Chronic Tophaceous Gout
These joint deformities occurred in a 61-year-old man with chronic tophaceous gout. The patient had had joint pain and swelling since he was 40 years old; the symptoms began in 2 fingers and were initially mild. He did not seek medical attention. Within 5 to 10 years, joint abnormalities had developed in the fingers and then in the left elbow and right ankle. The toes were not affected. He had no family history of joint pain or swelling. Serum uric acid level was 9.7 mg/dL.
These joint deformities occurred in a 61-year-old man with chronic tophaceous gout. The patient had had joint pain and swelling since he was 40 years old; the symptoms began in 2 fingers and were initially mild. He did not seek medical attention. Within 5 to 10 years, joint abnormalities had developed in the fingers and then in the left elbow and right ankle. The toes were not affected. He had no family history of joint pain or swelling. Serum uric acid level was 9.7 mg/dL.
The 4 main phases of gout are asymptomatic hyperuricemia, acute gouty arthritis, intercritical (asymptomatic) gout, and chronic tophaceous gout. The last is characterized by hyperuricemia (serum uric acid level above 7 mg/dL) and large accumulations of monosodium urate (MSU) crystals in joints, bones, and soft tissues. After many untreated attacks of gout, MSU crystals form tophi that can cause erosion and resorption of bone. Tophi generally develop within affected joints, although the location may vary.
MSU crystal deposits are especially prevalent in distal areas because of precipitation at cooler temperatures. Although tophi may not be painful, periodic acute inflammation around the site can cause intense pain.
When treatment is started before tophi are visible or palpable and before bone destruction occurs, drug therapy can control the disease.1 Patients with gout require long-term treatment with uricosuric agents or xanthine oxidase inhibitors to lower the serum uric acid level.2 Maintaining a level below 6 mg/dL may increase dissolution of MSU crystals, lower the risk of recurrent gout attacks, and reduce tophaceous deposits.3-5
Start antihyperuricemic medications at a low dose, and gradually increase the dosage.6 Lowering serum urate levels can take weeks or months. Rapid urate lowering can cause shedding of crystals from urate deposits, which can result in an acute gout flare or urinary stone formation.4 To avoid an acute flare, colchicine or an NSAID should be used concomitantly until the serum urate level remains below 6 mg/dL for 6 months in patients without apparent tophi.7 The optimal duration of prophylactic therapy for patients who have tophi is uncertain. In patients with tophi that persist despite normouricemia, continuation of prophylactic colchicine therapy indefinitely is not recommended because of the risk of neuromyopathy associated with this drug.7
Hyperuricemia and gout are often associated with hypertension, obesity, diabetes, hyperlipidemia, atherosclerosis, and ethanol abuse. Thus, encourage patients to achieve an ideal body weight, reduce dietary protein intake, and limit alcohol consumption. In addition, advise patients to increase fluid intake to 2 L/d to promote uric acid excretion. Patients with chronic tophaceous gout will probably need antihyperuricemic treatment with uricosuric agents and allopurinol in addition to lifestyle changes.
This patient continues to have periodic bouts of severe pain despite treatment with allopurinol (300 mg qd) and colchicine (0.6 mg qd). Multiple large tophi have erupted through the skin and caused ulceration on the right ankle. His most recent uric acid level was 6.6 mg/dL.
References:
REFERENCES:
1
. O’Duffy JD, Hunder GG, Kelly PJ. Decreasingprevalence of tophaceous gout. Mayo Clin Proc.1975;50:227-228.
2.
Wallace SL, Singer JZ. Therapy in gout. RheumDis Clin North Am. 1988;14:441-457.
3
. McLean L. The pathogenesis of gout. In:Hochberg MC, Silman AJ, Smolen JS, et al, eds.Rheumatology. 3rd ed. Edinburgh: Mosby; 2003:1903-1918.
4.
Yamanaka H, Togashi R, Hakoda M, et al. Optimalrange of serum urate concentrations to minimizerisk of gouty attacks during anti-hyperuricemictreatment. Adv Exp Med Biol. 1998;431:13-18.
5.
Emmerson BT. The management of gout. In:Hochberg MC, Silman AJ, Smolen JS, et al, eds.Rheumatology. 3rd ed. Edinburgh: Mosby; 2003:1929-1936.
6.
Dalbeth N, Kumar S, Stamp L, Gow P. Doseadjustment of allopurinol according to creatinineclearance does not provide adequate control ofhyperuricemia in patients with gout. J Rheumatol.2006;33:1646-1650.
7.
Borstad GC, Bryant LR, Abel MP, et al. Colchicinefor prophylaxis of acute flares when initiating allopurinolfor chronic gouty arthritis. J Rheumatol. 2004;31:2429-2432.
