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A nterior and intermediate uveitis are inflammatory processes of diverse causes, including among others, infections, trauma, lymphoproliferative disorders, and ischaemia. The remainder are considered to have an immune pathogenesis with an autoimmune component. For example, uveitis is a common manifestation of spondyloarthropathy (SpA), a related group of disorders, with common clinical, biological, genetic, and therapeutic characteristics.1 Within the SpA group of diseases, considerable overlap between the different disease entities can occur—for example, during the course of ankylosing spondylitis, 40% of the patients will develop acute anterior uveitis (AUU).2 In addition, in patients with AUU, SpA is the most commonly identified systemic disease.3 Moreover, as is true for other diseases within the SpA group, subclinical gut inflammation has been found in patients with AUU.4,5
From a therapeutic perspective, the management of patients with AAU is targeted at stopping the inflammatory process, in the shortest time possible, as otherwise it might result in irreversible damage leading to impaired visual acuity. Most attacks can be managed by topical steroids and mydriatic agents; in severe episodes of iritis periocular injection of corticosteroids may be beneficial. Occasionally, oral administration of steroids is necessary, sometimes in combination with immunosuppressive agents. However, in some patients the uveitis appears to be treatment resistant; in others, the use of steroids is restricted owing to a lack of response, intolerance, or side effects.
The beneficial effects of tumour necrosis factor α (TNFα) blockade with infliximab (Remicade) are well established in Crohn's disease and, more recently, open and placebo controlled studies indicated a significant improvement of articular symptoms of this treatment in patients with SpA.6–8 Considering the disease overlap within the SpA group and the promising therapeutic results of TNFα blockade in this group of diseases, we suggested that this treatment might possibly provide a clinical benefit in SpA related uveitis. Here, we report the effect of TNFα blockade with infliximab on chronic treatment resistant uveitis in a patient with SpA.
CASE REPORT
A 45 year old male patient, with pre-existing SpA (fulfilling ESSG criteria), who was HLA-B27 positive, had been known since 1995 to have recurrent anterior uveitis of the left eye, resulting in reactional vitritis, and ultimately evolving into chronic anterior and intermediate uveitis. Topical treatment with steroid drops failed; subconjunctival injections and systemic steroids were repeatedly needed, with only partial improvement. No consistent benefit with sulfasalazine or cyclosporin was seen. As part of an open label pilot programme for SpA, an induction scheme with infliximab (5 mg/kg at baseline, week 2 and 6) was started. At baseline visual acuity of the left eye was impaired to 0.63, with a Tyndall phenomenon ++. One week after treatment, visual acuity substantially improved to 1.00, with a Tyndall + to +/−. This improvement was sustained up to week 14—that is, eight weeks after the last infusion, after which a relapse occurred. Retreatment (5 mg/kg) at week 14 was, however, again followed by significant improvement of ocular inflammation and visual acuity. From then on, the patient was re-treated every eight weeks and the ocular inflammation stabilised up to 58 weeks. No subconjunctival injections or systemic steroids were needed during this period, so that steroid administration was substantially reduced.
CONCLUSION
In view of the beneficial effects of infliximab in Crohn's disease and in SpA, and the observation of clinical benefit in this patient with steroid resistant SpA related uveitis after treatment with infliximab, further exploration of the therapeutic potential of TNFα blockade in SpA related uveitis seems warranted.