Gout is a common systemic metabolic disease, affecting more than 1% of the population. It is the most common inflammatory arthritis, afflicting 1 or more joints in men older than 40 years of age.¹ The majority of patients have primary gout, meaning that no identifiable underlying disease causing the hyperuricemia can be found. Secondary gout, which is less common, can result from many conditions (Table 1).

To understand gout adequately, it is important to define the relationship between uric acid, hyperuricemia, and gout. Humans do not express the enzyme urate oxidase (uricase), because of a mutation during evolution of the uricase gene, which converts urate to the more soluble and easily excreted compound allantoin. Among mammals, only humans and other primate species excrete uric acid as the end product of purine metabolism. Uric acid is a weak organic acid that exists mainly as the urate ion at pH >5.75 and as the un-ionized uric acid form at more acidic (lower) pH levels. Thus, the urate form predominates in all extracellular fluids, including serum, in which physiological pH is 7.4. In urine, which is usually acidic, the un-ionized uric acid form predominates.

When overproduction or underexcretion of uric acid occurs, the serum urate (SU) concentration may exceed the solubility of urate (a concentration approximately >6.8 mg/dL), and supersaturation of urate in the serum (and other extracellular spaces) results. This state, called hyperuricemia, imparts a risk of crystal deposition of urate in tissues from the supersaturated fluids.

Four clinical stages result from hyperuricemia, including asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout (intervals between acute attacks), and chronic tophaceous gout.² Inflammatory arthritis in patients with gout is caused by crystals of monosodium urate (MSU) that form as a result of chronically elevated levels of urate in plasma and extracellular fluids.

Although the first descriptions of gout can be traced to the dawn of recorded medical history, questions remain regarding the diagnosis of gout.³ The gold standard for establishing a definite diagnosis of gout is the presence of MSU crystals in aspirated joint fluid or tophus.⁴ Physicians, however, do not routinely perform synovial fluid (SF) analysis, even in hospitalized patients with acute gout,⁵ opting instead to reach a diagnosis based on clinical features and demonstration of hyperuricemia.

There are many limitations to this diagnostic approach. In a study of 9108 consecutive new patients seen in an outpatient rheumatology clinic, 155 (1.7%) were diagnosed with gout. A higher number of patients (164, 1.8%) had been incorrectly diagnosed with gout in the community.⁶  Some have maintained that gout can be diagnosed clinically by the triad of inflammatory arthritis, elevated SU level, and response to colchicine.⁶

In the absence of demonstrating the presence of MSU crystals in aspirated joint fluid or tophus, clinical, radiologic, and laboratory criteria are helpful. It is important to diagnose gout early so that underlying hyperuricemia and the acute attack can be treated appropriately. This article describes current knowledge regarding the diagnosis of gout and provides an overview of the various classification criteria and clinical examination, laboratory, and radiologic findings needed to make the diagnosis of gout.

Classification Criteria

The first criteria for the classification of gout were proposed at the Rome symposium on population studies in the rheumatic diseases.⁷ According to the Rome criteria, to be diagnosed with gout, patients must meet 2 of the following 4 criteria: (1) an SU level >7 mg/dL in men or >6 mg/dL in women; (2) the presence of tophi; (3) the presence of MSU crystals in SF or tissues; and (4) a history of painful joint swelling with abrupt onset and remission within 2 weeks.

These criteria were modified in an international symposium held in New York in 1966. The major changes were the addition of a response to colchicine and the removal of SU levels from the list of criteria.⁸ The New York criteria are still helpful in routine clinical practice. They include the presence of a clear history of at least 2 attacks of painful joint swelling with complete resolution within 2 weeks, a clear history or observation of podagra, the presence of a tophus, and a rapid response to colchicine within 48 hours of starting treatment. Two of these criteria are required for a clinical diagnosis, but a definitive diagnosis can be made if MSU crystals are seen in SF or in the tissues.

Rigby and Wood⁹ compared the New York and Rome criteria in 59 patients with gout and 761 patients with other arthropathies. They found that the best individual criterion was 1 or more attacks of podagra (New York criteria). In contrast, the presence of a tophus was the least valuable criterion. The New York criteria were more sensitive and specific than the Rome criteria. Rigby and Wood also investigated the value of determining the SU level in new patients in a rheumatology outpatient clinic. The gold standard in this study was clinical assessment by rheumatologists. Determining the SU level was a criterion for the diagnosis of gout in the Rome criteria but not in the New York criteria. Rigby and Wood concluded that in a clinical picture resembling gout, with a low SU level independent of the gouty attack, the diagnosis of gout is very unlikely. 

In 1977, the American College of Rheumatology published preliminary criteria for the classification of gout for use in either clinical settings or population-based epidemiologic studies.¹⁰ Subjects were classified as having gout when they had MSU crystals in their SF, the presence of a proven tophus, or at least 6 of the remaining 11 criteria (Table 2). These criteria were extrapolated from a rheumatic population in which 6 or more of the 11 criteria were present in 87.6% of the 178 patients with acute gout.¹⁰ Tophi were present or suspected in 30% of the 178 patients with acute gout, with a specificity of 99%. Most likely, the specificity was not 100% because there were 1 or more cases of bacterial arthritis in gouty patients with tophi.