Erythema Elevatum Diutinum

Laymon, Carl W.

doi:10.1001/archderm.1962.01590010028004

Cited by 17 publications

(2 citation statements)

References 12 publications

(4 reference statements)

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“…IC deposition plays a central role in the pathogenesis of HV ( 2 ), IgA vasculitis ( 6 ), UV ( 7 ) and EED ( 1 , 10 ) through complement activation, neutrophilic infiltration, and the release of destructive enzymes leading to vessel damage. Immobilized ICs have been reported recently to induce the release of NETs from human neutrophils in vitro ( 36 ).…”

Section: Discussionmentioning

confidence: 99%

“…Neutrophils degranulate and release free oxygen radicals, vasoactive amines and lysosomal proteolytic enzymes, which cause damage to the vessel wall ( 3 , 4 ). Hypersensitivity vasculitis (HV) ( 2 , 5 ), IgA vasculitis ( 6 ) and urticarial vasculitis (UV) ( 7 – 9 ) are acute SVV, and erythema elevatum diutinum (EED) is a chronic SVV ( 1 , 10 ), which all share IC deposition as a central role in their pathogenesis, and LCV in their histology. Cutaneous polyarteritis nodosa (PAN) is predominantly a medium-sized vessel vasculitis.…”

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confidence: 99%

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Neutrophil Extracellular Traps are Present in Immune-complex-mediated Cutaneous Small Vessel Vasculitis and Correlate with the Production of Reactive Oxygen Species and the Severity of Vessel Damage

Bergqvist

Safi²,

Hasbani³

et al. 2019

Acta Derm Venerol

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Formation of neutrophil extracellular traps has been implicated in autoimmunity. However, the presence and clinical relevance of neutrophil extracellular traps in immune-complex-mediated cutaneous small and medium vessel vasculitides has not been investigated. This study retrospectively analysed 72 patients with histology-proven hypersensitivity vasculitis ( n = 21), IgA vasculitis ( n = 22), urticarial vasculitis ( n = 22), erythema elevatum diutinum ( n = 3) and polyarteritis nodosa ( n = 4). Neutrophil extracellular traps were detected in hypersensitivity vasculitis, IgA vasculitis, urticarial vasculitis and erythema elevatum diutinum, but not in polyarteritis nodosa lesions. Neutrophil extracellular traps were found around inflamed vessels, and their formation was highest early after the onset of vasculitis and decreased progressively thereafter. Neutrophil extracellular traps were strongly correlated with the histological severity of vasculitis and the production of reactive oxygen species. Both hypersensitivity vasculitis and IgA vasculitis showed significantly more neutrophil extracellular traps than did urticarial vasculitis, independent of the histological severity and duration of vasculitis. These results provide evidence on the implication of neutrophil extracellular traps in the early phases of immune-complex-mediated small vessel vasculitis.

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