Gout is an inflammatory arthritis associated with elevated serum levels of urate (hyperuricemia). Hyperuricemia results from increased production or impaired excretion of uric acid. Acute inflammatory arthritis results when crystals of uric acid are deposited in joints. The synovium subsequently be- comes hyperemic and swollen, but pannus formation does not occur in acute cases. Neutrophils ingest urate crystals and release me- diators of inflammation. With treatment, these crystals can be removed, and the joint can be returned to normal. Gout has a chronic form in which tophi (chalky deposits of urate surrounded by inflammatory cells) are formed adjacent to the joint. In chronic gout, the synovium reacts to the formation of these tophi by becoming hyperplastic, and pannus is formed that leads to erosion of bone. Tophi typically arise close to the joints, but they may also appear in the soft tissue at some distance from the joint or even in other tis- sues located far from joints (eg, the ear).
Gout is less common than RA. Unlike RA, it is more prevalent in men by a factor of 9:1. Elevated levels of urate are not synonymous with the presence of gouty arthritis.13 Many people with transiently elevated urate levels will never have arthritis; in those who do, however, the urate levels are often elevated for years before the disease is manifest in the joints.
The most common form of gout occurs be- cause of decreased excretion of urate by the kidney. Less common causes of this condition include enzymatic defects or diseases with increased nucleotide production. Diet tends to have a direct effect on gout. Excessive organ meat consumption can lead to in- creased urate levels, and drinking alcohol tends to block the excretion of urate. Taken together, a diet rich in alcohol and organ meats is likely to aggravate gout.
Most people with hyperuricemia are asymptomatic. Some will have an acute gouty flare and experience increasing pain over a short number of hours, which typically occurs in only one joint—most often the metatarsophalangeal joint of the great toe. People who experience these types of episodes may re- port recent alcohol consumption or have a known history of asymptomatic hyperuricemia. Objective findings include marked tenderness, erythema, warmth, swelling, and severe limitation of motion. Patients with chronic forms of the disease may also have palpable tophi.14
In its initial stage, gout is comparable on radiographs to RA because only soft-tissue swelling is seen; however, as the disease progresses, erosions and ultimately joint destruction may be apparent. The erosions that occur with gout are characteristic and may be easily discerned from those that occur with RA. In patients with gout, new bone formation partially surrounding a tophus creates a characteristic overhanging margin (Fig. 5).
The measurement of serum urate levels is not particularly helpful in diagnosing gout because gout will not develop in many patients with elevated urate levels. Some patients with active gout may have a normal serum urate level at the time of presentation. Other circumstances may result in hyperuri- cemia, such as renal insufficiency or inges- tion of drugs (eg, thiazide diuretics).
Gout is diagnosed by laboratory testing of the synovial fluid. This fluid will show high levels of white blood cells and, more importantly, characteristic needle-shaped monosodium urate crystals. Because monosodium urate crystals are negatively birefringent (doubly refractive), the precise identification of crystals is made with polarized light. Calcium pyrophosphate may also deposit as crystals in the joint (a condition called pseudogout); these crystals are positively bi- refringent.
Treatment and Prevention
Gouty arthritis can be prevented by reducing elevated urate levels with diet modification or medication. Dietary recommendations include decreased ingestion of purines and decreased alcohol consumption. Drugs that lower serum urate levels include probenecid, which promotes the excretion of urate in the urine, and allopurinol, a xanthine oxidase in- hibitor that decreases the synthesis of uric acid.
Colchicine can be used to treat acute episodes of gout because it blocks neutrophil phagocytosis of urate crystals. NSAIDs, of course, can be used to relieve pain and acute inflammation. Historically, indomethacin has been the agent of choice, but other NSAIDs can be equally effective.15 For patients with chronic renal insufficiency, corti- costeroids are the drug of choice.