Literature DB >> 27512196

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Farid E Stephan1, Elio G Kechichian1, Roger N Haber1, Francois G Kamar2.   

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Year:  2016        PMID: 27512196      PMCID: PMC4966409          DOI: 10.4103/0019-5154.185724

Source DB:  PubMed          Journal:  Indian J Dermatol        ISSN: 0019-5154            Impact factor:   1.494


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Sir, Thank you for your comment. Drugs can induce a wide range of severe cutaneous reactions from toxic epidermal necrolysis to hypersensitivity syndromes.[12] These reactions are potentially lethal, and early intervention with drug cessation followed by adequate care is paramount. Tumor necrosis factor (TNF)-alpha inhibitor-induced pseudolymphoma is an important emerging reaction as it was outlined by Lahiri.[1] CD30/Ki-1 is a cell surface molecule of the TNF receptor family that is expressed on a subset of activated lymphocytes. Blockade of the TNF-alpha pathway, while being effective in controlling many autoimmune and chronic inflammatory diseases, may trigger the development of a benign lymphoproliferative process mimicking lymphomas.[3] Five relatively recent cases of TNF-alpha inhibitor-induced pseudolymphomas have been reported in the literature.[34] Infliximab, etanercept, and adalimumab have been implicated. The mean time of onset of pseudolymphoma after drug initiation is 15.55 months. This long interval should raise the awareness of the prescribing physician even if confronted with a relatively late-appearing lesion. Clinical findings range from a solitary infiltrated lesion to erythroderma associated with edema, fever chills, and general status deterioration requiring cyclosporine at doses up to 5 mg/kg/day.[5] Interestingly, infliximab and adalimumab, when used for psoriasis, cleared the psoriatic plaques and induced the appearance of biopsy-proven pseudolymphomas instead of these lesions. Imafuku et al. described an “immunological converse of psoriasis to pseudolymphoma” by stating that while both manifestations might have a common trigger (i.e., trauma), different intrinsic biomolecular pathways can lead to one clinical manifestation or the other.[3] Of note, prognosis is excellent even for the erythrodermic patient and all of the lesions healed in the following months after stopping the TNF-alpha inhibitor. With the increased frequency and ease of prescription of TNF-alpha inhibitors, by both dermatologists and other physicians, the number of reports of these kinds of reactions is expected to grow. Early recognition and biopsy of any suspicious lesion are to be done, and in case of a lymphoid infiltration, the diagnosis of drug-induced pseudolymphoma should be considered.

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  4 in total

1.  Cutaneous pseudolymphoma induced by adalimumab and reproduced by infliximab in a patient with arthropathic psoriasis.

Authors:  S Imafuku; K Ito; J Nakayama
Journal:  Br J Dermatol       Date:  2011-11-08       Impact factor: 9.302

2.  Erythrodermic CD8+ pseudolymphoma during infliximab treatment in a patient with psoriasis: use of cyclosporine as a rescue therapy.

Authors:  Gilles Safa; Karine Luce; Laure Darrieux; Laurent Tisseau; Nicolas Ortonne
Journal:  J Am Acad Dermatol       Date:  2014-10       Impact factor: 11.527

3.  Cutaneous Pseudolymphoma in a Patient With Crohn's Disease Under Infliximab: First Report.

Authors:  Sofia Carvalhana; Ana Gonçalves; José Velosa
Journal:  J Clin Gastroenterol       Date:  2016 May-Jun       Impact factor: 3.062

4.  Lamotrigine-induced Hypersensitivity Syndrome with Histologic Features of CD30+ Lymphoma.

Authors:  Farid Stephan; Roger Haber; Elio Kechichian; Francois Kamar
Journal:  Indian J Dermatol       Date:  2016 Mar-Apr       Impact factor: 1.494

  4 in total

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