Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antineutrophil cytoplasmic antibody (ANCA) test is now available in most routine diagnostic immunology laboratories. Improvement, simplification and standardisation of the testing methodology have enabled it to become more reliable and accessible to clinicians. ANCA has strong association with and is most useful in the diagnosis and management of the ANCA-associated vasculitides which include Wegener's granulomatosis, microscopic polyarteritis, Churg-Strauss syndrome and primary pauci-immune necrotising and crescentic glomerulonephritis. It is found in lower frequency in the other vasculitides and collagen vascular diseases, in chronic inflammatory bowel disease and autoimmune liver disease, and in miscellaneous infective and neoplastic disorders. While the gold standard for ANCA testing remains the indirect immunofluorescence (IIF) assay, identification of ANCA-specific antigens such as proteinase 3 and myeloperoxidase has enabled the development of antigen-specific tests. The antigen-specific solid-phase assays have comparable sensitivity with IIF assays and improved specificity in some instances. However, appropriate use of the ANCA test requires full knowledge of its capabilities and limitations, and the results should always be correlated with clinical data. In particular, it is important to understand that it is not only test sensitivity and specificity, but patient selection that contributes to the positive predictive value and clinical relevance of the test result.
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PMID:The appropriate use of antineutrophil cytoplasmic antibody (ANCA) testing in rheumatic diseases. 958 76

We present the case of a 67-year-old woman with myeloperoxidase (MPO)-antineutrophil cytoplasmic antibody (ANCA)-positive pauci-immune crescentic necrotizing glomerulonephritis and tubulointerstitial nephritis with renal eosinophilic infiltration and peripheral blood eosinophilia. Staining for eosinophil cationic protein indicated that activated eosinophils were involved in the tubulitis, as well as in the glomerular injury. Marked peripheral blood eosinophilia is uncommon in ANCA-positive crescentic necrotizing glomerulonephritis associated with tubulointerstitial nephritis, except in Churg-Strauss syndrome. However, our patient had no clinical history or signs of asthma, no other signs suggestive of allergic diseases, and no histologic findings of granulomas in the kidney, thus failing to fulfill the criteria for Churg-Strauss syndrome.
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PMID:MPO-ANCA-positive crescentic necrotizing glomerulonephritis and tubulointerstitial nephritis with renal eosinophilic infiltration and peripheral blood eosinophilia. 963 50

Anti-neutrophil cytoplasmic antibodies, as detected by indirect immunofluorescence, have limited diagnostic significance as they occur in a variety of inflammatory disorders. The presence of antibodies to defined target antigens of anti-neutrophil cytoplasmic antibodies, that is proteinase 3 and myeloperoxidase, is, however, highly specific for one of the systemic vasculitides, in particular Wegener's granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome, and idiopathic pauci-immune necrotizing crescentic glomerulonephritis. In general, anti-proteinase-3-positive patients show more widespread organ involvement, more granuloma formation, and a more severe initial course of their renal lesions than anti-myeloperoxidase-positive patients; however, there is considerable overlap, and either antibody specificity may be found in the different clinical syndromes. In vitro, anti-neutrophil cytoplasmic antibodies are able further to activate pre-activated neutrophils and monocytes, which can result in endothelial damage. A direct activating effect of anti-neutrophil cytoplasmic antibodies on endothelial cells has been suggested, but those studies should be confirmed. In vivo, experimental data support a pathogenetic role for anti-neutrophil cytoplasmic antibodies, particularly anti-myeloperoxidase, but besides anti-neutrophil cytoplasmic antibodies a second pro-inflammatory stimulus seems to be required to induce lesions. Whether anti-neutrophil cytoplasmic antibodies can be a direct target for treatment has still to be proved. Current immunosuppressive treatment regimens for the anti-neutrophil cytoplasmic antibody-associated vasculitides are, however, unsatisfactory because of side-effects, that is opportunistic infections and malignancies. New treatment regimens, based on new pathogenetic concepts, are currently being tested.
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PMID:What is new with anti-neutrophil cytoplasmic antibodies: diagnostic, pathogenetic and therapeutic implications. 1045 61

Haemosiderin-laden alveolar macrophages are a common finding in patients with alveolar bleeding. Iron-positive macrophages, suggestive of subclinical alveolar bleeding, were found to be fairly common in bronchoalveolar lavage (BAL) fluid in primary systemic vasculitis but uncommon in collagen vascular diseases (CVDs) and rheumatoid arthritis (RA). To substantiate the impression that subclinical alveolar bleeding may be a feature distinguishing between these disorders, fibreoptic bronchoscopy and BAL were performed in 49 patients with active Wegener's granulomatosis or Churg-Strauss syndrome and 44 patients with CVDs or RA, all of them without clinically manifest alveolar bleeding. The percentage of iron-positive cells was compared with clinical and radiological findings. Only a minority of the CVD and RA patients had iron-positive alveolar macrophages; the 95th percentile of the median number of such cells was 5%. Fifty-three per cent of the patients in the vasculitis group had >5% iron-positive cells, with individual counts ranging up to 95%. Patients with iron-positive macrophages had more extensive disease, more frequent microhaematuria, a higher antineutrophil cytoplasmic antibody titre, a higher myeloperoxidase concentration in the BAL fluid and somewhat more frequent low-attenuation opacities in pulmonary high-resolution computed tomography than the patients with a low iron-positive cell count. In conclusion, subclinical alveolar bleeding was, indeed, a common finding in antineutrophil cytoplasmic antibody-associated vasculitis, which distinguished these disorders from lung disease due to collagen vascular diseases or rheumatoid arthritis. Its association with indices of disease activity, although weak in this cross-sectional study, merits a longitudinal study of its value for the long-term monitoring of vasculitis patients.
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PMID:Subclinical alveolar bleeding in pulmonary vasculitides: correlation with indices of disease activity. 1048 38

Wegener granulomatosis (WG), microscopic polyangiitis (MP), and Churg Strauss syndrome (CSS) are rare systemic autoimmune disorders. Common features are anti-neutrophil cytoplasmic antibodies (ANCA) in patient sera. Whereas WG patients show mainly anti-proteinase 3 ANCA, MP and CSS patients typically present anti-myeloperoxidase (MPO) ANCA. ANCA play an important role in the pathogenesis in the vessel wall by activating polymorphonuclear cells (PMN) and increased adhesivity between PMN and endothelial cells via adhesion molecules. Here we investigated major adhesion molecules as predisposition factors via common polymorphisms in or in the vicinity of the candidate genes ICAM-1, e-selectin, PLAUR, CD11b, and CD18. A restriction fragment-length polymorphism in exon 11 of the CD18 gene was associated with MPO-ANCA(+) systemic vasculitis. Our data indicate that a common variant of the CD18 gene confers increased risk for CSS and MP, supporting that genetic factors are involved in the etiology and pathogenesis of ANCA-associated systemic vasculitides.
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PMID:The association of CD18 alleles with anti-myeloperoxidase subtypes of ANCA-associated systemic vasculitides. 1060 85

A 64-year-old Japanese male was admitted to Kotoh General Hospital because of fever and cough on July, 14, 1997. Laboratory data showed hypereosinophilia (11,500/microliter) and high titer of anti-myeloperoxidase antineutrophil cytoplasmic antibody (319 EU). A physical examination revealed progressive peripheral neuropathy. He had been diagnosed as having bronchial asthma since November, 1996. Therefore, he was diagnosed as having Churg-Strauss syndrome (CSS). He was treated with methylprednisolone pulse therapy (500 mg/day for 3 days) and oral prednisolone (PSL, 60 mg/day). However, peripheral neuropathy was rapidly progressive, and echocardiogram revealed cardiac hypofunction (ejection fraction (EF); 39%). He was refereed to Akita University Hospital for further examination. On admission, laboratory data showed hyponatremia (125 mEq/l) with inappropriate secretion of antidiuretic hormone (ADH, 13.0 pg/ml). Atrial natriuretic peptide was normal (26 pg/ml). Urinary osmorality was 488 mOsm/l, and urinary sodium excretion was 86 mEq/l. Renal, adrenal, and thyroid functions were normal. From these data, his hyponatremia was caused by syndrome of inappropriate secretion of ADH (SIADH). After cyclophosphamide-pulse therapy (500 mg) and oral administration of cyclophosphamide (50 mg/day) and PSL (50 mg/day), peripheral neuropathy improved gradually, and his serum sodium returned to normal, but cardiac hypofunction continued. A possible relationship between SIADH and CSS is discussed.
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PMID:[Severe peripheral neuropathy, cardiac hypofunction, and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in a patient with Churg-Strauss syndrome]. 1061 73

We herein describe the case of a 77-year-old woman, who presented clinical and histopathological evidence of giant cell arteritis (GCA) involving the temporal artery, together with a Churg-Strauss syndrome (CSS). Our patient presented positive anti-neutrophil cytoplasmic antibodies (ANCA), with cytoplasmic staining pattern (C-ANCA) that was specific against proteinase 3 (PR3), and also a perinuclear pattern (P-ANCA) with specificity against myeloperoxidase (MPO). To our knowledge, the simultaneous presence in the same patient of both types of antibodies has not been previously reported.
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PMID:Simultaneous presence of C-ANCA and P-ANCA in a patient with concurrent Churg-Strauss syndrome and giant cell temporal arteritis. 1072 62

Antineutrophil cytoplasmic antibodies (ANCA) have proved to be useful serological markers for a subset of vasculitic diseases, including Wegener's granulomatosis, microscopic polyangiitis, and the Churg-Strauss syndrome. The pathogenesis of the ANCA vasculitides remains less clear, including what role, if any, genetic factors play in the expression of ANCA-associated diseases. Familial cases of systemic vasculitis have been reported, and a number of studies have addressed HLA associations of Wegener's and microscopic polyangiitis, but the results have been confusing and inconsistent. We report the first case of P-ANCA-positive vasculitis presenting in a Native American father and daughter. Both patients had systemic vasculitis and were P-ANCA positive with anti-myeloperoxidase (MPO) antibodies.
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PMID:A familial case of P-ANCA glomerulonephritis presenting in a father and daughter. 1079 52

Microscopic polyangiitis, Wegener's granulomatosis, Churg-Strauss syndrome, and pauci-immune necrotizing glomerulonephritis share pathogenic, pathological, and clinical features. They all involve capillaries, venules, arterioles, and small arteries. Approximately 90% of patients have autoantibodies either to myeloperoxidase (MPO-ANCA) or to proteinase 3 (PR3-ANCA). The clinical manifestations of ANCA-small vessel vasculitis are protean. These can be limited to the kidney alone, or may involve the upper respiratory tract, the lungs, the skin, or a number of other organs in various combinations. The characteristic feature of the glomerular lesion is a focal necrotizing glomerulonephritis associated with crescent formation and little or no glomerular staining for immunoglobulin by immunofluorescence microscopy. The renal manifestations can present as a rapidly progressive glomerulonephritis or that of a more indolent, remitting, and relapsing course that leads to substantial glomerulosclerosis. The two main prognostic markers of the long-term outcome are the presence of pulmonary hemorrhage (which accounts for at least half of all deaths) and the entry serum creatinine. The higher the entry serum creatinine, the higher the risk of developing end-stage renal disease. The treatment of ANCA-small vessel vasculitis and glomerulonephritis rests primarily on the use of induction high-dose corticosteroids and cyclophosphamide. Patients with pulmonary hemorrhage also benefit from plasmapheresis. With the use of an alkylating agent, the rate of remission is of the order of 75%, but relapses occur in about 30% of patients who achieve a remission, and in about 17% of patients after renal transplantation. Despite the improved outcome of patients with ANCA vasculitis in the recent decade, their long-term prognosis continues to be primarily determined by a rapid diagnosis, and the prompt institution of therapy.
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PMID:ANCA glomerulonephritis and vasculitis: a Chapel Hill perspective. 1085 33

Microscopic polyangiitis is a non-granulomatous necrotizing vasculitis involving small vessels. Clinical manifestations are highly polymorphic, but rapidly progressive glomerulonephritis is one of the most frequent and most severe manifestations of the disease. Biopsy of an affected organ and detection of circulating anti-neutrophil cytoplasmic antibodies (ANCA) are key elements for the positive diagnosis of microscopic polyangiitis. Biopsies can disclose necrotizing vasculitis affecting small vessels, without granulomas and without immune deposits. ANCA are very specific for microscopic polyangiitis, Wegener's granulomatosis and Churg-Strauss syndrome when they are positive by indirect immunofluorescence and are directed against myeloperoxidase or proteinase 3. Such ANCA are found in about 70% of patients with microscopic polyangiitis. Treatment of severe forms of microscopic polyangiitis is based on the administration of pulse methylprednisolone, oral corticosteroids and cyclophosphamide. In the mildest forms of the disease, one can probably try either to competely avoid using immunosuppressive drugs, or to replace cyclophosphamide with azathioprine. Treatment induces a complete remission of the disease in more than 90% of cases, but about 30% of the patients will experience a relapse, and progressive worsening of renal function can occur in patients with severe chronic renal failure.
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PMID:[Microscopic polyangiitis]. 1089 71


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