NEW ORLEANS – Induction or exacerbation of psoriasis is a common and paradoxical side effect of anti–tumor necrosis factor-alpha therapy for rheumatologic and inflammatory bowel diseases.

The paradox lies in the fact that anti-TNF agents are a tremendously effective therapy for moderate to severe psoriasis.

So when a patient with Crohn's disease or rheumatoid arthritis in remission induced by anti-TNF therapy suddenly develops severe psoriasis, it creates a clinical conundrum, observed Dr. Brian F. Mandell at the meeting Dr. Mandell is a rheumatologist who is professor and chairman of the department of medicine at the Cleveland Clinic.

Dr. Alice Gottlieb noted that psoriasis induced by TNF blockers is a class effect that, although rare, can be severe and debilitating, especially in cases of palmar-plantar psoriasis.

Unfortunately, palmar-plantar psoriasis is much more common in TNF-blocker-induced/flared psoriasis than it is in the general psoriasis population, Dr. Gottlieb said in an interview.

In his report, Dr. Mandell noted that a strikingly unusual feature of this cutaneous drug reaction is how long it takes to appear. In a recent study by European gastroenterologists and dermatologists, the median interval between the start of infliximab (Remicade) for inflammatory bowel disease (IBD) and the occurrence of psoriasis was 17 months; for adalimumab (Humira), the median interval was 12 months; and with certolizumab (Cimzia), it was 4.5 months, noted Dr. Mandell.

The European study involved 85 patients being treated with anti-TNF agents for Crohn's disease or ulcerative colitis who developed severe skin lesions while their IBD remained quiescent.

Sixty-two patients developed dermatologist-diagnosed psoriasis marked by the classic histologic features, including epidermal hyperplasia, parakeratosis, agranulosis, elongated rete ridges, and dilated dermal capillaries.

Fourteen patients had a history of psoriasis prior to anti-TNF therapy, and another 8 had a family history of the skin disease.

The most frequently affected site was the scalp, in 40 patients. A total of 27 patients had involvement at the axillae, groin, and other flexural sites, which are not typical locations for psoriasis; 21 had both scalp and flexural lesions; and 22 had palmar-plantar psoriasis.

Dr. Mandell's data shed some light on treatments: All 62 patients were promptly placed on topical therapy with corticosteroids, vitamin D analogs, keratolytics, and emollients, with phototherapy being prescribed in selected cases.

Twenty-five patients showed a favorable response, while the remaining 37 had no response at all to topical therapy.

Eighteen patients discontinued anti-TNF therapy altogether, of whom 16 experienced complete regression of their psoriasis. Twenty-six patients switched to a second TNF inhibitor; only 1 showed improvement in skin lesions.

Ten of the 23 patients who developed eczematous lesions had a history of atopy. The median duration of anti-TNF therapy prior to onset of the skin lesions was 11 months for infliximab, 6 months for adalimumab, and 14 months for certolizumab.

The histology was consistent with eczema. The lesions were equally distributed on the scalp, flexural areas, trunk, face, and limbs. Sixteen of 23 patients had a favorable response to topical steroids and emollients. Five patients were switched to a second anti-TNF biologic, but only one experienced resultant skin improvement. Four patients were eventually taken off anti-TNF therapy altogether, with complete clearing of skin lesions in a median of 3 months.

Dr. Gottlieb, chair of dermatology at the Tufts Medical Center, Boston, noted that the best clinical results are obtained when the TNF blocker is discontinued. Often systemic immunosuppression/immunomodulation is required to control psoriasis induced by a TNF blocker (J. Dermatolog. Treat. 2009;20:100-8).

Altogether, recurrent severe skin lesions caused one-third of IBD patients in this study to discontinue anti-TNF therapy. Extrapolating from the broader Lille University gastroenterology experience, the French investigators estimated that patients on anti-TNF therapy have roughly a 5% risk of developing inflammatory skin lesions, and that the need to halt biologic therapy due to an inability to gain control of the skin eruption is around 1% (Clin. Gastroenterol. Hepatol. 2010;8:1048-55).

Dr. Mandell said the European report on anti-TNF-treated IBD patients accurately reflects his own experience in using the biologics for rheumatoid arthritis, although he's had more success than the gastroenterologists in switching patients to a different agent within the anti-TNF class in order to continue with treatment.

But he noted that it's necessary to discontinue anti-TNF therapy altogether in a minority of Rheumatology patients, and even then the psoriasiform reactions don't always resolve.

Dr. Mandell said he had no relevant commercial interests. Dr. Gottlieb declared financial relationships with the following makers of anti–tumor necrosis factor agents: Abbott, Amgen, Centocor, Pfizer, and UCB.

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One striking feature of this anti-TNF-induced cutaneous drug reaction is how long it takes to appear.

Source DR. MANDELL

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Systemic immuno-suppression may be needed to control the psoriasis in some patients.

Source DR. GOTTLIEB

Anti-TNF Therapy May Induce Psoriasis