Chapter 255. Gout, Pseudogout, and Osteoarthritis

1. Why do patients have acute flares of crystal arthropathies?

2. How is gout distinguished from other monoarthropathies?

3. What are the appropriate therapies for acute and chronic gout and pseudogout?

4. What are the pathophysiologic features of osteoarthritis (OA), and how do these relate to clinical manifestations?

5. How is OA differentiated from other types of arthritis?

6. What are the nonpharmacologic, pharmacologic, and surgical treatment options for OA?

Gout, pseudogout, and osteoarthritis make up perhaps the largest portion of the rheumatic diseases that affect primarily joints. Although these three disease entities are quite different, they share a number of features in common: all tend to be diseases seen at older ages; all three are not uncommonly seen in overlap with each other; and all three are characterized primarily by inflammatory and/or mechanical abnormalities, rather than autoimmune ones. Whereas gout and pseudogout constitute diseases of abnormal crystal formation and its resultant responses, osteoarthritis is primarily a disease of cartilage loss and autodestruction. In the following sections, we discuss these three important diseases, their pathogenesis, and management.

Gout currently affects more than 3 million Americans, usually presenting with severe acute episodic arthritis, which may evolve into chronic destructive tophaceous disease. It is more common in men than women, and more common in African-Americans than whites. The prevalence of gout rises with age, from 17 per 1000 among individuals 45 to 64 years old, to as high as 41 per 1000 in those 75 years and older. When hospitalized for other conditions, elderly patients with gout are more likely to have their hospital discharge delayed than those without gout. The annual incidence of gout rose from 45 per 100,000 in 1977–1978 to 64 per 100,000 in 1995–1996, and is estimated to have continued to rise over the last decade. Overall, the prevalence of gout has nearly quadrupled over the past half-century. Despite being the most common inflammatory arthropathy, gout is frequently misdiagnosed and mistreated.

Pathophysiology

The most important risk factor for gout is hyperuricemia, or an excess of serum uric acid, the end product of purine metabolism. Serum concentrations are determined by the balance between urate production and elimination. Hyperuricemia may be caused by either overproduction or underexcretion of urate, or a combination of both. Consumption of meat or seafood promotes hyperuricemia and gout, a phenomenon related to the high purine content of these foods. Alcohol has been known to predispose to gout since the days of Hippocrates. Alcohol consumption increases urate production through multiple mechanisms, including generation and turnover of ATP, diuresis and dehydration, production of lactic and ketoacids (which block renal urate excretion), and the consumption of purines in alcoholic beverages. Beer and ale ingestion are most strongly correlated with the presence of hyperuricemia and gout (presumably because of their higher purine content), while hard liquor increases serum urate and gout risk to an intermediate degree. Moderate wine consumption has a lesser effect on serum urate and the ...