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Psoriasis often responds well to biologic inhibitors of tumor necrosis factor-α (TNF-α). Paradoxically, it also appears that psoriasis or psoriatic palmoplantar pustulosis sometimes develops in patients being treated with TNF-α inhibitors.
De Gannes and co-workers describe new-onset psoriasis (13 cases) or severe exacerbation of psoriasis (2 cases) in patients receiving TNF-α inhibitors for various rheumatologic conditions. Ubriani and Van Voorhees describe three more such cases. Add these to more than 50 other reports, and the sum suggests a causal relationship between the agents etanercept, infliximab, and adalimumab and the development of psoriasis.
What is happening? The de Gannes group suggests that interferon-α (INF-α) is involved. INF-α is an essential element in the development of early psoriasis, and TNF-α downregulates INF-α production. Therefore, the use of TNF-α inhibitory drugs neutralizes TNF-α and facilitates INF-α production, which allows psoriasis to develop.
de Gannes GC et al. Psoriasis and pustular dermatitis triggered by TNF-α inhibitors in patients with rheumatologic conditions. Arch Dermatol 2007 Feb; 143:223-31.
Ubriani R and Van Voorhees AS. Onset of psoriasis during treatment with TNF-α antagonists: A report of 3 cases. Arch Dermatol 2007 Feb; 143:270-2.
Fiorentino DF. The yin and yang of TNF-α inhibition. Arch Dermatol 2007 Feb; 143:233-6.
Comment
For clinicians, several points are relevant: First, TNF-α inhibitors may precipitate psoriasis, palmoplantar pustulosis, or new-onset psoriasis, perhaps after a delay of months or years. Second, the induced psoriasis will often respond to local therapies and even to continued treatment with TNF-α inhibitors. Third, many exacerbations are pustular, and many affect the palms and soles. Fourth, this development was the exception rather than the rule. Some difference in these patients led them to develop psoriasis, and understanding this difference will probably tell us something important about the disease.