Atypical pigmentary purpura: A clinical, histopathologic, and genotypic study

Crowson, A. Neil; Magro, Cynthia M.; Zahorchak, Robert J.

doi:10.1016/s0046-8177(99)90216-2

Cited by 64 publications

(52 citation statements)

References 29 publications

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“…In this context, in half of our cases a monoclonal population of T lymphocytes was observed, confirming previous observations by Toro and coworkers 11 and by Crowson and coworkers. 23 A similar finding was recently published by Magro and coworkers. 24 However, their inclusion criteria differed, and approximately 40% of patients with PPPD having monoclonal populations of T lymphocytes were reported to have clinicopathologic features consistent with MF.…”

Section: Commentsupporting

confidence: 86%

Lichen Aureus

Fink‐Puches¹,

Wolf²,

Kerl³

et al. 2008

Arch Dermatol

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Section: Commentsupporting

confidence: 86%

Lichen Aureus

Fink‐Puches¹,

Wolf²,

Kerl³

et al. 2008

Arch Dermatol

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“…Although the aetiopathogenesis is unknown, steroids, antihistaminics, griseofulvin, ciclosporin, systemic steroids, psoralens, carbromal, carbutamide, meprobamate, glipizide, acetaminophen, zomepirac sodium, interferon α, diuretics, chlordiazepoxide and aminoglutethimide are implicated in a minority of cases 3 7 – 9. A cell-mediated immune reaction has been proposed as the pathomechanism 7 10. Drugs that precipitate PPD act as haptens, leading to the formation of antibody–antigen complexes that deposit in the endothelium causing vascular disruption 11 12.…”

Section: Predominantly Perivascular Dermatitismentioning

confidence: 99%

Drug-induced cutaneous pathology

Ramdial¹,

Naidoo²

2009

J Clin Pathol

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Drug-induced cutaneous rashes, whether confined to the skin or part of a systemic disease, are characterised by a spectrum of inflammatory disease patterns that include perivascular dermatitis, nodular and diffuse dermatitis, vesiculobullous lesions, pustular eruptions, sclerodermoid reactions, vasculitis, folliculitis/perifolliculitis and panniculitis. While a single drug can elicit a range of reaction patterns, no reaction pattern is specific for a particular drug. Although the temporal link between initiation of drug therapy and the onset of the drug rash is critical to the diagnosis, drug reactions may also occur during the course of chronic drug ingestion. Clues to the drug-induced nature of the cutaneous eruption include the presence of overlapping histological reaction patterns and incongruent clinical and histopathological features. While eosinophils are an important tell-tale sign of a drug-induced reaction, they may also be conspicuous in skin rashes devoid of a drug association. Furthermore, eosinophils may be sparse or absent in some drug exanthems. Heightened awareness of the mimicry of a wide spectrum of cutaneous pathology by an ever-increasing range of therapeutic agents is pivotal to the diagnosis of drug-induced skin pathology.

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“…Thus, it is not possible to know if histological signs of MF were present from the beginning. However, histology, immunohistochemistry and TCR gene analysis are not always sufficient to distinguish PPD from early MF [3,4].…”

Section: Discussionmentioning

confidence: 99%

“…Since the beginning of the 1990s, MMF has been used as an immunosuppressive agent to prevent acute rejection after organ transplantation [2]. MMF has also been used alone or in combination with corticosteroids in autoimmune blistering diseases such as bullous pemphigoid [3][4][5], pemphigus vulgaris [4][5][6] and pemphigus foliaceus [4,7]. Recently, 2 reports on the therapeutic effect of MMF in epidermolysis bullosa acquisita (EBA) have been published with conflicting results [8,9].…”

Section: Discussionmentioning

confidence: 99%