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KMID : 0363220170550070480
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Korean Journal of Dermatology
2017 Volume.55 No. 7 p.480 ~ p.481
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New-onset Psoriasis Induced by Adalimumab Administered for Rheumatoid Arthritis
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Suh Hyun-Yi
Kim Kyung-Ho
Ahn Ji-Young
Park Mi-Youn
Youn Jai-Il
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Abstract
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Tumor necrosis factor alpha (TNF-α) is a cytokine central to the pathological responses involved in rheumatoid arthritis (RA), psoriasis, and psoriatic arthritis1. Adalimumab, a recombinant human IgG monoclonal antibody, selectively blocks TNF-α and is considered an alternative therapeutic agent for treatment of RA. However, new-onset psoriasis or the worsening of pre-existing psoriasis is reportedly an adverse effect associated with its use and is defined as a “paradoxical reaction”.
A 54-year-old woman with known history of RA refractory to conventional therapies was treated with adalimumab (40 mg every 2 weeks). She related no history of skin rashes or psoriasis. Throughout the 4 months (until the 8th injection) following treatment initiation, she reported no skin problems, and her arthritis was well controlled. After the 9th injection of adalimumab, she developed erythematous patches with scales on her back. Physical examination showed scattered erythematous patches and plaques on her lower back and legs. Erythematous papules with pustules appeared on the hypothenar area of her left palm (Fig. 1A∼C). A punch biopsy performed on the left leg revealed histopathological findings characteristic of psoriasis. The lesions resolved with use of topical calcipotriol (Daivonexⓡ cream). The biologics that were being administered were changed, and treatment with tocilizumab (interleukin-6 receptor antagonist) was continued for her arthritis, and there were no psoriatic skin lesions noted.
High levels of TNF-α have been found in the synovial fluid of patients diagnosed with RA and psoriatic skin lesions1. The concomitant presence of RA and skin psoriasis in the same patient is rare. The German National Data Bank for Rheumatological Diseases has reported that only 0.2% of patients with RA and 0.3% of patients with seropositive rheumatoid arthritis simultaneously exhibited psoriasis2. The British Society for Rheumatology Biologics Register has reported an incidence of 1.04 per 1000 person-years for the development of psoriasis following treatment with TNF-α inhibitors3. Many of these cases of psoriasis occurred within 9 months of initiating anti-TNFα therapy (median 6 months). Adalimumab, in particular, has been noted to cause new-onset pustular and palmoplantar psoriasis unlike in our case3. The role of TNF-α inhibitors in the etiology of new-onset psoriasis remains unclear. RA patients receiving systemic TNF-α inhibitors exhibit an increased number of Th1 lymphocytes in their peripheral circulation, a possible secondary effect of decreased exchange between previous regions of inflammation (i.e., the joints)4. However, overexpression of interferon alpha (IFN-α) in the tissue could induce T-cell migration to the psoriatic dermis and subsequent cell homing to the epidermis1. Another potential explanation could be related to the heterogeneity of psoriasis. Polymorphisms in the TNF receptor II gene have not only been associated with a lower clinical response to anti-TNF therapy5, but may also play a role in the paradoxical response to TNF-α inhibitors. In the current case, clinical manifestations included a plaque on the trunk and pustular lesions on the palm. TNF-α is a recognized contributor to the development of plaque psoriasis. However, lower expression of this cytokine has been demonstrated in the palmar eccrine sweat glands and in the skin of patients with palmoplantar pustulosis5. This implies the wide variation in clinical symptoms based on levels of TNF-α measured following administration of TNF-α inhibitors. We describe the case of a Korean patient treated with TNF-α inhibitors for the management of rheumatic disease who subsequently developed new-onset psoriasis. We propose that further studies would be needed to investigate risk factors involved in the induction of such paradoxical psoriasis.
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KEYWORD
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Adalimumab, Rheumatoid arthritis, New-onset psoriasis
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