Psoriasis and palmoplantar pustulosis associated with tumor necrosis factor-α inhibitors: The Mayo Clinic experience, 1998 to 2010

被引:81
作者
Shmidt, Eugenia [2 ]
Wetter, David A. [1 ]
Ferguson, Sara B. [3 ]
Pittelkow, Mark R. [1 ]
机构
[1] Mayo Clin, Dept Dermatol, Rochester, MN 55905 USA
[2] Mayo Clin, Mayo Med Sch, Coll Med, Rochester, MN 55905 USA
[3] Ctr Med & Surg Associates PC, State Coll, PA USA
关键词
adalimumab; etanercept; infliximab; palmoplantar pustulosis; plaque psoriasis; psoriasis; tumor necrosis factor-alpha inhibitor; TNF-ALPHA; INTERLEUKIN-1-RECEPTOR ANTAGONIST; ARTHRITIS; THERAPY; EXACERBATION; BIOLOGY;
D O I
10.1016/j.jaad.2011.05.038
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Background: Tumor necrosis factor (TNF)-alpha antagonists have been associated with the induction of de novo or worsening psoriasis. Objective: We sought to retrospectively examine the clinical characteristics and outcomes of patients with psoriasis associated with anti-TNF-alpha therapy. Methods: We performed a retrospective review of patients with new-onset or worsening psoriasis during TNF-alpha inhibitor therapy between 1998 and 2010. Results: Of the 56 patients (mean age at psoriasis onset, 48.1 years), 41 (73%) were female. In all, 22 patients (39%) had Crohn's disease and 14 (25%) had rheumatoid arthritis. Thirty patients (54%) were treated with infliximab, 19 (34%) with adalimumab, and 7 (12%) with etanercept. New-onset or worsening psoriasis occurred after a mean treatment duration of 17.1 months. Plaque psoriasis (n = 27), palmoplantar pustulosis (n = 25), scalp psoriasis (n = 12), generalized pustular psoriasis (n = 7), erythrodermic psoriasis (n = 2), and inverse psoriasis (n = 2) were the cutaneous presentations. Among the 39 patients for whom full treatment response data were available, 33 (85%) had a complete or partial response; combined response rates (complete and partial) were slightly higher among those who discontinued anti-TNF-alpha therapy (16 of 17 patients [94%]) than among those who continued anti-TNF-alpha therapy (17 of 22 patients [77%]). Limitations: Retrospective nature, possible referral bias, and lack of complete follow-up for some patients are limitations. Conclusion: Although some patients sufficiently controlled their psoriasis while continuing anti-TNF-alpha therapy, those who discontinued therapy achieved higher rates of complete response. Further studies should explore the efficacy and safety of switching to an alternative anti-TNF-alpha agent. (J Am Acad Dermatol 2012;67:e179-85.)
引用
收藏
页码:E179 / E185
页数:7
相关论文
共 24 条
[1]   An Autoinflammatory Disease with Deficiency of the Interleukin-1-Receptor Antagonist [J].
Aksentijevich, Ivona ;
Masters, Seth L. ;
Ferguson, Polly J. ;
Dancey, Paul ;
Frenkel, Joost ;
van Royen-Kerkhoff, Annet ;
Laxer, Ron ;
Tedgard, Ulf ;
Cowen, Edward W. ;
Pham, Tuyet-Hang ;
Booty, Matthew ;
Estes, Jacob D. ;
Sandler, Netanya G. ;
Plass, Nicole ;
Stone, Deborah L. ;
Turner, Maria L. ;
Hill, Suvimol ;
Butman, John A. ;
Schneider, Rayfel ;
Babyn, Paul ;
El-Shanti, Hatem I. ;
Pope, Elena ;
Barron, Karyl ;
Bing, Xinyu ;
Laurence, Arian ;
Lee, Chyi-Chia R. ;
Chapelle, Dawn ;
Clarke, Gillian I. ;
Ohson, Kamal ;
Nicholson, Marc ;
Gadina, Massimo ;
Yang, Barbara ;
Korman, Benjamin D. ;
Gregersen, Peter K. ;
van Hagen, P. Martin ;
Hak, A. Elisabeth ;
Huizing, Marjan ;
Rahman, Proton ;
Douek, Daniel C. ;
Remmers, Elaine F. ;
Kastner, Daniel L. ;
Goldbach-Mansky, Raphaela .
NEW ENGLAND JOURNAL OF MEDICINE, 2009, 360 (23) :2426-2437
[2]   THE CUTANEOUS LYMPHOCYTE ANTIGEN IS A SKIN LYMPHOCYTE HOMING RECEPTOR FOR THE VASCULAR LECTIN ENDOTHELIAL CELL-LEUKOCYTE ADHESION MOLECULE-1 [J].
BERG, EL ;
YOSHINO, T ;
ROTT, LS ;
ROBINSON, MK ;
WARNOCK, RA ;
KISHIMOTO, TK ;
PICKER, LJ ;
BUTCHER, EC .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 174 (06) :1461-1466
[3]   IL-1RL2 and Its Ligands Contribute to the Cytokine Network in Psoriasis [J].
Blumberg, Hal ;
Dinh, Huyen ;
Dean, Charles, Jr. ;
Trueblood, Esther S. ;
Bailey, Keith ;
Shows, Donna ;
Bhagavathula, Narasimharao ;
Aslam, Muhammad Nadeem ;
Varani, James ;
Towne, Jennifer E. ;
Sims, John E. .
JOURNAL OF IMMUNOLOGY, 2010, 185 (07) :4354-4362
[4]   Psoriasiform lesions induced by tumour necrosis factor antagonists: a skin-deep medical conundrum [J].
Carter, J. D. ;
Gerard, H. C. ;
Hudson, A. P. .
ANNALS OF THE RHEUMATIC DISEASES, 2008, 67 (08) :1181-1183
[5]   Psoriatic Skin Lesions Induced by Tumor Necrosis Factor Antagonist Therapy: Clinical Features and Possible Immunopathogenesis [J].
Collamer, Angelique N. ;
Battafarano, Daniel F. .
SEMINARS IN ARTHRITIS AND RHEUMATISM, 2010, 40 (03) :233-240
[6]   Psoriasis and pustular dermatitis triggered by TNF-α inhibitors in patients with rheumatologic conditions [J].
de Gannes, Gillian C. ;
Ghoreishi, Mchran ;
Pope, Janet ;
Russell, Anthony ;
Bell, David ;
Adams, Stewart ;
Shojania, Kamran ;
Martinka, Magdalena ;
Dutz, Jan P. .
ARCHIVES OF DERMATOLOGY, 2007, 143 (02) :223-231
[7]  
Flier J, 2001, J PATHOL, V194, P398, DOI 10.1002/1096-9896(200108)194:4<397::AID-PATH899>3.0.CO
[8]  
2-S
[9]  
Furst DE, 2001, ANN RHEUM DIS, V60, pIII2
[10]  
Guilloteau K, J IMMUNOL, DOI [10.4049/jimmunol.0902464, DOI 10.4049/JIMMU-NOL.0902464]