Background Acromegalic arthropathy is a noninflammatory condition in which cartilage hypertrophy and hyperplasia lead to the disruption of joint geometry and chondrocyte metabolism, and ultimately to degenerative changes. It is reversible in cases of early and prompt diagnosis. Rheumatoid arthritis is an inflammatory disease with joint destruction. Erosion in rheumatoid arthritis is caused by invasion of articular cartilage by the synovial pannus. Erosion in rheumatoid arthritis may be regressed with early and aggressive treatment. In this report we present a case of acromegaly who developed rheumatoid arthritis.

Methods Case report:A 64-year-old male was admitted in April 2000 for evaluation of a 2-year history of polyarthritis. He was followed in 1985 with symptoms and signs of acromegaly, which was confirmed by radiology and a basal GH level of 30 mU/l. His acromegalic features improved after he had been operated. In 1995, therapy with sandostadin was started. In 1997, he was given external radiation. In 1998, he started to complain symmetric polyarthritis in proximal interphalangial and metacarpophalangial, wrist, and knee joints. In laboratory evaluation, erythrocyte sedimentation rate (ESR) was 93 mm/hour and rheumatoid factor was 685 IU/l. No improvement was observed with the treatment protocol consisting of non-steroid anti-inflammatory drug and exercise which was given in another hospital. Two years later, he was evaluated in our rheumatology clinic. At that time, he had arthritis in PIF, MCF, and wrist joints and three-hour morning stiffness. Bilateral ulnar deviation at MCF joint and interosseous muscle atrophy were observed. In laboratory examination, ESR, CRP, Hb, RF, platelet count were 89 mm/hour, 6.7 mg/dL, 12.6 gr/dL, 789 IU/L, 540000/ml respectively. In radiological evaluation, osteoporosis in lumbar vertebrae and in hand graph were observed. Widening and tufting of distal phalanx and subchondral erosive and cystic changes in PIF and MCF joints were seen. In MRI, synovitis and erosive changes were marked. The patient was diagnosed as rheumatoid arthritis and treated with methotrexate, sulfasalazine, and hydroxychloroquine. After three months of treatment, the patient improved regarding in clinical and laboratory values. He is still being followed by our clinic in good health.

Conclusion The incidence of significant joint complains in large series of acromegalic patients have been reported to be 15%-64%. The changes seen in acromegaly are similar to those seen in degenerative joint disease. The occurrence of rheumatoid arthritis and acromegaly in the same patient are not reported, except one case. The slow progression of the erosive changes in this case proposed that GH might modify the catabolic effect of rheumatoid arthritis. Evaluation of laboratory parameters such as ESR, CRP, RF, thrombocytosis and anaemia help us to make a differential diagnosis of rheumatoid arthritis and acromegaly arthropathy.