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Feb12
POLY ARTICULAR GOUT-A CASE REPORT
Unusual case of poly articular gout-a case report.

Abstract-
Gout is a common inflammatory arthritis caused by deposition of monosodium urate crystals in the joints. It classically affects the first metatarsophalangeal joint and less commonly other joints, such as wrists, elbows, knees and ankles.
We report the case of a 65-year-old man with tophaceous polyarticular gout, soft-tissue involvement of elbow joint with secondary infection leading to septicemia.
Key words—
Gout, monosodium urate crystals, tophi, arthropathy,Febuxostat,Colchicine
Introduction-

Gout is a common disorder of uric acid metabolism, characterized by recurrent episodes of inflammatory arthritis, tophaceous soft tissue deposits of monosodium urate crystals, uric acid renal calculi and chronic nephropathy. We report the case of a 65-year-old man suffering from tophaceous polyarticular gout and soft-tissue involvement, presenting with ulcerated tophi overlying the left elbow. We also emphasize the disabling effects of the untreated hyperuremic arthropathy.
Case presentation
A 65-year old man with a long-standing history of tophaceous gout and several recurrent episodes of arthritis during the past five years presented with a large, painful, ulcerated tophus located on the left elbow joint to the emergency department. He tried a course of non-steroidal anti-inflammatory drugs (NSAIDs) without improvement.
On physical examination he had a mild fever of 37.8°C. A grayish, voluminous and ulcerated nodule containing chalky material was located on the left elbow. Further examination revealed multiple other tophi overlying the 4th and 5th PIP joints (proximal interphalangeal joint) of his right hand and the first interphalangeal joints of his left hand(Figure 1). Other joints involved were wrists, elbows, ankles, interphalangeal and metatarsophalangeal joints of the feet and heels. Many joints were also deformed. The first metatarsophalangeal joint of his left foot was totally nonfunctional.
Laboratory workup revealed leukocytosis (11.000/mm3), elevated C-reactive protein (60.21 mg/dl) and elevated serum uric acid (11 mg/dl) and normal serum creatinine (0.9mg/dl). Radiographs of the hands showed showing soft tissue swelling and destruction of both wrist, left IP thumb, right 4th and 5th PIP joints, calcified tophi seen in right 2nd MCP joint(meta carpo phalangeal joint)(Figure 2). A culture from the ulcerated tophus was positive for staphylococcus aureus (Methicillin sensitive). Two days after admission, the tophus burst releasing a viscous, chalk-like material. Polarized microscopy confirmed presence of needle shaped monosodium urate crystals (Figure 3).
Antibiotic treatment with IV Ciprofloxacin (1000 mg/day) and intravenous administration of NSAIDs (Diclofenac 100 mg/day) was initiated.
A surgical debridement with lavage of the joint was performed. Debridement was also performed on the minor ulcers. Five days after admission treatment with Febuxostat (80 mg/day) along with Colchicine 0.5mg twice daily was initiated. The patient improved clinically and was discharged two days later. Six months after treatment, he remains symptom free.
Discussion:
Gout is the most common inflammatory arthropathy, reported to affect 2.13% of the population of the United States of America in 2009 [1]. Older age, male sex, postmenopausal state and black race are related to a higher risk for development of the disease [2]. Elevation of uric acid levels above the saturation point for urate crystal formation (6.8 mg/dl) usually results from an impaired renal uric acid excretion and although necessary, it is not sufficient to cause gout. Hyperuricemia and gout can be attributed to uric acid elevating drugs, genetic polymorphisms in genes controlling renal urate transport and predisposing dietary factors, such as consumption of red meat, seafood, alcohol and fructose containing soft beverages [3]. Other conditions associated with the disease include insulin resistance, obesity, hypertension, renal insufficiency, congestive heart failure, and organ transplantation [2].
Over time, poorly controlled gout may progress to a chronic phase, characterized by polyarticular attacks, painful symptoms between acute flares and monosodium urate crystal deposition (tophi) in soft tissues or joints [2]. Tophi are typically found on the helix of the ears, on fingers, toes, wrists and knees, on the olecranon bursae, on the Achilles tendons and also rarely on the sclerae, subconjuctivally, [4] and on the cardiac valves [5]. They can cause pain and dysfunction and are rarely associated with ulcerations [6], bone fractures [7], tendon and ligament rupture [8], carpal tunnel [9] and other nerve compression syndromes [10]. Differential diagnosis for subcutaneous or articular nodules includes septic arthritis, synovial cysts, nodal osteoarthritis, rheumatoid arthritis, sarcoidosis, lymphoma or neoplasms [11]. Synovial fluid or tophus aspiration permits diagnosis through demonstration of negatively birefringent monosodium urate crystals [2].
Treatment options for acute gouty attacks include dietary and lifestyle modifications, NSAIDs, colchicine, oral or topical steroids and corticotropin (ACTH). Interleukin-1 (IL-1) antagonists, such as anakinra, a human recombinant IL-1 receptor antagonist and canakinumab, a monoclonal antibody against IL-1β, have also shown promising results in the treatment of refractory cases or cases intolerant to classical therapy [2]. Even without treatment acute attacks usually resolve spontaneously within seven to 10 days. Normalizing hyperuricemia is of cardinal significance for the control of recurrent attacks and for the regression of tophi. This is achieved with drugs, which either favor uric acid excretion (probenecid), convert uric acid into soluble allantoin (pegloticase), or inhibit uric acid production (allopurinol, febuxostat) [2].
Surgical treatment is seldom required for gout and is usually reserved for cases of recurrent attacks with deformities, severe pain and joint destruction [11]. The main indication for surgery in patients with tophaceous gout is sepsis or infection of ulcerated tophi, followed by mechanical problems, confirmation of diagnosis and pain control [12]. Removal of tophaceous deposits from the hands can be achieved through tenosynovectomy for heavily infiltrated tendons, through a soft-tissue shaving technique for heavy skin infiltration with ulceration and draining fissures [13], or through more complex surgical approaches involving large skin incisions and excision of the tophi [14]. A hydrosurgery system applying a highly pressurized saline stream has also been used with good results for the debridement of tophi [15]. In the early stages, surgical arthroplasty can be carried out, but simple enucleation of the tophi may lead to complications such as skin necrosis, tendon and joint exposures [11]. Amputation is always a valid option for untreatable and infected ulcerations [16].
Conclusion
Secondary infection of tophaceous gout are not uncommon can lead to septicemia. Surgical treatment is required for such cases along with medical therapy.

References:
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12.Kumar S, Gow P. A survey of indications, results and complications of surgery for tophaceous gout. N Z Med J. 2002;115:U109.
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14.Tripoli M, Falcone AR, Mossuto C, Moschella F. Different surgical approaches to treat chronic tophaceous gout in the hand: our experience. Tech Hand Up Extrem Surg. 2010;14:187–190.
15.Lee JH, Park JY, Seo JW, Oh DY, Ahn ST, Rhie JW. Surgical treatment of subcutaneous tophaceous gout. J Plast Reconstr Aesthet Surg. 2010;63:1933–1935.
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16.Ertugrul Sener E, Guzel VB, Takka S. Surgical management of tophaceous gout in the hand.Arch Orthop Trauma Surg. 2000;120:482–483.


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