Key Clinical Questions
Why do patients have acute flares of crystal arthropathies?
How is gout distinguished from other monoarthropathies?
What are the appropriate therapies for acute and chronic gout and pseudogout?
What are the pathophysiologic features of osteoarthritis (OA), and how do these relate to clinical manifestations?
How is OA differentiated from other types of arthritis?
What are the nonpharmacologic, pharmacologic, and surgical treatment options for OA?
Gout, pseudogout, and osteoarthritis make up the largest portion of the rheumatic diseases that affect primarily joints. Although these three disease entities are quite distinct, they share a number of features in common: all tend to be diseases seen at older ages; all three are often 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 are diseases of abnormal crystal formation and resultant inflammation, osteoarthritis is primarily a disease of mechanically driven, biochemically propagated cartilage loss and autodestruction. In the following sections, we discuss these three important diseases, their pathogenesis, and management.
Gout currently affects more than 8 million Americans, usually presenting with severe acute episodic arthritis that may evolve over time into chronic destructive tophaceous disease. Gout is more common in men (6.1 million US males vs 2.2 million US females), and is slightly more common among African Americans (5% of the African American population vs 4% of the US white population). The prevalence of gout rises with age, from 3.3% among individuals 40 to 49 years old, to 8.0% among individuals 60 to 69, to as high as 12.6% in those 80 years and older. The annual incidence of gout rose from 4.5 per 10,000 in 1977 to 1978 to 6.4 per 10,000 in 1995 to 1996, and to 12.4 per 10,000 from 1994 to 2007. Overall, the prevalence of gout has more than quadrupled over the past half-century. Despite being the most common inflammatory arthropathy, gout is frequently misdiagnosed and mismanaged.
The most important risk factor for gout is hyperuricemia, or an excess of serum urate, the end product of purine metabolism. Serum urate 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 as a result of the high-purine content of these foods. In contrast, alcohol consumption increases urate production through multiple mechanisms, including generation and turnover of ATP (a purine base), 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 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 ...