As more rheumatologists and dermatologists have begun to use biological agents such as TNF-α blocker, they have been confronted with an unexpected complication: psoriasis was paradoxically aggravated or induced by the TNF-α blocker (). This paradoxical onset or aggravation of psoriasis is both interesting and embarrassing because TNF-α blocker is considered a drug that controls psoriasis. Aggravation, as in this case, can develop regardless of the type of TNF-α blocker and, among the subtypes of psoriasis, palmoplantar pustulosis develops most commonly8
Case reports of new onset or exacerbation of preexisting psoriasis following treatment with anti-TNFα therapy (6; our case)
Although the exact mechanism of this paradoxical skin condition has not yet been determined, several theories have been proposed. First, TNF-α blocker activates the auto-reactive T-cells causing autoimmune-related tissue destruction9
. Second, TNF-α blocker induces IFN-α over-expression in the tissue, which could also cause psoriasis7
. Third, considering the heterogeneity of psoriasis, TNF-α blocker reduces some plaque types of psoriasis while pustular psoriasis appears to be induced by TNF-α blocker2,9
. Fourth, antibody formation against infliximab contributes to development or aggravation of psoriasis3
In this case, the deterioration of psoriasis cannot simply be explained as an association with the underlying CD or its disease activity, although the prevalence of psoriasis with CD is three times more than that in the general population1
. In this patient, there was no flare up of CD during the treatment with infliximab and some laboratory data, including erythrocyte sediment rate or C-reactive protein, remained within the normal range. In addition, it was not until the fourth infusion of infliximab that her psoriasis became aggravated, which could be explained by the fact that T-cells generally reactivate after prolonged repeated use of TNF-α blocker3
. Lastly, withdrawal of infliximab reduced her psoriasis while infusion of infliximab worsened her psoriasis repeatedly.
We report a case in which preexisting psoriasis vulgaris was repeatedly aggravated during treatment with infliximab for CD, which is a rare rheumatologic disease in Korea. Most previously reported cases were confined to new onset of pustular psoriasis induced by TNF-α blocker for underlying rheumatologic disease.
New onset or aggravation of TNF-α blocker-induced psoriasis is regarded as a more common phenomenon than previously recognized and users of TNF-α blockers should pay attention to complications in such cases.