Malignant Papulosis of Skin and Cerebrum

Winkelmann, R. K.; Howard, Frank M.; Perry, Harold O.; Miller, Ross H.

doi:10.1001/archderm.1963.01590130060011

Cited by 41 publications

(14 citation statements)

References 5 publications

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“…Anticoagulation with heparin has been utilized in the acutely ill. 31 Other anticoagulation strategies with coumadin have been unsuccessful. 32 Fibrinolytics such as phenformin and ethylestrenol have yielded mixed results. 33,34 Other largely unsuccessful therapies have included sulphonamides, streptomycin, tetracycline, penicillin, corticosteroids, arsenic, chloroquine, azathioprine, methotrexate, low molecular weight dextran, and phenylbutazone.…”

Section: Discussionmentioning

confidence: 99%

Is Degos' disease a clinical and histological end point rather than a specific disease?

High¹,

Aranda²,

Patel³

et al. 2004

Journal of the American Academy of Dermatology

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Section: Discussionmentioning

confidence: 99%

Is Degos' disease a clinical and histological end point rather than a specific disease?

High¹,

Aranda²,

Patel³

et al. 2004

Journal of the American Academy of Dermatology

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“…1,9 Degos 1 suggested that anticoagulants might be beneficial, although they have been ineffective when used by others. 26 We considered the use of oral anticoagulants in our patient in view of the presence of a lupus anticoagulant with its well-recognized association with thrombosis. However, in view of the absence of previous thromboembolic events and the apparent benefit of aspirin in halting the development of new skin lesions, it was decided not to treat with warfarin unless further lesions developed.…”

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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“…23,24 Aspirin plus dipyridamole was used in the two patients with increased platelet aggregation, and the cessation of formation of new lesions coincided with platelet aggregation returning to normal. 26 We considered the use of oral anticoagulants in our patient in view of the presence of a lupus anticoagulant with its well-recognized association with thrombosis. 9 Other treatments that have been tried in the past without success include sulphonamides, streptomycin, tetracycline, penicillin, corticosteroids, arsenic, chloroquine, azathioprine, methotrexate, low molecular weight dextran and phenylbutazone.…”

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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Malignant Papulosis of Skin and Cerebrum

Cited by 41 publications

References 5 publications

Is Degos' disease a clinical and histological end point rather than a specific disease?

Is Degos' disease a clinical and histological end point rather than a specific disease?

Benign Cutaneous Degos' Disease

Benign cutaneous Degos' disease

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