LEEDS, UK—Three patients who developed new-onset psoriasis after rituximab (Rituxan®) treatment have raised a troubling new concern about the growing use of this B-cell depleting therapy in a widening group of rheumatic diseases. The cases are reported in the August issue of Arthritis & Rheumatism.¹

"These cases suggest that the pathogenesis of psoriasis may not require normal numbers of B-cells and that proposed treatment of psoriasis and psoriatic arthritis with rituximab may result in unpredictable responses," wrote the research team led by Shouvik Dass, MA, MB, BChir, MRCP, of the University of Leeds, in the UK. "The interpretation of this possible side effect of rituximab remains unclear, but a B-cell-depleted environment may induce abnormal T-cell responses, possibly provoked either by subclinical infection or by the removal of mechanisms whereby B-cells regulate T-cells."

New-onset psoriasis in three patients treated with rituximab

The researchers described the cases of three patients who had no known risk factors for psoriasis but developed them after receiving rituximab for a variety of indications including seropositive and seronegative rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). One of the patients also developed features of psoriatic arthritis following B-cell depletion with rituximab.
The underlying disease responded well to rituximab in all these cases.

The first case was a 17-year-old girl with seronegative RA who was treated with a standard course of rituximab. Her B-lymphocyte cells were depleted within 4 months of the second infusion. She saw an improvement of symptoms immediately after administration, but the improvement lasted for only 6 weeks. Six months after rituximab therapy, she developed scalp psoriasis, onycholysis, pan-uveitis, and ruptures on her Achilles tendon. She received systemic and topical therapy, but both the skin and joint disease are still active.

The second case was a 52-year-old woman with RA. She did not respond to anti-TNF therapy and received standard rituximab treatment. She showed sustained B-cell depletion for about 1 year, and her rheumatoid factor (RF) levels also decreased. She developed psoriatic plaques on her knees and thighs 4 months after the second infusion at a time of complete B-lymphocyte depletion. The lesions were treated with topical steroids for 3 months and have not since recurred.

The third case, a 26-year-old with SLE, received a standard course of rituximab. She achieved B-lymphocyte depletion within 1 month, and it was sustained for 16 months after therapy ceased. Four months after therapy, however, the patient developed widespread psoriasis on her elbows, arms, thighs, and trunk. The skin lesions were accompanied by onycholysis. She partially responded to steroids and now takes azathioprine and oral prednisolone.

"Our experience with these ceases suggest that it ought to be used with caution in patients in whom the diagnosis of RA, as opposed to psoriatic arthritis, is uncertain," the researchers conclude.

Skin tissue studies needed

"I am aware that studies are under way regarding the use of rituximab in psoriasis and psoriatic arthritis and we hope to gain greater understanding about the biology of B-cell depletion in psoriasis with more focused clinical and skin tissue studies," said Philip J. Mease, MD, at the department of internal medicine at the Swedish Medical Center and Rheumatology Associates, in Seattle, Washington.

"I certainly take heed of the new findings and its important information to consider as we gain further understanding about the potential pros and cons of using B-cell depletors or modulators in the context of autoimmune disease," he told CIAOMed.

"It was not until after we had learned about the highly significant benefits of anti-TNF drugs for psoriasis that we learned about the rare chance of anti-TNF drugs stimulating the appearance of psoriasis," Dr. Mease ended.

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