Pictorial CME

Chronic Gout and Osteoarthritis

          

A 75-year-old female underwent kidney transplantation nine years ago for epimembranous glomerulonephritis. Her immunosuppressive regimen consisted of cyclosporine. Over the last few years she noticed progressive increase in swelling of her finger joints. Due to progressive renal failure a Cimino shunt operation was performed on her left arm. Shortly after this procedure she noted a swelling of the right index finger (Fig. 1). Serum-urate and creatinine clearance (Cockcroft-Gault formula) was 570 µmol/l (9.58 mg/dl) and 17 ml/min respectively. A fine needle aspiration of the lesion showed monosodium urate crystals (Fig. 2) without growth of pathogens in the synovial fluid culture. Plain radiograph demonstrated signs of chronic osteoarthritis (Bouchard and Heberden nodes - Fig. 3). In the past, a short course of loop diuretics along with long term cyclosporine-treatment had led to an acute exacerbation of gouty arthritis.

Hyperuricaemia occurs in 5-84% and gout in 1.7-28% of recipients of solid organ transplants.1 Beside hyperuricaemia, obesity, weight gain, hypertension and diuretic use, treatment with cyclosporine is an additional risk factor for the development of gout.1 Cyclosporine may lower glomerular filtration rate which leads to uric acid retention and can cause tubular damage that can reduce urate secretion.2 Chronic osteoarthritis with underlying low grade inflammation can be a site at risk for tophus formation.3,4 In patients suffering from chronic renal dysfunction and hyperuricaemia tophi formation may preferentially occur in joints having low grade inflammation due to chronic osteoarthritis. Effective treatment of the acute exacerbation as well as medication to lower hyperuricaemia should be undertaken. Non-steroidal anti-inflammatory drugs (NSAIDs) are relatively contraindicated in the setting of cyclosporine therapy or renal insufficiency and allopurinol therapy with concomitant azathioprine may result in significant neutropenia. Intraarticular or systemic corticosteroids may be the safest treatment options for acute gouty attacks. Synovial fluid cultures should be performed routinely. Uricosurics are often ineffective in these patients as a result of a glomerular filtration rate of <50 ml/min. Allopurinol, at a dose adjusted for renal function, can be used cautiously in transplant patients taking cyclosporine because rare, severe cases of myoneuropathy have been reported in patients receiving cyclosporine and colchicine.5

This patient was successfully treated with low dose allopurinol and a short course of prednisone.

D Miedinger*, PN Chhajed*, T Daikeler **

*Internal Medicine; **Rheumatology, University Hospital Basel, CH-4031, Switzerland.

Received : 15.1.2007; Revised : 23.2.2007; Re-revised : 4.4.2007; Accepted : 5.4.2007

References

1.     Stamp L, Searle M, O’Donnell J, Chapman P. Gout in solid organ transplantation: a challenging clinical problem. Drugs 2005;65:2593-611.

2.     Lin HY, Rocher LL, McQuillan MA, et al. Cyclosporine-induced hyperuricemia and gout. N Engl J Med 1989;321:287-92.

3.     Simkin PA, Campbell PM, Larson EB. Gout in Heberden’s nodes. Arthritis Rheum 1983; 26:94-7.

4.     Lally EV, Zimmerman B, Ho G Jr, Kaplan SR. Urate-mediated inflammation in nodal osteoarthritis. Arthritis Rheum 1989;32:86-90.

5.     Rana SS, Giuliani MJ, Oddis CV, Lacomis D. Acute onset of colchicine myoneuropathy in cardiac transplant recipients: case studies of three patients. Clin Neurol Neurosurg 1997;99:266-70.