RESEARCH - TNF-alpha inhibitor-induced psoriasis or psoriasiform exanthemata: first 120 cases from the literature including a series of six new patients

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Am J Clin Dermatol. 2008;9(1):1-14.

Tumor necrosis factor-alpha inhibitor-induced psoriasis or

psoriasiform exanthemata: first 120 cases from the literature

including a series of six new patients.

Wollina U, Hansel G, Koch A, Schönlebe J, Köstler E, Haroske G.

Departments of Dermatology and Allergology, Academic Teaching Hospital

Dresden-Friedrichstadt, Dresden, Germany.

Tumor necrosis factor-alpha (TNFalpha) inhibition is effective in the

treatment of moderate-to-severe psoriasis. We report on 120 patients

from the literature including six new patients (three women and three

men) who developed pustular lesions during treatment with TNFalpha

inhibitors. We identified 72 women and 36 men (several papers did not

specify the gender of patients) with an age range of 13-78 years (mean

42.3 years). The primary diagnoses were rheumatoid arthritis (n = 61),

ankylosing spondylitis (n = 21), psoriasis (n = 10), Crohn disease (n

= 8), SAPHO (synovitis acne pustulosis hyperostosis osteitis) syndrome

(n = 3), psoriatic arthritis (n = 2), and other diagnoses (n = 15).

Psoriasis (except palmoplantar pustular type) was the most common

adverse effect during anti-TNFalpha treatment (n = 73), followed by

palmoplantar pustular psoriasis (n = 37) and psoriasis of the nail (n

= 6), sometimes combined in the same patient. Palmoplantar pustulosis

and psoriasiform exanthema was the diagnosis in ten patients each. A

positive personal history of psoriasis was recorded in 25 patients. A

positive family history was noted in eight patients. No data about

personal (n = 7) or family history (n = 46) were available in a number

of patients. Newly induced psoriasis was diagnosed in 74 patients

whereas an exacerbation or aggravation of a pre-existing psoriasis was

noted in another 25 patients. All three TNFalpha inhibitors available

on the market were involved: infliximab (63 patients), etanercept (37

patients), and adalimumab (26 patients). Several patients were treated

with more than a single TFNalpha inhibitor. The timing of cutaneous

adverse effects (psoriasis and psoriasiform rash) varied considerably

among patients, ranging from after a single application to a delayed

response of up to 63 months after initiation of treatment. The mean

time to appearance of the cutaneous adverse effect for all TNFalpha

inhibitors was 9.5 months. Cessation of the responsible TNFalpha

inhibitor was carried out in 47 patients either alone or in

association with adjuvant anti-psoriatic therapy (mostly topical).

This resulted in complete remission in 21 patients, partial remission

in 20 patients, and stable disease in another three patients; in the

other three patients, the outcome was not reported. TNFalpha

inhibition was continued in 47 patients but anti-psoriatic adjuvant

therapy was introduced. The outcome in this group was complete

remission in 22 patients, partial remission in 25 patients, and stable

disease in 2 patients. The response rate (complete remission plus

partial remission) was 93.2% and 95.9%, respectively, in each group.

In six patients, switching from one TNFalpha inhibitor to another one

immediately after cutaneous adverse effects occurred resulted in an

improvement in five patients. In nine patients, a second TNFalpha

inhibitor was initiated after a break in TNFalpha inhibition. The

response to a second or third drug in these patients was mixed. The

underlying pathomechanisms of induction of psoriasis or psoriasiform

exanthemata by TNFalpha inhibitors remain elusive but there is reason

to assume that induction of such adverse events has more than one

pathophysiology.

PMID: 18092839

http://www.ncbi.nlm.nih.gov/pubmed/18092839

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