Co-present rheumatoid arthritis and gout successfully treated with abatacept

Abstract

Dear Editor, We have read with much interest the article by Kuo et al., ‘Rare co-present rheumatoid arthritis and gout: comparison with pure rheumatoid arthritis and literature review’ [1], presenting eight new cases of concomitant rheumatoid arthritis and gout and summarizing 32 reported cases. The authors noticed that over 85% of co-present patients experienced at least one acute gout attack after continuous disease modifying antirheumatic drugs (DMARDs) and nonsteroidal anti-inflammatory drugs administration, while only one patient became totally quiescent after etanercept therapy. It is similar to our observation of a 45-year-old patient with gout and rheumatoid arthritis successfully treated with abatacept. He was admitted to our department in 2001 because of a 12-year experience of recurrent arthritis, associated with erythema, warmth, and swelling. Likemost co-present patients, he had more comorbidities [1–3], i.e., hypertension, glucose intolerance, but, interestingly, no kidney dysfunction. Laboratory tests revealed erythrocyte sedimentation rate (ESR) of 37 mm/h, C-reactive protein (CRP) of 5 mg/L, uric acid (UA) of 0.49 mmol/L, and rheumatoid factor (RF) of 1:40. There were no significant changes in X-rays of his hands and feet. While the diagnosis of gout was confirmed by the presence of monosodium urate crystals on polarized light microscopy (synovial fluid aspirated from left knee), oral colchicine and allopurinol were introduced with improvement. He was readmitted to our department in 2006 due to a 6-month history of persistent pain and swelling of joints of hands and feet, exudation in left knee, and morning stiffness lasting over 2 h. In laboratory tests, ESR revealed 72 mm/h, CRP 58.7 mg/L, UA 0.2 mmol/L, RF 1:80, and anticyclic citrullinated peptide antibodies 136 IU. In synovial fluid aspirated from left knee, not only monosodium urate crystals were found but also rheumatoid factor (1:40), which was previously negative. X-rays of feet revealed symmetrical erosive changes typical for RA with no changes in X-rays of hands and narrowing of left knee joint space. DAS28 score was 6.14. Oral methylprednisolone 6 mg was administered, and the patient was introduced to the program of abatacept therapy for early RA. He had obtained several courses of abatacapt from April 2006 to March 2008. Since the abatacept administration, no further gout attacks were observed, and DAS28 score decreased to 1.86. Both, the patient described by Kuo et al. and our patient, responded very well to biologics, etanercept and abatacept, respectively, with no gout attacks after the introduction of therapy. They were both younger than ‘average’ co-present patients and did not respond well to DMARDs (in 2001, before gout was diagnosed, our patient obtained 6 months MTX therapy, but without any improvement). This might suggest that the introduction of biologics in co-present patients may not only inhibit RA activity but also decrease the frequency of gout attacks.