Dermatology Online Journal

Development of new-onset psoriasis in a patient receiving infliximab for treatment of rheumatoid arthritis
Chung-Yin Stanley Chan MD¹ John C Browning MD¹, Fiona Larsen MB ChB², Sylvia Hsu MD¹
Dermatology Online Journal 14 (9): 12

1. Department of Dermatology, Baylor College of Medicine, Houston, Texas. shsu@bcm.edu
2. University of Texas Southwestern Medical Center, Dallas, Texas

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Abstract

Infliximab is a chimeric monoclonal antibody that selectively blocks tumor necrosis factor-alpha (TNF-α). It is indicated for the treatment of numerous inflammatory diseases, including rheumatoid arthritis, Crohn disease, ulcerative colitis, ankylosing spondyilitis, and psoriatic arthritis. Infliximab has also been shown to be a well tolerated and highly effective treatment for psoriatic skin lesions. We report an interesting case of unexpected, new-onset psoriasis in a patient on infliximab for rheumatoid arthritis.

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Figure 1

A 68-year-old woman with a history of rheumatoid arthritis presented complaining of red, pruritic papules and plaques on her trunk and extremities for five months. She had been receiving monthly infusions of infliximab for treatment of her rheumatoid arthritis, with development of the lesions. She experienced more lesions as well as increased pruritus following each treatment. Before infliximab, the patient had received etanercept without appearance of the skin lesions. She had not changed any other medications. Review of systems did not yield any history of recent illness or constitutional symptoms. The patient had no family history of psoriasis. Her rheumatoid factor level was 74 U/mL (normal 0-20 U/mL). Physical examination revealed generalized 3-10 mm erythematous, drop-like papules with mild scale on her trunk and extremities (Fig. 1). The lesions spared her palms and soles.

Figure 2

Histologic examination of a biopsy specimen taken from the active lesion on the right upper arm revealed slight acanthosis, focal loss of the granular layer, mounds of parakeratosis containing neutrophils and a sparse infiltrate of lymphocytes in the upper dermis consistent with psoriasis (Fig. 2).

Discontinuation of the infliximab and topical treatment with halobetasol propionate 0.05% ointment led to improvement in the lesions.

Discussion

Infliximab has been shown to be a well tolerated and highly effective treatment for psoriatic skin lesions [1]. Psoriasis can be induced or aggravated by various medications such as beta-blockers, lithium, antimalarial drugs, nonsteroidal anti-inflammatory agents, and tetracyclines [2]. Infliximab has been associated with adverse cutaneous reactions [3], however infliximab-induced psoriasis has not been described until recently. An increasing number of reports in the literature have described the unexpected appearance or worsening of psoriatic skin lesions in patients treated with TNF-α inhibitors, such as infliximab [4-11].

The appearance of psoriasis is counterintuitive as clinical trials have shown that TNF-α inhibitors improve psoriasis [1, 12]. Tumor necrosis factor-alpha appears to play a vital role in the development of psoriasis by increasing keratinocyte hyperproliferation and altering recruitment-effector function of memory T cells. It has been hypothesized that in a select group of patients with genetic predisposition, TNF-α inhibitors could promote an inflammatory autoimmune process in the skin [6]. The development of autoimmunity is evidenced by the induction of antinuclear antibodies in some patients. [14]. Furthermore, TNF-α inhibitors have been shown to potentially increase peripheral T cell reactivity, increasing the likelihood of autoimmunity [15].

The exact cause for this paradoxical worsening of psoriasis while on TNF-α inhibitors has yet to be determined. Because psoriasis is a heterogeneous disease, the complex mechanisms behind this paradoxical phenomenon require further reports and investigation of similar cases. We report this case in order to raise awareness of a possible side effect of infliximab therapy.

References

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