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					The

n e w e ng l a n d j o u r na l

of

m e dic i n e

Psoriasis
To the Editor: In their review of psoriasis, Nestle et al. (July 30 issue)1 focus only on the genetic aspect of this disease. Drugs are not included as a possible trigger of psoriasis. Certain drugs may precipitate psoriasis in persons without a family history of the disease or in predisposed persons, and they may induce psoriatic lesions on clinically uninvolved skin in patients with psoriasis or exacerbate preexisting disease.2 Drugs with undoubted causal associations with psoriasis are beta-blockers, lithium, synthetic antimalarial agents, inhibitors of tumor necrosis factor α, and tetracyclines.3,4 The clinical and histologic features of drug-associated psoriasis do not differ considerably from those of idiopathic psoriasis.5 Complete remission or a return to initial status after drug withdrawal is the sole evidence of drugassociated psoriasis. Chaker Ben Salem, M.D. Houssem Hmouda, M.D. Kamel Bouraoui, M.D.
Faculty of Medicine of Sousse Sousse, Tunisia
1. Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med

our understanding of the genetic and immunologic basis of psoriasis, insights into mechanisms and clinicopathological phenotypes of drug-induced psoriasis are still limited. Current knowledge relies mostly on case reports with inherent problems of scientific validity. As we pointed out in our article, ongoing efforts in the establishment of drug registries1 could address some of these issues. One trigger of psoriasis that might provide important insights into disease mechanisms is imiquimod, a topical immunomodulator and agonist of toll-like receptor (TLR) 7 and 8,2 which induces psoriasiform lesions in mice.3 The triggering of psoriasis with the use of imiquimod is in agreement with a potential role of TLR7-positive plasmacytoid dendritic cells and their secretion of interferon alpha in patients with psoriasis.4 Thus, careful studies of drugs that trigger psoriasis might lead to a better understanding of disease mechanisms. Frank O. Nestle, M.D.
King’s College London London, United Kingdom frank.nestle@kcl.ac.uk

2009;361:496-509. 2. Dika E, Varotti C, Bardazzi F, Maibach HI. Drug-induced psoriasis: an evidence-based overview and the introduction of psoriatic drug eruption probability score. Cutan Ocul Toxicol 2006;25:1-11. 3. Wollina U, Hansel G, Koch A, Schönlebe J, Köstler E, Haroske G. Tumor necrosis factor-alpha inhibitor-induced psoriasis or psoriasiform exanthemata: first 120 cases from the literature including a series of six new patients. Am J Clin Dermatol 2008;9:1-14. [Erratum, Am J Clin Dermatol 2008;9:347.] 4. Fry L, Baker BS. Triggering psoriasis: the role of infections and medications. Clin Dermatol 2007;25:606-15. 5. Tsankov N, Angelova I, Kazandjieva J. Drug-induced psoriasis: recognition and management. Am J Clin Dermatol 2000;1: 159-65.

Dan Kaplan, M.D., Ph.D.
University of Minnesota Minneapolis, MN

Jonathan Barker, M.D.
King’s College London London, United Kingdom
1. Gladman DD, Rahman P, Krueger GG, et al. Clinical and

The authors reply: In Figure 3 of our review article, we list all the major environmental triggers of psoriasis, including drugs. Although important scientific progress has been achieved in

genetic registries in psoriatic disease. J Rheumatol 2008;35:145863. 2. Gilliet M, Conrad C, Geiges M, et al. Psoriasis triggered by toll-like receptor 7 agonist imiquimod in the presence of dermal plasmacytoid dendritic cell precursors. Arch Dermatol 2004;140:1490-5. 3. van der Fits L, Mourits S, Voerman JS, et al. Imiquimodinduced psoriasis-like skin inflammation in mice is mediated via the IL-23/IL-17 axis. J Immunol 2009;182:5836-45. 4. Nestle FO, Conrad C, Tun-Kyi A, et al. Plasmacytoid predendritic cells initiate psoriasis through interferon-alpha production. J Exp Med 2005;202:135-43.

FOXP3 Forkhead Domain Mutation and Regulatory T Cells in the IPEX Syndrome
To the Editor: The immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome, a rare disorder characterized by multiorgan autoimmunity, often results in death in
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infancy.1 The IPEX syndrome results from mutations in the forkhead box P3 (FOXP3) gene, which encodes a transcriptional repressor considered to be the master regulator of differentiation in CD4+

n engl j med 361;17

nejm.org

october 22, 2009

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