Objective.

We sought to examine primary care providers' gout knowledge and reported treatment patterns in comparison with current treatment recommendations.Methods. We conducted a national survey of a random sample of US primary care physicians to assess their treatment of acute, intercritical and tophaceous gout using published European and American gout treatment recommendations and guidelines as a gold standard.

Results.

There were 838 respondents (response rate of 41%), most of whom worked in private practice (63%) with >16 years experience (52%). Inappropriate dosing of medications in the setting of renal disease and lack of prophylaxis when initiating urate-lowering therapy (ULT) accounted for much of the lack of compliance with treatment recommendations. Specifically for acute podagra, 53% reported avoidance of anti-inflammatory drugs in the setting of renal insufficiency, use of colchicine at a dose of ≤2.4 mg/day and no initiation of a ULT during an acute attack. For intercritical gout in the setting of renal disease, 3% would provide care consistent with the recommendations, including initiating a ULT at the appropriate dose with dosing titration to a serum urate level of ≤6 mg/dl and providing prophylaxis. For tophaceous gout, 17% reported care consistent with the recommendations, including ULT use with dosing titration to a serum urate level of ≤6 mg/dl and prophylaxis.

Conclusion.

Only half of primary care providers reported optimal treatment practices for the management of acute gout and <20% for intercritical or tophaceous gout, suggesting that care deficiencies are common.

Gout is an ancient disease. Despite significant advances in the understanding of its risk factors, etiology, pathogenesis, prevention, and treatment, millions of people with gout experience repeated attacks of acute arthritis and other complications. The incidence of gout is increasing, most likely reflecting increasing rates of obesity and other lifestyle factors, including diet. Comorbid conditions that often accompany gout, including chronic kidney disease and diabetes mellitus, present challenges for the management of gout. Using the case of Mr R, a 57-year-old man with a history of podagra, hyperuricemia, and mild renal insufficiency, the diagnosis and treatment of gout are discussed. For those with moderate to severe gout, urate-lowering treatment can eliminate acute attacks of arthritis and prevent complications. In the near future, it is likely that new risk factors for gout will be identified and new ways of preventing and managing this common disease will become available.

The prevalence of gout increases with age. Up to 7% of men > 65 and 3% of women > 85 have gout. Risk of gout increases significantly with increasing serum uric acid levels. Alcohol consumption and purine-rich foods such as red meat and seafood increase the risk of incident gout significantly. Loop and thiazide diuretics are also associated with increased risk. Gout is frequently associated with the metabolic syndrome. Dehydration, increasing creatinine levels, and surgery are also known to precipitate flares. Acute gout manifests as severe joint pain, of rapid onset, reaching maximal intensity within a few hours. Gout has a predilection for lower extremity joints. It often starts at the first metatarsophalangeal joint, a condition termed podagra. Other common sites of gouty flares include: tarsal and subtalar joints; ankle; knee; wrist; small joints of the hands; Achilles tendon; and olecranon bursae. The joint affected is usually hot, red, swollen and very painful. This is often associated with skin erythema. Identification of MSU crystals in the synovial fluid of an inflamed joint or from tophi allows a definite diagnosis of gout to be made. Hyperuricaemia does not confirm or exclude gout as most people with hyperuricaemia are asymptomatic, while serum uric acid levels tend to decrease during acute attacks. Short-acting NSAIDs should be used at maximal dose as first drug of choice if not contraindicated. In patients at risk of GI complications, co-prescription of a proton pump inhibitor or the use of COX-2 selective agents should be considered. Colchicine can be particularly useful in patients with heart failure in whom NSAIDs are contraindicated but should be avoided in patients with severe renal impairment. Joint aspiration and injection of intra-articular steroids is one of the most effective ways of treating acute monoarthritic gout. Uric acid lowering therapy is initiated if a patient suffers two or more attacks in one year. Many rheumatologists will start this therapy in hyperuricaemic patients whose first attack is very severe or in polyarticular gout.

Gout is an often-overlooked and undertreated inflammatory arthritis that is most frequently managed in the primary care office. Its initial clinical presentation may include acute-onset pain that is most typically associated with the big toe (podagra) or knee. Most patients with gout can be successfully treated from the primary care physician's office with little or no need for referral to a rheumatology practice. Prompt recognition, diagnosis, and management can greatly improve the lives of patients with gout. Patient education is important; addressing modifiable risk factors promptly after initial presentation can arrest the development of serious debilitating effects and improve, or occasionally replace, pharmacologic intervention. This article will discuss the epidemiology, pathophysiology, and diagnosis of gout, as well as management of the acute flare and management of chronic gout with urate-lowering therapy, including prophylaxis.

The purpose of this study is to determine the diagnostic properties of the clinical gout diagnosis (CGD) proposal in patients with gout and other rheumatic diseases. We investigated the presence of current or past history of the previously published CGD criteria: (1) >1 attack of acute arthritis, (2) mono/oligoarthritis attacks, (3) rapid progression of pain and swelling (<24 h), (4) podagra, (5) erythema, (6) unilateral tarsitis, (7) probable tophi, and (8) hyperuricemia. CGD was established in patients with greater than or equal to four out of eight of these criteria. Demographic data and comorbidities were also considered. Statistical analysis included diagnostic test evaluation (sensitivity, specificity, likelihood ratios, positive predictive values and receiving operating characteristic curves). One hundred and sixty-seven patients with the following diagnoses were included: gout (most in intercritical period, n = 75), rheumatoid arthritis (RA, n = 30), osteoarthritis (OA, n = 31) and spondyloarthritis (SpA, n = 31). All gout patients had MSU crystal demonstration and constituted the gold standard for diagnostic test evaluation. There were significant differences across diagnostic groups in most demographic variables and comorbidity. The presence of greater than or equal to four out of eight of the CGD criteria were found in 97% patients with gout, in two patients with SpA, and one each with RA and OA. The sensitivity, specificity, and LR+ of greater than or equal to four out of eight of the CGD criteria were 97.3%, 95.6%, and 22.14, respectively. The presence of more than or equal to four out of eight items from the CGD proposal is highly suggestive of gout.

Crystal-induced arthritis (CIA) is easy to diagnose as soon as the physician might suspect the diagnosis. Indeed, CIA can be readily ascertained since one single gold standard is available: identification of microcrystals in synovial fluid or in other materials (tophus, synovial tissue biopsy, periarticular tissues). It is therefore mandatory to perform joint aspiration and to get synovial fluid sample for microscopic examination. Monosodium urate crystals are the key feature of gout, and calcium pyrophosphate (CPP) crystals are associated with CPP disease, also called "chondrocalcinosis" in France. Diagnosis of gout can be readily suspected when considering typical clinical presentations such as podagra, presence of tophi, cardiovascular comorbidities, and diuretics use. Plain radiographs, as long as technical quality is present, are an easy way to suspect and eventually to diagnose CPP disease or apatite deposits in any articular or periarticular site. Joint ultrasonography when performed by skilled physicians can easily help in displaying crystal deposits at the cartilage surface (gout) or within the cartilage (CPP), along with peri-tophaceous inflammatory reaction as evidenced by power Doppler.

Joint diseases in antiquity and the Renaissance were generally known by the all-encompassing term, gout (podagra or gotta). Only in later centuries was there a differentiation in the types of joint diseases, distinguishing gout in the modern sense from other arthritic and rheumatic disorders. The present article illustrates one pictorial representation of joint disease from the early sixteenth century, a case that seems typical of gouty tophi.

This invited paper provides a summary of a keynote lecture delivered at the 2011 Australasian Podiatry Conference. Gout is the most prevalent inflammatory arthropathy. It displays a striking predilection to affect the first metatarsophalangeal joint as well as joints within the mid-foot and ankle. A number of factors are known to reduce urate solubility and enhance nucleation of monosodium urate crystals including decreased temperature, lower pH and physical shock, all of which may be particularly relevant to crystal deposition in the foot. An association has also been proposed between monosodium urate crystal deposition and osteoarthritis, which also targets the first metatarsophalangeal joint. Cadaveric, clinical and radiographic studies indicate that monosodium urate crystals more readily deposit in osteoarthritic cartilage. Transient intra-articular hyperuricaemia and precipitation of monosodium urate crystals is thought to follow overnight resolution of synovial effusion within the osteoarthritic first metatarsophalangeal joint. The proclivity of gout for the first metatarsophalangeal joint is likely to be multi-factorial in origin, arising from the unique combination of the susceptibility of the joint to osteoarthritis and other determinants of urate solubility and crystal nucleation such as temperature and minor physical trauma which are particularly relevant to the foot.

Observation of monosodium urate (MSU) crystal is the gold standard for diagnosis of gout, but is rarely performed in daily clinical practice, and diagnosis is based on clinical judgment. Our aim was to identify clinical and paraclinical data included in the European League Against Rheumatism recommendations (EULARr) and American College of Rheumatology proposed criteria (ACRp) for diagnosis of gout in patients with chronic gout according to their attending rheumatologists.This cross-sectional and multicenter study included consecutive patients from outpatient clinics with a diagnosis of gout by their attending rheumatologists according to their expertise. The frequency of each item from the ACRp and EULARr was determined. Possible combinations of the items that were frequent, clinically relevant, and simple to evaluate in daily practice were determined.We studied 549 patients (96% men), mean age 50 +/- 14 years. Analysis of MSU crystals was performed in 15%. We selected 7 clinical criteria and 1 laboratory measure because of their frequency, importance, and simplicity to obtain: current or past history of: > 1 attack of acute arthritis (93%); mono or oligoarthritis attacks (74%); rapid progression of pain and swelling (< 24 hours; 74%); podagra (70%); erythema (56%); unilateral tarsitis (33%); tophi (52%); and hyperuricemia (93%). The chronic gout diagnosis (CGD) proposal comprised >or= 4/8 of these; 88% of patients had the criteria of the CGD proposal while 75% had 6/11 ACRp criteria (p = 0.001). When analysis of MSU crystals was added, 90.1% (CGD) and 83.9% (ACRp) met the criteria (p = 0.004).Current or past history of >or= 4/8 CGD parameters is highly suggestive of chronic gout.

Many patients with gout present with an acute attack (flare) of gouty arthritis. In its early stages, gout is a chronic, often silent disorder punctuated by acute, extremely painful arthritic flares. Over time, untreated or insufficiently treated gout may progress, with more frequent flares and formation of urate crystal deposits (tophi) and associated chronic, deforming arthritis (gouty arthropathy). About 20% of patients with gout have urinary tract stones and can develop an interstitial urate nephropathy. Gout (also called urate crystal deposition disease) is characterized by reduced renal clearance or, less frequently, an overproduction of uric acid. When the serum urate acid (sUA) level persistently exceeds 6.8 mg/dL, extracellular fluids become saturated and hyperuricemia occurs. Hyperuricemia is also very common among adult men and postmenopausal women, most of whom remain asymptomatic with respect to gout throughout their lives. Nevertheless, hyperuricemia is the major risk factor for gout because it predisposes to urate crystal formation and deposition, particularly in and around joints and in other soft tissue structures. The symptoms and signs of gout result from acute and chronic inflammatory responses of the body to urate crystal deposits. Although any joint may be affected, the metatarsophalangeal (MTP) joint of the great toe (podagra) is the first joint affected in half of all cases. One major goal in managing gout is to treat the pain of acute flares aggressively with anti-inflammatory agents to reduce flare intensity and duration. In addition, most patients with gout eventually require long-term treatment with urate-lowering therapy (ULT) to reverse the chronic urate crystal deposition and to prevent recurrent flares that can cause permanent joint damage.