Dermatology Case Answer C: May

Correct!

C) Tumor necrosis factor (TNF)–α-induced palmoplantar pustular psoriasis

Though anti–TNF-α treatments are very effective in treating psoriasis, they may paradoxically induce psoriasis, including a variant of pustular psoriasis. Most frequently, anti–TNF-α-induced psoriasis occurs in the setting of rheumatologic disease, but cases associated with inflammatory bowel disease and with native psoriasis are well documented. Women aged 40 to 50 years are most commonly affected, though cases in men are not uncommon, and cases in children have been described.^1-3 The duration of treatment with anti–TNF-α prior to the development of psoriatic lesions is variable, but the lesions tend to occur beyond the first two weeks of treatment. This delay helps distinguish this condition from a hypersensitivity drug reaction.^1,2

The clinical presentation of anti–TNF-α–induced psoriasis can vary. In some cases, patients present with widespread, well-demarcated erythematous plaques with silvery adherent scale, typical of plaque-type psoriasis. In other patients, the clinical picture is dominated by pustular patches and plaques confined to the palms and soles, resembling palmoplantar pustular psoriasis. The latter form best describes this patient’s case. A recent review confirmed the frequent observation that, while palmoplantar psoriasis accounts for only 1.7% of patients with native psoriasis, it is the most common manifestation of TNF-α–induced psoriasis, with 42.9% of TNF-α–induced cases in the literature reported to be of this subtype.¹ Scalp psoriasis is also common.⁴

Infliximab has been implicated as the most common anti–TNF-α drug to induce psoriasis.^1,5,6 Cases associated with etanercept, adalimumab, and certolizumab pegol have also been described, and most authors believe that anti–TNF-α therapy–induced psoriasis is a class effect.

In patients who are being treated for native psoriasis, anti–TNF-α therapy–induced psoriasis can present with lesions that are distinct and show a different distribution pattern from the original psoriasis.^1,6 This distinction holds true if the patient develops psoriasis when rechallenged with a second anti–TNF-α therapy. Thus, it appears anti–TNF-α medications can cause de novo psoriasis in psoriatic patients, rather than simply exacerbating a preexisting condition.

The management of patients with anti–TNF-α therapy–induced psoriasis is not well established. Many authors recommend initiating or increasing topical therapy (corticosteroids, calcipotriene, or retinoids) for psoriasis as initial therapy. If this is not successful, the anti–TNF-α therapy may need to be discontinued, and/or additional systemic therapy initiated. Discontinuation of the anti–TNF-α agent results in complete or partial resolution in the majority of cases, and switching to a different anti–TNF-α may occasionally be helpful despite the apparent class effect.^2,6,7 In cases with refractory and severe skin disease, the addition of methotrexate, ultraviolet therapy, phototherapy, cyclosporine, or oral retinoinds may be helpful.8 Recently, the use of cyclosporine with transition to ustekinumab has been advocated.⁹