Malignant atrophic papulosis: Absence of circulating immune complexes or vasculitis

Tribble, Karen; Archer, Matt; Jorizzo, Joseph L.; Sánchez, Ramón L.; Solomon, Alvin R.; Gardner, Frank H.; Cavallo, T

doi:10.1016/s0190-9622(86)70180-1

Cited by 34 publications

(17 citation statements)

References 11 publications

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“…There is no strong evidence for an immunological basis-studies of immunofluorescence, circulating immune complexes and lymphocyte transformation tests have been unrevealing. 4,5 Disturbances of coagulation or fibrinolysis have been demonstrated in some cases. Black et al 5 observed complete loss of fibrinolysis in the centre of both early and established papules in two patients.…”

Section: Discussionmentioning

confidence: 99%

Benign Cutaneous Degos' Disease

Harvell

Williford²,

White³

2001

The American Journal of Dermatopathology

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The following case report details a 53-year-old man with a 6-year history of the benign cutaneous or skin-limited form of Degos' disease. Clinically, the patient demonstrated a diffuse eruption of papules on the upper trunk and arms. Many papules demonstrated the classic porcelain-white centers characteristic of Degos' disease, but others exhibited different clinical morphologies that corresponded to the evolutionary stages of papules originally described by Degos. Over the course of several clinic visits, the patient underwent a total of 5 punch biopsies, the histologies of which were correlated with their clinical morphologies. Early papules were skin-colored and demonstrated a superficial and deep perivascular, periadnexal, and perineural chronic inflammatory cell infiltrate associated with interstitial mucin deposition. The overlying epidermis showed a mild vacuolar interface reaction and the histologic appearances at this early stage resembled tumid lupus erythematosus. Fully developed papules were raised with umbilicated porcelain-white centers and a surrounding erythematous rim. Histologically these exhibited a prominent interface reaction with squamatization of the dermo-epidermal junction, melanin incontinence, epidermal atrophy, and a developing zone of papillary dermal sclerosis that resembled the early stages of lichen sclerosus et atrophicus in miniature. These interface reactions were invariably confined to the central portion of the punch biopsy specimen, corresponding to the central porcelain-white area seen clinically. Additional features of fully developed papules included a prominent lymphocytic vasculitis affecting venules, a mild periadnexal infiltrate of neutrophils and/or eosinophils, and interstitial mucin deposition. In late-stage papules, the porcelain-white areas were better developed and the lesion flattened. Histologically, the degree of inflammation was generally sparse and the overall picture mirrored the classic histologic description of Degos' disease with a central roughly wedge-shaped zone of sclerosis surmounted by an atrophic epidermis and hyperkeratotic compact stratum corneum. These late-stage papules closely resembled a miniaturized version of fully developed lichen sclerosus et atrophicus confined to the center of the punch biopsy specimen.

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Section: Discussionmentioning

confidence: 99%

Benign Cutaneous Degos' Disease

Harvell

Williford²,

White³

2001

The American Journal of Dermatopathology

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“…4,5 Disturbances of coagulation or fibrinolysis have been demonstrated in some cases. Although there are a few reports of Degos' disease occurring in two or more first-degree relatives, 2,3 the majority of cases appear to be sporadic.…”

Section: Discussionmentioning

confidence: 99%

Benign cutaneous Degos' disease

Farrell

Moss

Costello

et al. 1998

British Journal of Dermatology

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We report the case of a 44-year-old woman with Degos' disease who also had a lupus anticoagulant. Electron microscopy of the mature lesions showed interwoven tubular structures within the endothelial cells, as have been observed in previous cases of Degos' disease. Four years after her first cutaneous lesions, there is no evidence of involvement of other organs. Aspirin (300 mg daily) has arrested the cutaneous disease.

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“…Die primäre Störung der Erkrankung wird daher auch auf der Ebene der Endothelzellen kleinerer Arterien vermutet [16,29], wobei auf der Basis eines unbekannten Reaktionsablaufes eine Permeabilitätsstörung gefolgt von Ödem und Intimaproliferation den Gefäßverschluss herbei führt [21,32].…”

Section: Pathogeneseunclassified

“…Andere wiesen wiederum IgG nach oder konnten keine Immunkomplexablagerungen finden [2]. Ebenso konnten keine zirkulierenden Immunkomplexe nachgewiesen werden [31,32]. Insgesamt lassen sich somit Immunkomplexen keine eindeutige Rolle in der Pathogenese dieser Erkrankung zuschreiben.…”

Section: Pathogeneseunclassified

Papulosis maligna atrophicans Degos

Mensing

2002

Der Hautarzt

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Malignant atrophic papulosis: Absence of circulating immune complexes or vasculitis

Cited by 34 publications

References 11 publications

Benign Cutaneous Degos' Disease

Benign Cutaneous Degos' Disease

Benign cutaneous Degos' disease

Papulosis maligna atrophicans Degos

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