Article Text

  1. C. C. Striebich
  1. University of Colorado Health Sciences Center, Denver


A 47-year-old African American male with a seven year history of plaque psoriasis was referred to rheumatology for the evaluation and management of arthritis. He had no history of previous joint pain or inflammatory arthritis associated with his psoriasis (psoriatic arthritis, PsA). He had participated in a three-month clinical trial of efalizumab for his psoriasis and had done well during the trail with an improvement in his skin disease. He was off efalizumab for approximately one month, and then obtained efalizumab on a compassionate basis. This course of therapy did not seem to improve the patients psoriasis to the extent experienced during the clinical trial. Over the next two months the patient developed worsening joint pain and stiffness, primarily in the knees and ankles. He presented to the emergency room where his left ankle joint was aspirated, yielding synovial fluid with a WBC count of 26,500. On exam in the rheumatology clinic, the patient was in moderate distress due to joint pain. There was synovitis of both knees and the left ankle. There was psoriatic involvement of 40% of his body surface area. Efalizumab in a humanized monoclonal antibody to CD11a that is FDA approved for the treatment of moderate to severe plaque psoriasis. Leukocyte function-associated antigen-1 (LFA-1) is a member of the β2 integrin family that mediates the adhesion of leucocytes to endothelial cells as part of the migration of cells into tissues. The β2 integrin family consists of heterodimers of unique α chains and a common β chain (CD18). There are four members of the family, LFA-1 (CD11a/CD18), Mac-1 or CR3 (CD11b/CD18), p150, 95 (CD11c/CD18), and CR4 (CD11d/CD18). Binding of LFA-1 by efalizumab disrupts the interaction of LFA-1 with ICAM -1 on vascular endothelial cells. It is believed that the mechanism of action of efalizumab is the blocking of cutaneous entry of CD8+ T cells into the skin. Discontinuation of efalizumab has been associated with worsening of psoriasis. PsA is a chronic inflammatory seronegative arthritis which occurs in approximately 7% of individuals with psoriasis. The onset of arthritis may be coincident with the development of psoriasis or may not appear for many years after the start of skin disease. This report describes the temporal association of the development of inflammatory arthritis with the worsening of psoriasis following the discontinuation of efalizumab. While worsening of psoriasis is well described, this is the first report of the new onset of inflammatory arthritis.

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