear peptide sequences on their target antigens. If common

Antibodies to selected minor target antigens in patients with anti-neutrophil cytoplasmic antibodies (ANCA).

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In patients with anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis, indirect immunofluorescence (IF) distinguishes between cytoplasmic (C-ANCA) and perinuclear (P-ANCA) neutrophil staining patterns. In patients with primary systemic vasculitis such as Wegener's granulomatosis,

Update on clinical, pathophysiological and therapeutic aspects in ANCA-associated vasculitides.

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Anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitides (AAV) comprise the most common group of primary systemic vasculitides and include Wegener;s granulomatosis (WG), microscopic polyangiitis (MPA), Churg-Strauss syndrome (CSS), and renal-limited vasculitis (RLV). AAV share the

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