Abstract

There is a significant advancement in the treatment of hyperuricemia and gouty in the current Taiwan, but gout was only a rare disease before the World War II. The first case was diagnosed in 1915, and the second was a tophaceous gout described by a Japanese Dr Tsuda in 1920. However, the case number increased dramatically after the War II, and it was majorly due to changing life style. A large-scaled community-based cohort study in a remote Kinmen island found the transformation with younger onset, increased female patients, and more with metabolic syndrome but less severe tophaceous gout. The most recent studies disclosed that the prevalence of hyperuricemia is around 20%, and gout 1-2%. The prevalence rate is much higher among aborigines, which genetically belong to Malayo-Polynesian, around 50% for hyperuricemia and 10% for gout. The studies found Atayal familial gout locus linked to ADMCKD on 1q21 region, HGPRT (Tsou) gene, and reduced fractional UA clearance, which connect to gout and hyperuricemia in aborigines. A prospective cohort study from the nationwide MJ Health Screening Centers reported hyperuricemia was an independent risk factor of mortality from all causes, total cardiovascular disease and ischemic stroke. Another study from databank of CGMH found that hyperuricemia is strongly associated with chronic kidney disease (CKD). Furthermore, from our national Longitudinal Health Insurance Database (LHID), gout linked to cancer risk and increased mortality from cardiovascular, endocrine and renal causes.

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