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New-onset psoriasis associated with adalimumab: A report of two cases

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Letter: New-onset psoriasis associated with adalimumab: A report of two cases
Candace J Glenn BS1, Katherina B Kobraei MD2, Jacqueline J Russo MD3
Dermatology Online Journal 17 (9): 15

1. University of Florida College of Medicine, Gainesville, Florida
2. Division of Dermatology, University of Florida, Gainesville, Florida
3. Division of Pathology, University of Florida, Gainesville, Florida


TNF-α inhibitors, including adalimumab, are increasingly used in the management of inflammatory cutaneous, gastrointestinal, and rheumatologic diseases. An untoward class effect of these medications is the development of new-onset psoriasis, particularly in patients treated for rheumatologic diseases without any personal or family history of cutaneous psoriasis. We report two patients that developed cutaneous and histologic changes consistent with psoriasis while receiving treatment with adalimumab for inflammatory arthridities: one patient with Crohn disease and ankylosing spondylitis who tolerated adalimumab for 15 months before developing psoriasis and another patient with rheumatoid arthritis who developed psoriasis 3 years after starting adalimumab. Both patients experienced rapid resolution of their psoriasis after discontinuation of adalimumab.

Case report 1

A 36-year-old white male with a long-standing history of HLA-B27 positive ankylosing spondylitis and Crohn disease, status post ileocolonic resection, was referred for evaluation of a new scaly eruption of 3 weeks duration on his back, upper extremities, and lower extremities. He had no family or personal history of psoriasis or psoriatic arthritis. He denied worsening of his joint or abdominal pain, preceding fever, infection, diarrhea, or urethritis since the onset of his rash. His medications included tramadol, losartan, baclofen, and adalimumab. He had been treated with adalimumab, 40 mg intramuscularly biweekly, for a total of 15 months without side effects. No medication changes were made since the initiation of adalimumab treatment 15 months prior to presentation.

Figure 1Figure 2
Figure 1. Salmon-colored scaly papules on the back

Figure 2. Abdominal scar from ileocolectomy illustrating the Koebner phenomenon with pink scaly plaques of psoriasis

Figure 3
Figure 3. Biopsy reveals dilated superficial dermal capillaries, sparse superficial perivascular lymphocytic infiltrate, hypogranulosis, and focal spongiform pustules.

Physical examination revealed salmon-colored scaly papules on his back and scattered on his upper and proximal lower extremities. Pink scaly plaques were noted to koebnerize to his abdominal scar. Examination of his mouth and nails was normal.

A punch biopsy specimen obtained from a representative lesion showed psoriasiform epidermal hyperplasia with thin club-shaped rete ridges. Dilated tortuous upper dermal capillaries and sparse lymphocytic infiltrate was seen superficially around blood vessels, and there was also hypogranulosis and focal spongiform pustule formation.

After discussion with his rheumatologist and gastroenterologist, adalimumab therapy was discontinued. Symptomatic treatment was initiated with triamcinolone 0.1 percent ointment and daily cetirizine. Four weeks after discontinuation of adalimumab, his psoriasis was nearly resolved with the remaining few papules improving on topical steroid therapy alone. In concurrence with his rheumatologist and gastroenterologist, we advised him to seek alternative treatment for his ankylosing spondylitis and Crohn disease.

Case report 2

A 57-year-old white male with a history of seropositive rheumatoid arthritis presented with a 4-week history of an intensely itchy eruption on his trunk and extremities. He denied a history of psoriasis or psoriatic arthritis and reported no worsening of his joint pain, diarrhea, fever, or infection. His daily medications included aspirin and colchicine for gout, neither of which had any dose adjustments for the last 4 years. He received adalimumab, 40 mg intramuscularly biweekly, for rheumatoid arthritis that he had been tolerating well for 3 years without any prior side effects. Prior ineffective therapies for his pruritic eruption included a medrol dose pack, hydroxyzine, topical fluocinonide 0.05 percent ointment, intramuscular corticosteroids, and colchicine cessation.

Figure 4Figure 5
Figures 4 and 5. Pink scaly papules on the trunk and annular plaques on the thighs

Physical examination revealed excoriated pink scaly papules and plaques on his trunk, and a few scattered on his lower extremities. There were annular pink papules on his anterior thighs and mild scaling of the scalp. Examination of the mouth and nails was normal.

Figure 6Figure 7
Figure 6. Biopsy demonstrates psoriasiform epidermal hyperplasia with dilated superficial dermal capillaries, perivascular lymphocytes, and hypogranulosis.

Figure 7. Neutrophilic microabscesses in the stratum corneum.

Skin punch biopsies of the patient’s thigh and forearm revealed psoriasiform epidermal hyperplasia with dilated tortuous upper dermal capillaries. Lymphocytic and neutrophilic infiltrate is present around blood vessels superficially, and there is loss of the granular layer. Neutrophilic microabscesses are noted within the stratum corneum. These results were discussed with the patient’s rheumatologist and attributed to the anti-TNF treatment, at which time adalimumab was stopped. Symptomatic treatment with topical fluocinonide 0.05 percent ointment and daily cetirizine were initiated. Weeks after discontinuation of the TNF-α inhibitor, the patient was seen for follow up with full resolution of his eruption. The decision was made with the patient and his rheumatologist to discuss other treatment options for his rheumatoid arthritis.


TNF-α inhibitors have impacted the management of inflammatory diseases across multiple medical specialties. Increasingly appreciated by the dermatologist are their various adverse cutaneous effects including eczematous dermatitis, cutaneous lymphoma, herpes simplex infection, bacterial infection, lichenoid dermatitis, erythema multiforme, lupus erythematosus, acute generalized exanthematous pustulosis, hyperhidrosis, urticaria, granuloma annulare, pruritus, folliculitis, xerosis, vasculitis, perniosis-like eruption, seborrheic dermatitis, rosacea, hyperkeratosis, and hyperpigmentation [1, 2].

Anti-TNF agents infliximab, etanercept, and adalimumab have only recently been associated with new-onset psoriasis [1-10]. Adalimumab, in particular, has been noted to cause pustular and palmoplantar psoriasis, but all clinical variants have been observed during treatment with the three anti-TNF agents. The etiology of TNF-α inhibitors and new-onset psoriasis remains uncertain. Several theories have been postulated, mostly involving autoimmune or infectious etiologies [3, 2]. TNF-α regulates production of INF-α, and TNF-α inhibitors may increase INF-α in some patients with a certain genetic susceptibility. This cytokine milieu engenders keratinocyte hyperproliferation, which creates the histological epidermal psoriasiform hyperplasia [4, 5].

The co-occurrence of rheumatoid arthritis and psoriasis of the skin in the same patient is rare. The German national data bank for rheumatologic diseases reported that 0.2 percent of patients with proven rheumatoid arthritis and 0.3 percent of patients with seropositive rheumatoid arthritis simultaneously had cutaneous psoriasis [4].

The British Society for Rheumatology Biologic Register report an incidence rate of 1.04 per 1000 person-years for the development of psoriasis in patients treated with TNF-α inhibitors [6]. Predisposing factors, gender or age predilection, or associated length of TNF-α treatment among reported cases of new psoriasis associated with TNF-α inhibitors are not yet fully elucidated [7]. As observed in our two patients, the latency from drug therapy initiation to skin eruption onset may be several years [2].

Patients with suspected psoriasis associated with anti-TNF therapy should be referred to a dermatologist for histologic confirmation and to exclude other inflammatory and infectious etiologies. Once the diagnosis of drug-induced psoriasis has been confirmed, the degree of tolerability and body surface area involved by psoriatic lesions is assessed to determine whether TNF-α therapy should be continued. Finally, clinical judgment and patient preferences are used to determine the treatment modality for their psoriasis, which may include topical keratolytics, topical corticosteroids, topical vitamin D analogs, PUVA, methotrexate, oral or topical retinoids, and cyclosporine when appropriate [3].

As observed with our patients, the majority of reported cases have improved with discontinuation of the TNF-α inhibitor and the initiation of standard psoriasis treatment. Notably, most patients improve with use of standard psoriasis treatments even when the TNF-α inhibitor is not discontinued [8, 4, 2].

Our cases serve to contribute to the growing subset of patients being treated with TNF-α inhibitors for rheumatologic diseases who have had subsequent development of new-onset psoriasis. Whereas this association is becoming well established, this area requires further study to elucidate pathophysiologic mechanisms and risk factors, as well as to clarify proper management of this specific psoriasis population.


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