Arthritis Bibliographi

Careless D, Inman RD. Etiopathogenesis of reactive arthritis and ankylosing spondylitis. Curr Opin Rheumatol 1995;7:290.

Clegg DO, et al. Comparison of sulfasalazine and placebo in the treatment of reactive arthritis (Reiter's syndrome). Arthritis Rheum 1996;39:2021.

Cremers MCW, et al. Second-line treatment in seronegative spondyloarthropathies. Semin Arthritis Rheum 1994;24:71.

Inman RD. Treatment of seronegative spondyloarthropathies. In: Klippel J, Weyand CM, eds. Primer on the rheumatic diseases. Atlanta: Arthritis Foundation, 1997:193. Thomson GT, et al. Post- Salmonella reactive arthritis: late clinical sequelae in a point source cohort. Am J Med 1995;98:13.

Theodore R. Fields and Nicholas P. Scarpa


Disease., classification Acutegout

Asymptomatic., ..hyperuricemia Interyalgout Chronicgout, The prognosis

The first clinical description of a syndrome called podagra, a classic pattern of gout, was in the fifth century b.c. Despite its early recognition, gout continued to plague humankind until the middle of the twentieth century, when practical and effective therapy emerged. The introduction of allopurinol and nonsteroidal antiinflammatory drugs (NSAIDs) has made it possible to alter the course of the disease dramatically.

Gout is a heterogeneous disorder with primary and secondary forms characterized by hyperuricemia and urate crystal-induced arthritis.

I. Epidemiology. In the United States, approximately 12% of family members of gout patients are affected. Ninety percent of primary gout patients are men. The peak age for the first attack of gout is during the fifth decade. Primary gout is thought to be a polygenic disease.

Arthritis Relief and Prevention

Arthritis Relief and Prevention

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