Incidence and Specificity of p-ANCA in Rheumatic Diseases

Braun, M G; Csernok, Elena; Schmitt, Wilhelm H.; Gross, Wolfgang L.

doi:10.1007/978-1-4757-9182-2_63

Cited by 9 publications

(8 citation statements)

References 2 publications

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“…However, our own observations do not confirm these findings. We and others see an association of pANCA with high Steinbrocker grades and rheumatoid factor positivity, but no significant association with vasculitis o r with a distinct subspecificity (Braun et al 1993). MPO-ANCA are not seen in rheumatoid vasculitis.…”

Section: Panca (Mpo-anca) and Disease Associationcontrasting

confidence: 46%

Antineutrophil cytoplasmic autoantibodies, autoantigens, and systemic vasculitis

Gross

Csernok

Helmchen

1995

APMIS

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Antineutrophil cytoplasmic antibodies (ANCA) encompass a heterogeneous group of autoantibodies targeting antigens in neutrophils (PMN), monocytes, and endothelial cells. ANCA are routinely detected by the indirect immunofluorescence technique (IFT) and at least three different patterns of fluorescence can be distinguished which have been assigned the acronyms cANCA, pANCA and aANCA. cANCA is mostly induced by proteinase 3 (PR3) antibodies (PR3‐ANCA), and pANCA by myeloperoxidase (MPO) antibodies (MPO‐ANCA), while aANCA has unidentified subspecificity. Over the past decade, ANCA have been the subject of extensive investigation. They have proved to be of significant value both as diagnostic tools and for follow‐up in several forms of systemic vasculitis (e.g. Wegener's granulomatosis, WG; microscopic polyarteritis, MPA; Churg‐Strauss syndrome, CSS) which are now termed ‘ANCA‐associated vasculitides’. Furthermore, it is suspected that the presence of ANCA is an important factor in the pathogenesis of these disease groups. Data regarding the detection of ANCA and their diagnostic value and role in the pathogenesis of vasculitic disorders will be discussed in this review. Growing evidence points to a pathophysiological and diagnostic relevance of the distribution of the ANCA target antigens PR3 and MPO (presence in the circulation, on cellmembranes, and in tissue extracellularly). An autoimmune process has been implicated in the pathogenesis of ANCA‐associated vasculitis, but it is uncertain which mechanism underlies the induction of the ANCA‐related immunoresponse. In this paper mechanisms such as antigenic cross‐reactivity between human PMN proteins and extrinsic antigens by molecular mimicry, idiotypic immunoglobulin regulation, and T‐cell reactivity to PR3 and MPO will be discussed.

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Section: Panca (Mpo-anca) and Disease Associationcontrasting

confidence: 46%

Antineutrophil cytoplasmic autoantibodies, autoantigens, and systemic vasculitis

Gross

Csernok

Helmchen

1995

APMIS

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“…Patients with rheumatoid arthritis and pANCA may have a more aggressive clinical course with more frequent systemic complications [35], while antilactoferrin [36] and antilysozyme antibodies [37] have been described in rheumatoid vasculitis [38], and anticathepsin G antibodies in Felty's syndrome [39].…”

Section: Discussionmentioning

confidence: 99%

Autoantibodies and target antigens in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides

Savige

Chang

Wilson³

et al. 1996

Rheumatol Int

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In this study of antineutrophil cytoplasmic antibody (ANCA)-associated diseases, we determined the prevalence of other autoantibodies and the antigen specificities of ANCA. ANA were common, occurring in 7 of 36 (19%) patients with Wegener's granulomatosis, in 16 of 34 (47%) patients with microscopic polyarteritis, in 6 of 11 (55%) patients with segmental necrotising glomerulonephritis and in 8 of 18 (44%) of those with ANCA-associated systemic vasculitis without renal involvement. ANA were associated more often with pANCA and microscopic polyarteritis than with cANCA (P < 0.05). Patterns were speckled (n = 23), homogeneous (n = 10) or nucleolar (n = 4). Anticardiolipin antibodies were also common, occurring in 10 of 25 (40%) patients with Wegener's granulomatosis, in 8 of 14 (57%) patients with microscopic polyarteritis and in 6 of 18 (33%) of those with a systemic vasculitis. However, anticardiolipin antibodies did not correlate with the presence of ANCA in any of the disease groups. Anti-GBM antibodies were demonstrated in only 2 of 25 (8%) patients with Wegener's granulomatosis, in 1 patient with microscopic polyarteritis (1/14, 7%) and in 1 with segmental necrotising glomerulonephritis (1/11, 9%). All four patients with anti-GBM antibodies had either cANCA or pANCA. In the second part of the study, the target antigens of ANCA were determined in Wegener's granulomatosis, microscopic polyarteritis, systemic vasculitis, inflammatory bowel disease, rheumatoid arthritis and systemic lupus erythematosus (SLE). Of the 19 sera with cANCA, 13 (68%) were directed against proteinase 3; other antigens were myeloperoxidase (1/19, 5%), elastase and lactoferrin together (1/19, 5%), lysozyme (1/19, 5%) or unknown (3/19, 16%). Of the 12 (58%) sera from patients with Wegener's granulomatosis who had cANCA, 7 bound to proteinase 3. Antimyeloperoxidase antibodies were present in 14 of 45 (31%) sera with pANCA; other antigens were proteinase 3 (5/45, 11%), elastase (3/45, 78%), lactoferrin (1/45, 2%), cathepsin G (5/45, 11%) or unknown (17/45, 38%). Antimyeloperoxidase antibodies were common in microscopic polyarteritis (6/14, 43%) and systemic vasculitis (5/16, 31%). However, the majority of target antigens in systemic vasculitis and rheumatoid arthritis with pANCA were not determined. "Atypical" ANCA were present in four patients, one with inflammatory bowel disease (1/8, 13%) and three with SLE (3/15, 20%). The specificities were cathepsin G, cathepsin G plus lactoferrin, or unknown in two sera. A recent report has suggested that bactericidal/permeability-increasing protein may be the target in patients with inflammatory bowel disease.

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“…IVIg is used as a form of established therapy or in experimental protocols in an increasing number of autoimmune and systemic innammatory diseases [7]. Tbe mechani.sms of rhe beneficial effect of IVIg are probably mtiltiplcand rely on the different functional portions of the IgG molecule.…”

Section: Modulation Of Pathological Autoimmunity By Ivigmentioning

confidence: 99%

“…The reason for this difference is unknown, although hypertension may contribute to a degree. It should be added that there are occasional cases of large vessel va.sculitis where the distinction between GCA and TA is very difficult if not impossible [7].…”

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confidence: 99%