Background Two treatment-resistant, HLA-B27 positive patients with ankylosing spondylitis (AS-pat.1&2) are described in whom etanercept led to a rapid profound improvement in symptoms as well as normalisation of CRP.
Methods AS-pat.1 is a 37 y.o. male with highly active AS with generalised stiffness and pain. Subcutaneous (s.c.) weekly MTX over one year in addition to the prior regimen of indomethacin 150 mg/d led to only moderate improvement in symptoms and reduction of CRP from 8 mg/dl to 4 mg/dl. A trial of I. V. pamidronate failed. Etanercept 25 mg s.c. twice/wk was added to MTX. He reported an immediate dramatic improvement of symptoms and stopped indomethacin the day after the first injection. CRP normalised. MTX was stopped after 1 month. He describes a “new life” and that he now plays badminton with his children which he was unable to do before.
AS-pat.2 is a 66 y.o. male with longstanding AS and a history of recurrent iritis. He suffered from morning stiffness and from repeated flarings of varying peripheral joints despite corticosteroid joint injections, indomethacin up to 150 mg/d and a 2 1/2 months trial of MTX 15 mg weekly. Etanercept 25 mg s.c. twice weekly led to rapid and dramatic improvement of pain and stiffness within 2 days, such that the patient did not continue MTX. CRP of 3 mg/dl normalised. No new flare of arthritis or iritis has occurred.
Results Both AS-pat. results (follow up of 8 months) appear particularly remarkable since none of the 9 RA pat. (disease duration more than 4 years, more than 3 failed DMARDs) treated with etanercept-DMARD combination in the same practice (community based, single practitioner rheumatology) in a one year period (9/99–8/2000) had a similar response. Only 4 stayed on etanercept, 3 withdrew due to lack of efficacy, 2 because of side effects.
Conclusion The herein described profound improvement of so far treatment resistant AS with etanercept and its superior efficacy for AS compared to RA warrants further confirmation. Etanercept’s only moderate benefit for RA in this setting might be explained by a selection of aggressive cases not having responded to prior DMARD combination therapy.
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