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Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...

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[Psoriasis induced by infliximab].

Iolanda C Fernandes¹, Tiago Torres, Madalena Sanches

¹Serviço de Dermatologia, Hospital de Santo António, Porto, Portugal.

Acta Medica Portuguesa

|August 4, 2012

Summary

This summary is machine-generated.

Tumor necrosis factor-α inhibitors (anti-TNF-α) can paradoxically induce psoriasis in patients treated for immune-mediated disorders. Discontinuation of infliximab was necessary due to severe skin lesions in a Crohn

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Area of Science:

Immunodermatology
Biologic therapy in immune-mediated disorders

Background:

Anti-tumor necrosis factor-α (anti-TNF-α) agents are widely used for immune-mediated conditions like inflammatory bowel disease and rheumatoid arthritis.
These biologics have also been employed in managing psoriasis.
The efficacy of anti-TNF-α therapy is well-established for various autoimmune diseases.

Observation:

A 35-year-old female with Crohn's disease, treated with infliximab for 10 months, developed severe psoriatic lesions.
Erythematous, scaling plaques appeared on the scalp, back, and umbilical fold.
Skin biopsy confirmed the diagnosis of psoriasis.

Findings:

The patient's psoriasis emerged during treatment with infliximab, a biologic agent.
The severity of the induced psoriatic lesions necessitated the discontinuation of infliximab.
This case highlights a paradoxical reaction to anti-TNF-α therapy.

Implications:

The development of psoriasis during anti-TNF-α therapy presents a clinical challenge.
The exact pathogenic mechanisms underlying drug-induced psoriasis by biologics remain unclear.
Further research is needed to elucidate the reasons for this paradoxical effect and guide treatment strategies.