Dear Editor,
We read with interest the editorial of Ritchlin and Tausk1 about psoriasiform lesions developed in patients receiving tumour necrosis factor (TNF)α antagonists. We would like to provide additional information. Indeed, we have recently reported 6 cases of psoriasiform lesions during TNFα antagonist therapy and described common characteristics of this paradoxical reaction with 40 cases already published in literature.2
To date, with our series1 and recent reports3-7 pooled together, 55 cases have been described, including one case in a patient with juvenile idiopathic arthritis 2 years after initiation of etanercept.5
One of these cases concerns psoriatic arthritis.6 Interestingly, after an initial resolution of plaque psoriasis with infliximab, the
patient developed an inverse psoriasis (axillae and groin). In this context of pre-existing psoriasis, other cases have been reported: exacerbation of plaque psoriasis treated with infliximab8, development of a guttate psoriasis and a worsening of psoriasis in 2 patients with plaque psoriasis treated with etanercept9, exacerbation of underlying psoriasis (asymptomatic for many years) in 3 patients with rheumatoid arthritis (RA)receiving etanercept or infliximab10, exacerbation of palmoplantar pustulosis (PPP) and apparition of erythematopapular scaly lesions in a patient with RA treated with infliximab.11 These cases of exacerbation
thus highlight that a change in clinical aspects of psoriasis can occur.
We also observed this characteristic in a woman with spondylarthropathy with Crohn’s disease but without a personal history of psoriasis. She developed follicular skin lesions over the trunk, back, pubis, buttocks,
and scalp with infliximab, and then inflammatory lesions over the upper eyelids, neck, and inner thighs with etanercept.2
Finally, we could compare these cases with PPP relapse described recently in 2 out of 4 cases of SAPHO treated with infliximab without active cutaneous manifestations before its initiation12. The latter support the specificity of this cutaneous manifestation for TNF antagonist-induced psoriasis.
Moreover, it is difficult to establish the prevalence of the phenomenon according to diagnosis. Admittedly, RA is the most common etiology in the case reports. Nevertheless, the hypothesis that this is due to the fact that more patients receive TNF antagonists for this
condition could not explain the low representativeness of Crohn’s disease.
This last remark contributes to the mystery of this paradoxical reaction.
REFERENCES
1 Ritchlin C, Tausk F. A medical conundrum: onset of psoriasis in patients receiving anti-tumour necrosis factor agents. Ann Rheum Dis 2006;65:1541-44.
2 Cohen JD, Bournerias I, Buffard V, Paufler A, Chevalier X, Bagot M, et al. Psoriasis induced by tumor necrosis factor-α antagonist therapy: a case series. J Rheumatol 2006 Oct 1; [Epub ahead of print]
3 Sari I, Akar S, Birlik M, Sis B, Onen F, Akkoc N. Anti-tumor necrosis factor-α-induced psoriasis. J Rheumatol 2006;33:1411-4.
4 Aslanidis S, Pyrpasopoulou A, Leontsini M, Zamboulis C. Anti-TNF-α-induced psoriasis: Case report of an unusual adverse event. Int J Dermatol 2006;45:982-3.
5 Peek R, Scott-Jupp R, Strike H, Clinch J, Ramanan AV. Psoriasis after treatment of juvenile idiopathic arthritis with etanercept. Ann Rheum Dis 2006;65:1259.
6 Matthews C, Rogers S, FitzGerald O. Development of new-onset psoriasis while on anti-TNFα treatment. Ann Rheum Dis 2006;65:1529-30.
7 Pirard D, Arco D, Debrouckere V, Heenen M. Anti-tumor necrosis factor alpha-induced psoriasiform eruptions: Three further cases and current overview. Dermatol 2006;213:182-6.
8 Bovenschen HJ, Van De Kerkhof PC, Gerritsen WJ, Seyger MM. The role of lesional T cells in recalcitrant psoriasis during infliximab therapy. Eur J Dermatol 2005;15:454-8.
9 Gottlieb AB, Matheson RT, Lowe N, Krueger GG, Kang S, Goffe B, et al. A randomized trial of etanercept as monotherapy for psoriasis. Arch Dermatol 2003;139:1627-32.
10 Kary S, Worm M, Audring H, Husher D, Renelt M, Soerensen H, et al. New onset or exacerbation of psoriatic skin lesions in patients with definite rheumatoid arthritis receiving TNF-α antagonists. Ann Rheum
Dis 2006;65:405-7.
11 Michaëlsson G, Kajermo U, Michaëlsson A, Hagforsen E. Infliximab can precipitate as well as worsen palmoplantar pustulosis: possible linkage to the expression of tumour necrosis factor-α in the normal
palmar eccrine sweat duct? Br J Dermatol 2005;153:1243-4.
12 Massara A, Cavazzini PL, Trotta F. In SAPHO syndrome anti-TNF-alpha may induce persistent amelioration of osteoarticular complaints, but may exacerbate cutaneous manifestations. Rheumatol 2006;45:730-3.
Dear Editor,
We read with interest the editorial of Ritchlin and Tausk1 about psoriasiform lesions developed in patients receiving tumour necrosis factor (TNF)α antagonists. We would like to provide additional information. Indeed, we have recently reported 6 cases of psoriasiform lesions during TNFα antagonist therapy and described common characteristics of this paradoxical reaction with 40 cases already published in literature.2
To date, with our series1 and recent reports3-7 pooled together, 55 cases have been described, including one case in a patient with juvenile idiopathic arthritis 2 years after initiation of etanercept.5
One of these cases concerns psoriatic arthritis.6 Interestingly, after an initial resolution of plaque psoriasis with infliximab, the patient developed an inverse psoriasis (axillae and groin). In this context of pre-existing psoriasis, other cases have been reported: exacerbation of plaque psoriasis treated with infliximab8, development of a guttate psoriasis and a worsening of psoriasis in 2 patients with plaque psoriasis treated with etanercept9, exacerbation of underlying psoriasis (asymptomatic for many years) in 3 patients with rheumatoid arthritis (RA)receiving etanercept or infliximab10, exacerbation of palmoplantar pustulosis (PPP) and apparition of erythematopapular scaly lesions in a patient with RA treated with infliximab.11 These cases of exacerbation thus highlight that a change in clinical aspects of psoriasis can occur. We also observed this characteristic in a woman with spondylarthropathy with Crohn’s disease but without a personal history of psoriasis. She developed follicular skin lesions over the trunk, back, pubis, buttocks, and scalp with infliximab, and then inflammatory lesions over the upper eyelids, neck, and inner thighs with etanercept.2
Finally, we could compare these cases with PPP relapse described recently in 2 out of 4 cases of SAPHO treated with infliximab without active cutaneous manifestations before its initiation12. The latter support the specificity of this cutaneous manifestation for TNF antagonist-induced psoriasis.
Moreover, it is difficult to establish the prevalence of the phenomenon according to diagnosis. Admittedly, RA is the most common etiology in the case reports. Nevertheless, the hypothesis that this is due to the fact that more patients receive TNF antagonists for this condition could not explain the low representativeness of Crohn’s disease.
This last remark contributes to the mystery of this paradoxical reaction.
REFERENCES
1 Ritchlin C, Tausk F. A medical conundrum: onset of psoriasis in patients receiving anti-tumour necrosis factor agents. Ann Rheum Dis 2006;65:1541-44.
2 Cohen JD, Bournerias I, Buffard V, Paufler A, Chevalier X, Bagot M, et al. Psoriasis induced by tumor necrosis factor-α antagonist therapy: a case series. J Rheumatol 2006 Oct 1; [Epub ahead of print]
3 Sari I, Akar S, Birlik M, Sis B, Onen F, Akkoc N. Anti-tumor necrosis factor-α-induced psoriasis. J Rheumatol 2006;33:1411-4.
4 Aslanidis S, Pyrpasopoulou A, Leontsini M, Zamboulis C. Anti-TNF-α-induced psoriasis: Case report of an unusual adverse event. Int J Dermatol 2006;45:982-3.
5 Peek R, Scott-Jupp R, Strike H, Clinch J, Ramanan AV. Psoriasis after treatment of juvenile idiopathic arthritis with etanercept. Ann Rheum Dis 2006;65:1259.
6 Matthews C, Rogers S, FitzGerald O. Development of new-onset psoriasis while on anti-TNFα treatment. Ann Rheum Dis 2006;65:1529-30.
7 Pirard D, Arco D, Debrouckere V, Heenen M. Anti-tumor necrosis factor alpha-induced psoriasiform eruptions: Three further cases and current overview. Dermatol 2006;213:182-6.
8 Bovenschen HJ, Van De Kerkhof PC, Gerritsen WJ, Seyger MM. The role of lesional T cells in recalcitrant psoriasis during infliximab therapy. Eur J Dermatol 2005;15:454-8.
9 Gottlieb AB, Matheson RT, Lowe N, Krueger GG, Kang S, Goffe B, et al. A randomized trial of etanercept as monotherapy for psoriasis. Arch Dermatol 2003;139:1627-32.
10 Kary S, Worm M, Audring H, Husher D, Renelt M, Soerensen H, et al. New onset or exacerbation of psoriatic skin lesions in patients with definite rheumatoid arthritis receiving TNF-α antagonists. Ann Rheum Dis 2006;65:405-7.
11 Michaëlsson G, Kajermo U, Michaëlsson A, Hagforsen E. Infliximab can precipitate as well as worsen palmoplantar pustulosis: possible linkage to the expression of tumour necrosis factor-α in the normal palmar eccrine sweat duct? Br J Dermatol 2005;153:1243-4.
12 Massara A, Cavazzini PL, Trotta F. In SAPHO syndrome anti-TNF-alpha may induce persistent amelioration of osteoarticular complaints, but may exacerbate cutaneous manifestations. Rheumatol 2006;45:730-3.