A 78-year-old male with a history of smoking, dietary excesses, hyperuricemia (serum uric acid level of 11 mg/dL) and renal chronic disease (creatinine clearance rate of 30 mL/min per 1.73 m2 of the body-surface area) presented with multiple tophi on the hands, elbows, feet, knees, and auricular surfaces, with hand bone associated deformities (Figure 1).

He described a long past of multiple episodes of confirmed acute uric arthritis improperly treated. He had also been medicated with allopurinol but with a patient poor concordance and advised to take a dietary regimen, which he refused. After thirty years, daily activities such as holding a fork, etc. were severely impaired.

Gout is the most common form of inflammatory arthropathy and affects at least 1% of the population in the western countries [1] [2]. Several studies suggest that its prevalence and incidence, in recent decades, have risen [1] [3]. Men have a greater risk of developing gout. The overall men and women ratio ranges between 7:1 and 9:1, but more recent studies suggest, a smaller difference and point ratios of 4:1 [1] . Gout prevalence also presents a direct association with age, and the increased population longevity may be contributing to its present higher prevalence [3].

Numerous risk factors seem to associate to the development of gout, such as hyperuricemia, genetics, diet and alcohol consumption, hypertension, obesity, diuretic use and chronic renal disease. Of these, hyperuricemia is considered to be the most important [1] [3].

As serum uric acid levels rise and its physiological saturation threshold in body fluids is exceeded, the formation and deposition of monosodium urate crystals occurs, in and around joints.

A typical gout attack is characterized by the sudden onset of severe pain, swelling, warmth, and redness of a joint. The joint most commonly involved is the first metatarsophalangeal joint but any joint may be involved. Some patients have a chronic form of gout with relapsing acute episodes.

Gout is strongly suspected by a clinical course of acute episodes of joint pain with complete resolution of symptoms between attacks associated with high levels of urate in blood analysis. However, the best way to diagnose gout is to examine synovial fluid from an affected joint to look for urate crystals in the sample. Crystals of monosodium urate appear as needle-shaped negatively birefringent (polarize microscopy) crystals [4].

Anti-inflammatory medications are the best treatment for acute gout attacks. Prophylactic therapy includes dietary changes and urate-lowering medications. These are effective options. Repeated episodes of acute gout when sustained for several years without treatment may lead to the accumulation of a large number of urate crystals in masses called tophi (potentially treatable) and to joint deformity and destruction (irreversible) [5].

Gout, if untreated, can be deforming and severally disabling.

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2. VanItallie TB. Gout: Epitome of painful arthritis. Metabolism 2010 Oct;59(Suppl 1):S32–6.   [CrossRef]   [Pubmed]    
3. Roddy E, Doherty M. Gout: Epidemiology of gout. Arthritis Res Ther 2010;12(6):223.   [CrossRef]   [Pubmed]    
4. Gupta A, Rai S, Sinha R, Achar C. Tophi as an initial manifestation of gout. J Cytol 2009 Oct;26(4):165–6.   [CrossRef]   [Pubmed]    
5. McQueen FM, Chhana A, Dalbeth N. Mechanisms of joint damage in gout: Evidence from cellular and imaging studies. Nat Rev Rheumatol 2012 Jan 10;8(3):173–81.   [CrossRef]   [Pubmed]