Lymphomatoid Papulosis Followed by Pityriasis Lichenoides: A Common Pathogenesis?

Vonderheid, Eric C.; Kadin, Marshall E.; Gocke, Christopher D.

doi:10.1097/dad.0b013e3181f4d8c3

Cited by 21 publications

(24 citation statements)

References 72 publications

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“…Some experts still believe, however, that PLEVA/PLC and LyP reside within a similar spectrum of often clonal T-cell lymphoproliferative disorders. 62,63 The histologic changes of PLEVA include those of interface dermatitis, with basal vacuolar degeneration and a sparse to moderately dense lymphocyte-predominant, superficial, and, typically, deep perivascular inflammatory infiltrate. [56][57][58]64 Scattered necrotic keratinocytes within the epidermis, not seen typically weeks to months and may recur.…”

Section: Pityriasis Lichenoidesmentioning

confidence: 99%

Mimics of Cutaneous Lymphoma

Sarantopoulos

Palla

Said

et al. 2013

American Journal of Clinical Pathology

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The Society for Hematopathology and European Association for Haematopathology workshop, from October 27 to 29, 2011, in Los Angeles, CA, exhibited many exemplary skin biopsy specimens with interesting inflammatory changes mimicking features of cutaneous lymphoma. This article reviews features observed in cutaneous lymphoid hyperplasia, cutaneous drug reactions, lupus-associated panniculitis, pityriasis lichenoides, hypereosinophilic syndrome, histiocytic necrotizing lymphadenitis, traumatic ulcerative granuloma with stromal eosinophils, and pigmented purpuric dermatosis, as well as a brief review of the pertinent literature and discussion of submitted conference cases. For the pathologist, it is important to be aware of diagnostic pitfalls as well as the limitations of ancillary testing (eg, clonality studies). Finally, correlation with total clinical information, good communication with clinical colleagues, close clinical follow-up with rebiopsy, and prudent use of laboratory studies are vital and will likely offer the best path toward a correct diagnosis.

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Section: Pityriasis Lichenoidesmentioning

confidence: 99%

Mimics of Cutaneous Lymphoma

Sarantopoulos

Palla

Said

et al. 2013

American Journal of Clinical Pathology

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“…The first theory implicates infections (Epstein-Barr virus or Toxoplasma gondii ) as the triggers of PL 21 22. The second includes PL as a primary lymphoproliferative disorder, based on studies with detection of clonal CD4+ T cell populations in patients with the disease 23. This last concept supports the link between PL and CD, since CD is presumed to be caused by and enhanced reactivity of CD4+ T cells to gluten 6.…”

Section: Discussionmentioning

confidence: 83%

Skin and coeliac disease, a lot to think about: a case series

Vaz¹,

Franco

Santos

et al. 2018

BMJ Case Reports

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Coeliac disease (CD) is an autoimmune disease, characterised by a permanent sensitivity to gluten. It is being progressively recognised as a multisystemic disease, with multiple extraintestinal manifestations. Skin conditions (eg, dermatitis herpetiformis) are an example of its manifestations; however, its underlying mechanisms are still not well understood. This article presents three cases of uncommon skin conditions in patients with a history of CD. Two of them concern linear IgA bullous dermatosis and erythema nodosum, which have been described in the literature as having potential associations with CD, though only a few cases were reported. The third case corresponds to pityriasis lichenoides-a rare lymphoproliferative disorder of unknown aetiology-, which has no correlation with CD in the literature reviewed. The authors aim to draw attention to the possibility of CD as a potential predisposing factor for the occurrence of these skin diseases.

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“…Although the pathogenesis of LyP and pcALCL is unknown, we and other investigators have speculated that a virus or other persistent antigen source acts to stimulate susceptible memory T cells that ultimately develop genetic alterations that favor disease development and progression [40,41]. In this regard, it might be informative to study CD30CLPD for IgE antibodies against staphylococcal and streptococcal superantigens, given the role of staphylococcal superantigens in the pathogenesis of atopic dermatitis [42], and the similar eruptive nature of LyP and acute guttate psoriasis which has been shown to be mediated by streptococcal superantigens [43,44].…”

Section: Discussionmentioning

confidence: 99%