Antineutrophil Cytoplasmic Antibodies of IgA Class in Neutrophilic Dermatoses With Emphasis on Erythema Elevatum Diutinum

Ayoub, N.; Charuel, Jean‐Luc; Diemert, Marie‐Claude; Barète, Stéphane; André, M.; Fermand, Jean‐Paul; Piette, Jean‐Charles; Françès, Camille

doi:10.1001/archderm.140.8.931

Cited by 53 publications

(37 citation statements)

References 40 publications

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“…Vários doentes têm doença inflamatória intestinal associada, e há relato de evolução para mieloma múltiplo tipo IgA. 58,[60][61][62][63][64] As lesões cutâneas podem manifestar-se como pápulas, placas papulosas ou nódulos não purpúricos, de curso crônico, eritematosos ou por vezes de cor acastanhada. Preferencialmente ocorrem na superfície extensora das extremidades (Figura 7 A), na pele sobre as articulações das mãos e joelhos, sendo essa distribuição extremamente característica.…”

Section: Erythema Elevatum Diutinumunclassified

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Vasculites dos médios e grandes vasos

Brandt

Arnone

Valente

et al. 2009

An. Bras. Dermatol.

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Resumo:As vasculites são constituídas por um grande grupo de síndromes caracterizadas por inflamação e necrose da parede dos vasos sangüíneos, resultando em estreitamento ou oclusão do lúmen. A distribuição dos vasos envolvidos varia consideravelmente e serve de base para a classificação das síndromes vasculíticas: grandes vasos (arterite de Takayasu, arterite temporal); pequenos e médios vasos (poliarterite nodosa, síndrome de Churg-Strauss, granulomatose de Wegener, vasculites nas doenças reumáticas); e pequenos vasos (vasculite de hipersensibilidade, púrpura de Henoch-Schonlein, poliangeíte microscópica, crioglobulinemia). Este artigo revisa as vasculites dos médios e grandes vasos e opções terapêuticas atuais; além de oferecer orientação sobre abordagem diagnóstica e tratamento dos pacientes com suspeita de vasculite cutânea. Palavras-chave: Anticorpos anticitoplasma de neutrófilos; Arterite de células gigantes; Arterite de Takayasu; Doenças reumáticas; Granulomatose de Wegener; Poliarterite nodosa; Púrpura; Síndrome de Churg-Strauss; Vasculite; Vasculite alérgica cutânea Abstract: Vasculitis comprises a broad group of syndromes characterized by inflammation and necrosis on the walls of blood vessels, resulting in narrowing or occlusion of the lumen. The distribution of involved blood vessel varies considerably and serves as the basis for one classification of vasculitic syndromes: large vessels (Takayasu arteritis, giant cell arteritis); medium and small muscular arteries (polyarteritis nodosa, Churg-Strauss syndrome, Wegener's granulomatosis, vasculitis in rheumatic diseases); and small vessels ("hypersensitivity" vasculitis, Henoch-Schonlein purpura, microscopic polyangiitis, cryoglobulinemia). This article reviews medium and large vessel vasculitis and current treatment options; it also presents a comprehensive approach to diagnosing and treating patients with suspected cutaneous vasculitis.

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Section: Erythema Elevatum Diutinumunclassified

“…O clima frio parece agravar a doença. 58,[60][61][62][63][64] O exame histopatológico das lesões agudas evidencia vasculite leucocitoclástica, podendo haver eosinófilos na derme superior e média. Nas lesões crônicas são observados fibrose, proliferação capilar e infiltrado de macrófagos, plasmócitos e linfócitos.…”

Section: Erythema Elevatum Diutinumunclassified

Vasculites dos médios e grandes vasos

Brandt

Arnone

Valente

et al. 2009

An. Bras. Dermatol.

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“…litis of the skin) (18), cutaneous vasculitis (19), ulcerative colitis (20), and Henoch-Schönlein purpura (21). Some of these IgA ANCA-associated diseases have clinical presentations similar to GPA, with renal and mucosal involvement because of vascular damage from excessive neutrophil activation (4,18). The proinflammatory and anti-inflammatory effects of IgA are determined through engagement with the FcR for IgA: FCAR (also known as FcαRI and CD89) (16).…”

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confidence: 99%

IgA and IgG antineutrophil cytoplasmic antibody engagement of Fc receptor genetic variants influences granulomatosis with polyangiitis

Kelley

Monach

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Granulomatosis with polyangiitis (Wegener's) is a rare autoimmune neutrophil-mediated vasculitis that can cause renal disease and mucosal manifestations. Antineutrophil cytoplasmic antibodies (ANCA) are present in many patients, vary in level over time, and induce neutrophil activation through engagement with Fc receptors (FcRs). Given roles for FcRs in ANCA-mediated neutrophil activation and IgA antibodies in mucosal immunity, we hypothesized that FcR genetics and previously unappreciated IgA ANCA affect clinical presentation. We assembled a total of 673 patients and 413 controls from two multicenter cohorts, performed ELISA and immunofluorescence assays to determine IgA and IgG ANCA positivity, and used Illumina, TaqMan, or Pyrosequencing to genotype eight haplotype-tagging SNPs in the IgA FcR ( FCAR ) and to determine NA1/NA2 genotype of FCGR3B, the most prevalent neutrophil IgG FcR. We evaluated neutrophil activation by measuring degranulation marker CD11b with flow cytometry or neutrophil extracellcular trap formation with confocal microscopy. Functional polymorphisms in FCGR3B and FCAR differed between patient groups stratified by renal involvement. IgA ANCA were found in ∼30% of patients and were less common in patients with severe renal disease. Neutrophil stimulation by IgA or IgG ANCA led to degranulation and neutrophil extracellcular trap formation in a FcR allele-specific manner (IgA:FCAR P = 0.008; IgG:FCGR3B P = 0.003). When stimulated with IgA and IgG ANCA together, IgG ANCA induced neutrophil activation was reduced ( P = 0.0001). FcR genotypes, IgA ANCA, and IgG ANCA are potential prognostic and therapeutic targets for understanding the pathogenesis and presentation of granulomatosis with polyangiitis (Wegener's).

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“…Grabbe et al [13] postulated that EED may be triggered by bacterial peptides via activation of cytokines such as interleukin-8, which induces neutrophil chemotaxis to tissue sites. IgA-ANCA and the antiphospholipid antibodies have been reported in patients with EED, but their contribution to the pathogenesis is unclear [14,15].…”

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confidence: 99%

Erythema elevatum diutinum in systemic lupus erythematosus

Chan

Mok

Tang³

2010

Rheumatol Int

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Erythema elevatum diutinum (EED) is a rare chronic form of leukocytoclastic vasculitis with unknown etiology. EED has been described in association with hematological malignancies, infections and a number of rheumatological diseases. We report a patient with systemic lupus erythematosus (SLE) who presented with intermittent attacks of tender nodules and plaques on the shins and ankles for 6 months. Skin biopsy confirmed the diagnosis of EED. Treatment with dapsone resulted in complete resolution of the skin lesions. EED is rarely reported in SLE, and its presentation and treatment is reviewed.

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Antineutrophil Cytoplasmic Antibodies of IgA Class in Neutrophilic Dermatoses With Emphasis on Erythema Elevatum Diutinum

Cited by 53 publications

References 40 publications

Vasculites dos médios e grandes vasos

Vasculites dos médios e grandes vasos

IgA and IgG antineutrophil cytoplasmic antibody engagement of Fc receptor genetic variants influences granulomatosis with polyangiitis

Erythema elevatum diutinum in systemic lupus erythematosus

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