Journal of Clinical Rheumatology | 2019

Multiarticular Deforming and Erosive Tophaceous Gout With Severe Comorbidities

 

Abstract


out is an increasingly common chronic metabolic disorder, G resulting from the inflammatory responses to monosodium urate crystals deposited in tissues. Tophaceous gout can occur years after recurrent attacks of acute inflammatory arthropathies. Microscopically, the tophus (the cardinal feature of advanced gout) is a foreign body, granuloma-like structure that contains lumps of monosodium urate crystals and is surrounded by inflammatory cells and connective tissue. Multiarticular chronic tophaceous gout causes progressive joint damage and the development of multiple, severe destructive ulcerations and reduces the quality of life. Although a few cases of erosive polyarticular tophaceous gout with severe osteolysis that require digital amputation have been identified in the literature, none of these have demonstrated extensive bone destruction. A 57-year-old white man with chronic tophaceous multiarticular gout was referred to our neurorehabilitation clinic. He presented with tophi on the right pinna and left knee, “white bumps” on the left elbow, multiple ulcerated tophi on his feet and hands, and necrotic lesions (distal right thumb and the distal phalanx of the little finger of the right hand). He was recently treated with vancomycin for a methicillin-resistant Staphylococcus aureus infection. He had a medical history of heavy smoking, longstanding and suboptimally treated gout (since 2004), previous partial amputation of the fourth right finger (2015), arterial hypertension (since 2012), renal lithiasis (since 2014), moderate kidney disease, myocardial infarction and coronary stent (2012), left sylvian ischemic stroke, and right hemiplegia and aphasia (in December 2018). Local physical and radiologic examination shows multiarticular deformities and deviations of the fingers and toes, soft-tissue involvement (multiple tophi, erosive and necrotic lesions; Fig. 1, Fig. 2). Laboratory testing revealed uric acid (UA) 7.5 mg/dL (446 μmol/L), erythrocyte sedimentation rate 130mm/h, white blood cells 6300/μL, 65.6% neutrophils, plasma fibrinogen 854 mg/dL, C-reactive protein 20.2 mg/L, and serum creatinine 1.70 mg/dL (glomerular filtration rate 44 mL/min per 1.73m). Patient s participation in the rehabilitation programwas limited by his dysfunctional medical comorbidities and neurologic status. Lifetime diet, long-term colchicine 0.5 mg twice daily and allopurinol 300 mg twice daily, neurotrophic factors, antihypertensive, antiplatelet therapy, and follow-up were indicated at discharge.

Volume 26
Pages e269 - e271
DOI 10.1097/RHU.0000000000001121
Language English
Journal Journal of Clinical Rheumatology

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