Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The specific antigens to antineutrophil cytoplasmic antibodies (ANCA) and their relations with renal diseases begin to be well-known. In patients with systemic vasculitis, two major antigens have been recognized: proteinase 3 and myoloperoxydase. These enzymes are located in the azurophilic granules of neutrophils and migrate to the surface of these cells when they are activated. Other antigens, such as elastase, lactoferrin, CAP57 and cathepsin G, have been identified, but they are less commonly encountered. The presence of ANCA is particularly frequent in Wegener's granulomatosis, microscopic periarteritis, crescentic necrotizing glomerulonephrites without immunoglobulin deposits; it is less frequent in periarteritis nodosa and in Churg-Strauss' syndrome. ANCA can now be considered as markers of vasculitis; they are related to disease activity and can be used to evaluate the effectiveness of treatments.
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PMID:[Anti-cytoplasmic antibodies of polynucle or "ANCA". A new class of autoantibodies]. 141 Nov 80

Antibodies against cytoplasm of neutrophil leucocytes (ANCA) with a high sensitivity are found in idiopathic necrotizing vasculitis and idiopathic glomerulonephritis with formation of sickles (IGS). C-ANCA are directed against the myeloid lysosomal enzyme--proteinase 3 and are found above all in Wegener's granulomatosis and microscopic polyarteritis. P-ANCA are directed mainly against myeloperoxidase, less against leucocytic elastase or lactoferrin and are found above all in microscopic polyarteritis, IGS, polyarteritis nodosa or Churg-Strauss syndrome. The elevated ANCA level correlates with the activity of the disease or precedes a relapse. These autoantibodies activate probably neutrophil leucocytes for respiratory exacerbation and degranulation which may lead to extensive tissue damage.
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PMID:[Antineutrophil cytoplasmic antibodies--ANCA]. 146 72

The diagnostic potential of assays detecting anti-neutrophil cytoplasm antibodies (ANCA), anti-GBM antibodies and anti-dsDNA antibodies was evaluated by examining sera from time of admission in a consecutive series of 455 patients with biopsy verified primary or secondary glomerulonephritis (GN). ANCA were classified into c- and p-ANCA by indirect immunofluorescence (IIF) and ELISAs using alfa-granule extract, proteinase-3, myeloperoxidase (MPO), elastase and lactoferrin. C-ANCA was virtually confined to 64 patients with systemic small vessel vasculitis, 66-74% being c-ANCA positive. P-ANCA against MPO, seen in 47 patients, segregated through many diagnostic categories of primary and secondary severe GN. ANCA against lactoferrin and elastase were rare. Anti-dsDNA positive patients constituted 57% of the 44 ANA-positive patients with systemic lupus erythematosus. It is concluded that the IIF and ELISAs for anti-proteinase-3, anti-MPO, anti-dsDNA and anti-GBM have an acceptable performance and are useful in the primary diagnostic work-up of patients suspected for secondary GN as the majority of such patients will be classified by these assays.
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PMID:Anti-neutrophil cytoplasm antibodies, anti-GBM antibodies and anti-dsDNA antibodies in glomerulonephritis. 147 49

The antigenic specificity and clinical distribution of the antineutrophil cytoplasmic antibodies (ANCA) in kidney diseases have recently been extensively studied. In patients with systemic vasculitis, the great predominance of two major ANCA antigens, proteinase 3 (PR3) and myeloperoxidase (MPO), is now established. PR3 and MPO are colocalized in the azurophilic granules of neutrophils and translocated to the cell surface during activation, and thus are able to interact with autoantibodies after neutrophil preactivation. Furthermore, by comparison of amino acid and DNA sequences, it has been shown that PR3 is identical to myeloblastin, which has been described independently and is involved in the control of growth and differentiation of leukemic cells. Aside from the two major ANCA antigens, a number of neutrophil cytoplasmic antigens recognized by ANCA have been identified, including human leukocyte elastase, lactoferrin, CAP57, and cathepsin G. These rare ANCA specificities occur in a limited number of patients. The variety of ANCA antigen specificities contrasts, however, with the fact that the vast majority of ANCA-positive sera are monospecific for one single ANCA antigen. With regard to clinical distribution, ANCA have major diagnostic significance in the four conditions in which they are frequently detected: Wegener's granulomatosis (WG), Churg and Strauss Syndrome (CSS), microscopic periarteritis (MPA), and necrotic and crescentic glomerulonephritis (NCGN). However, the initial dichotomy between MPO-associated vasculitis (NCGN, MPA) and that associated with anti-PR3 antibodies (WG) appears far from absolute.
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PMID:Antigen specificities and clinical distribution of ANCA in kidney diseases. 172 65

The authors studied the dynamics of C4-component of complement (C4), lactoferrin (LF), leukocytic thermostable alpha-glycoprotein (LT alpha G) in the blood serum of 54 patients with rheumatoid arthritis, 32 patients with systemic lupus erythematosus, 8 patients with systemic vasculitis under the effect of hemosorption (HS), enterosorption (ES) and also immunosuppressants (IS). In severe forms of systemic rheumatic diseases the blood serum exhibits a decreased content of C4 but an elevated level of LF and LT alpha G. It has been established that HS is more active than ES or IS, and it influences the mechanisms of humoral immunity. This finds its expression in normalization of C4 level. The favourable clinical effect of HS correlates with a decrease in the level of LF and LT alpha G in the blood serum of patients during treatment.
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PMID:[Levels of the C 4 component of the complement, lactoferrin and leukocytic thermostabile alpha glycoprotein during the treatment of patients with systemic rheumatic diseases]. 267 97

Previously it was shown that tissue injury occurring in acute immune-complex-induced vasculitis, which is complement and neutrophil-dependent, is significantly attenuated by the presence of catalase, suggesting the pathogenic role of H2O2 generated from activated neutrophils. We now show that significant protection is also afforded by pretreatment of animals with apolactoferrin , a naturally occurring chelator of iron. Iron-saturated lactoferrin is devoid of protective effects. Deferoxamine mesylate, a synthetic iron chelator, also has protective effects. Infusion of ionic iron, especially Fe(III), potentiates the tissue injury. Significant protection from tissue injury is also produced by treatment of rats with dimethyl sulfoxide, a potent hydroxyl radical scavenger. Morphologically, animals treated with these protective interventions show the influx of neutrophils into sites of immune complex deposition, but there is markedly attenuated edema, little or no hemorrhage, and little evidence of endothelial cell injury, in contrast to the findings in nonprotected animals. These data support the suggestion that immune-complex-induced injury may be linked to generation of H2O2 from activated neutrophils and the subsequent conversion of H2O2 to the hydroxyl radical.
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PMID:Evidence for a role of hydroxyl radical in immune-complex-induced vasculitis. 623 6

In a serological laboratory with a routine service for determining autoantibodies to human neutrophils, antibodies giving a selective or preferential reaction with the nucleus or perinuclear area of neutrophils are not uncommon. The aim of this study was to look for clinical correlates with the presence of such neutrophil-reactive autoantibodies. The specificity of such antibodies for nuclear or cytoplasmic antigens was studied in 65 consecutive sera displaying nuclear/perinuclear reactivity at a titre of at least 80 using the indirect immunofluorescence technique (IIF) on ethanol-fixed leucocytes. The sera were also investigated by IIF on formalin-acetone fixed leucocytes and on HEp-2 cells. ELISA techniques were used to measure antibodies to azurophil granule constituents (ANCA), purified myeloperoxidase (MPO-ANCA), and lactoferrin (LF-ANCA). Furthermore a qualitative spot immunoassay was used for the detection of antibodies to alpha, beta, and gamma fractions, and the nuclear fraction of neutrophils, purified proteinase 3 (PR3), MPO, enolase, lysozyme, elastase, lactoferrin, and cathepsin G. The diagnoses linked to such GS-ANA/pANCA positivity were arthritides, vasculitides, inflammatory bowel disease and chronic hepatic conditions. MPO was the main antigen recognized in the vasculitis group, but apart from that, rather limited antigen reactivity was demonstrable by these techniques, lysozyme being the most frequently recognized autoantigen in patients with arthritides. Human lymphocytes served as a suitable control substrate when distinguishing between GS-ANA/pANCA and ANA, whereas HEp-2 cells usually could not be used if both classes of antibodies were present in a sample. Furthermore, formalin-acetone fixation is not recommended for routine use.
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PMID:Clinical correlates and substrate specificities of antibodies exhibiting neutrophil nuclear reactivity--a methodological study. 749 88

Sera from 85 HIV-infected patients were tested for the presence of antilactoferrin antibodies (anti-LF Abs) by specific ELISA. Fifty-seven sera were found positive, including sera from asymptomatic (18/28, 64.3%, mean O.D.: 0.27 +/- 0.05) and symptomatic patients (39/57, 68.4%, mean O.D.: 0.82 +/- 0.15). In the control group, only one out of 26 normal donors show any reactivity (mean O.D.: 0.06 +/- 0.01). None of the tested patients had clinical evidence of vasculitis, the previous reported antilactoferrin-associated pathology and if, in both groups, a similar frequency of anti-LF Abs was found, the autoantibody level was significantly higher among the symptomatic patients (p < 0.01). However, correlation was found neither with polymorphonuclear cell counts nor with the level of circulating lactoferrin. The characterization and the clinical significance of the autoantibodies are under investigation.
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PMID:Antilactoferrin autoantibodies associated with HIV infection. 788 52

This review discusses recent developments in infectious tubulointerstitial nephritis, including bacterial virulence factors, the interaction between leukocytes and bacteria, and early events in inflammation. In the area of vasculitis, little-studied specificities of antineutrophil cytoplasmic antibodies (ANCAs), including lactoferrin and elastase, plus newly described ANCAs with alpha-enolase specificity are discussed, along with newer studies on the pathogenesis of ANCA-mediated damage and animal models for ANCA-related vasculitis.
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PMID:Tubulointerstitial nephritis and vasculitis. 792 64

We aimed at confirming the antigen specificity recognized by anti-neutrophil cytoplasm antibodies (ANCA) in patients presenting systemic vasculitis with anti-myeloperoxidase (MPO) activity on ELISA. Thirty-five consecutive patients with reactivity in anti-MPO ELISA and systemic microscopic vasculitides were tested in slot and Western blot analyses. Eleven of 35 sera exhibited binding in Western blot studies with the MPO preparation used in the ELISA: five sera bound at the size of MPO, but five sera reacted with a 78 kD species (p78) co-purifying with MPO, and one serum blotted both MPO and p78. Sequence analysis and antigen-specific assays including Western blot studies showed that p78 is lactoferrin. All anti-lactoferrin positive sera, but no anti-MPO positive sera, also exhibited anti-nuclear binding on HEp2 cells with specificity for histone. We concluded that: (a) a subgroup of patients presenting systemic vasculitis with false anti-MPO reactivity on ELISA had anti-lactoferrin antibodies; (b) anti-lactoferrin was associated with anti-nuclear activity with specificity for histone; (c) these patients had systemic vasculitis without histological evidence of immune complex deposition.
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PMID:Autoantibodies to lactoferrin and histone in systemic vasculitis identified by anti-myeloperoxidase solid phase assays. 793 32


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