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We report the case of a 53 year old man with a history of gouty arthritis extending over several years. He had had an acute kidney failure 2 years previously because of nephrolithiasis with urate calculi.
At the first consultation the patient had severe painful gouty arthritis (three to four attacks a week) of the joints of the big toes, the ankle joints, and different finger joints as well as in joints of the hands, shoulders, and knees. In addition to the polyarticular joint manifestation, multiple gouty tophi were present in the subcutaneous tissue (fig 1).
The medical history of the patient showed he had arterial hypertension and hypertriglyceridaemia. He consumed 20–25 units of alcohol weekly. Standard treatment was impractical because the patient had developed incompatibility with allopurinol and benzbromarone, which manifested as diarrhoea and a generalised exanthema.
Laboratory tests showed a raised white blood cell count (WBC) of 9.4×109/l; an erythrocyte sedimentation rate (ESR) 55 mm/1st h, C reactive protein (CRP) 61.0 mg/l, serum uric acid 580 μmol/l. Transaminases were normal apart from a γ-glutamyltransferase of 282 U/l. Clinical examination, including cardiovascular and respiratory systems, an electrocardiogram, and a chest radiograph were normal. Abdominal ultrasound was also normal apart from showing hepatomegaly. The radiographs of all symptomatic joints showed impressive signs of destructive gouty arthritis (fig 2).
Despite exhaustive treatment with colchicine, diclofenac, methylprednisolone, and opioids, the arthritis attacks did not improve considerably (table 1).
After obtaining the latest detailed information about the patient and his informed consent, treatment with etanercept (Enbrel) 25 mg subcutaneously twice weekly was started. As table 1 shows the frequency (gouty attacks per week) and the intensity (number of painful joints) of the gouty arthritis decreased considerably after four injections of etanercept. Laboratory tests showed a noticeable decrease of the inflammation, with WBC of 7.4×109/l; ESR 6 mm/1st h, CRP 6.1 mg/l. During the anti-inflammatory treatment, antihyperuricaemic treatment with probenecid and urine alkalisers was maintained; the level of serum uric acid remained roughly the same.
Thus, treatment with the tumour necrosis factor α (TNFα) inhibitor etanercept in a patient with a complex gouty arthritis impressively reduced the clinical manifestations of gout, and uric acid depots were depleted generally.
Effective treatment exists to prevent the complications of symptomatic hyperuricaemia. However, severe gouty arthritis together with tophaceous manifestations are rarely seen. In most cases standard treatment with colchicine, non-steroidal anti-inflammatory drugs, and moderate doses of glucocorticosteroids is sufficient to control the inflammation of gouty attacks.1,2 In our patient the conservative treatment of the gout, including opioids for analgesia, did not control the attacks. The use of etanercept produced a noticeable decrease in all the pathological clinical and laboratory findings (table 1).
Acute and chronic gouty arthritis is an inflammatory disease, in which activation of certain white blood cells occurs owing to the presence of a foreign substance—namely, urate crystals. The activation of monocytes and macrophages releases TNFα into the synovial fluid.7,8 Increased concentrations of TNFα are detectable in joints of gouty arthritis.9 In certain cases, gout can mimic rheumatoid arthritis.10
We describe the first published case of severe, recurrent tophaceous gouty arthritis refractory to anti-inflammatory treatment in a patient who was subsequently treated successfully with a TNFα inhibitor. Of particular interest is the possibility of maintaining antihyperuricaemic treatment during the antiphlogistic protection of etanercept, especially as there is a massive excavation of uric acid from the depots owing to the antihyperuricaemic treatment.
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