Introduction: Gout is the most common inflammatory arthritis worldwide and is the only type of chronic arthritis that potentially can be ‘cured’. However, data on gout incidence, prevalence and management, assessed at multiple time points in the same population, are sparse, particularly in Asian populations. The aim of this study was to describe trends in the epidemiology of gout in the general population of Taiwan. Methods: The National Health Insurance Research Database was used to identify patients with gout and to estimate the prevalence and incidence of gout for each calendar year from 2005 to 2010. The pattern of gout management was also examined. Results: Of 23,371,362 beneficiaries in 2010, there were 1,458,569 prevalent and 56,595 incident cases of gout, giving a prevalence of 6.24% (95% confidence interval (CI), 6.23% to 6.25%) and an incidence of 2.74 (95% CI, 2.72 to 2.76) per 1,000 person-years. The annual percentage change (APC) of the standardised prevalence was −0.7% (95% CI, −1.7% to 0.3%; P = 0.14), suggesting that the prevalence of gout was essentially the same throughout the study period. However, The APC of incidence was −13.4 (95% CI, −16.1 to −10.6) between 2005 and 2007 and −2.1 (95% CI, −10.4 to 7.1) between 2007 and 2010. Regions with the highest prevalence and incidence were eastern coastal counties and offshore islets, where indigenous people are clustered. Among prevalent gout cases in 2010, only 22.93% (95% CI, 22.87% to 23.00%) were prescribed urate-lowering treatment (ULT), which remained unchanged between 2005 and 2010 at an APC of 0.0 (95% CI, −3.8 to 4.0). Uricosuric agents were more commonly prescribed than xanthine oxidase inhibitors in Taiwan. Conclusions: In Taiwan, 1 in 16 people have gout. Whereas the incidence has decreased recently, the prevalence remains unchanged. Management of gout in Taiwan is poor, with only one in five affected people being treated with ULT.

Objective: To investigate familial aggregation of Sjögren's syndrome (SS) and the relative risks (RRs) of other autoimmune disease in relatives of patients with SS.Methods: We identified 23,658,577 beneficiaries enrolled in the Taiwan National Health Insurance system in 2010, of whom 12,754 had SS. We identified 21,009,551 parent–child relationships and 17,168,340 pairs of full siblings. The familial risks of SS and other autoimmune diseases, tetrachoric correlation, and familial transmission were estimated.Results: We identified 105 patients with SS who had an affected first‐degree relative. The RR of SS was 18.99 (95% confidence interval [95% CI] 9.76–36.93) in siblings of patients with SS, 11.31 (95% CI 8.34–15.33) in offspring, and 12.46 (95% CI 9.34–16.62) in parents. Tetrachoric correlation coefficients were 0.53 (95% CI 0.41–0.65) for cotwins of affected individuals and 0.21 (95% CI 0.16–0.26) for full siblings. The familial transmission (heritability plus shared environmental contribution) was 0.54 (95% CI 0.44–0.77). In first‐degree relatives of patients with SS, the RRs were 2.95 (95% CI 2.33–3.73) for rheumatoid arthritis, 6.25 (95% CI 5.15–7.58) for systemic lupus erythematosus, 2.39 (95% CI 0.77–7.41) for systemic sclerosis, 0.71 (95% CI 0.10–5.07) for idiopathic inflammatory myopathy, 1.97 (95% CI 1.29–3.02) for type 1 diabetes mellitus, 3.38 (95% CI 1.26–9.05) for multiple sclerosis, 1.67 (95% CI 0.83–3.33) for myasthenia gravis, 1.25 (95% CI 1.04–1.50) for psoriasis, 1.21 (95% CI 0.39–3.76) for inflammatory bowel disease, and 2.29 (95% CI 1.19–4.40) for vasculitis.Conclusion: The risk of SS and other autoimmune diseases is increased in relatives of patients with SS, and more than one‐half of phenotypic variance in SS can be explained by familial factors.

Introduction: We explored the risk of end-stage renal disease (ESRD) among gout patients in a representative cohort in Taiwan. Methods: The primary database used was the Taiwan National Health Insurance Research Database. Subjects older than 20 years without ESRD, coronary heart disease, or stroke were included in the study. The case definition of gout in the present study was gout diagnosis and medical treatment for gout. An ESRD case was defined by the presence of chronic renal failure necessitating long-term renal replacement therapy. Multivariate Cox proportional hazards models were used to evaluate the risk of ESRD among gout patients. Results: The analysis included data of 656,108 patients who were followed up for a mean of 8.0 years. Among them, 19,963 (3.0%) patients had gout. At the end of 2008, 2,377 individuals (gout, n = 276; non-gout, n = 2,101) had ESRD, and 861 individuals (gout, n = 77, 27.9%; non-gout, n = 521, 24.8%) died due to ESRD. The rates of incidence of ESRD were 1.73 and 0.41 cases per 1,000 patient-years in the gout and non-gout groups. After adjustment for age, sex, and history of diabetes mellitus and/or hypertension, gout was associated with a hazard ratio (HR) of 1.57 for ESRD (95% confidence interval [CI], 1.38-1.79; P < 0.001). In patients with ESRD, the adjusted HR for death in patients with gout was 0.95 (0.74-1.23, P = 0.71), which was similar to the HR obtained in patients without gout. Conclusions: Gout is associated with an increased hazard for development of ESRD.

Objective.: The relationship among serum uric acid (SUA), metabolic syndrome, and chronic kidney disease (CKD) is unclear. We examined whether SUA level is an independent risk factor for chronic kidney disease and whether the association between SUA and metabolic syndrome is affected by kidney function.Methods.: We analyzed 28,745 subjects (17,478 men, 11,267 women, age 20–49 yrs) who underwent health examinations at this hospital between 2000 and 2007. Hyperuricemia was defined as SUA level > 7.7 mg/dl in men or > 6.6 mg/dl in women. Kidney function was assessed by estimated glomerular filtration rate (eGFR) using the Modification of Diet in Renal Disease Study equation modified for Chinese subjects. Impaired renal function with low GFR was defined as eGFR < 90 ml/min/1.73 m². The UA-low GFR groups were defined according to the observed combination of hyperuricemia and low GFR: Group A (absence of both hyperuricemia and low GFR); Group B (presence of low GFR but no hyperuricemia); Group C (presence of hyperuricemia but not low GFR); and Group D (presence of both hyperuricemia and low GFR).Results.: The prevalence of hyperuricemia, metabolic syndrome, and impaired kidney function with low GFR was 20.3% (27.6% in men, 8.9% in women), 7.6% (10.6% in men, 3.0% in women), and 9.9% (11.6% in men, 7.1% in women), respectively. The Pearson correlation between SUA and eGFR was only −0.26 (−0.21 in men, −0.22 in women; p < 0.001). In men, the age-adjusted odds ratio (OR) of metabolic syndrome was 1.41 (Group B), 2.45 (Group C), and 2.58 (Group D) in comparison with Group A. In women, the age-adjusted OR of metabolic syndrome was 0.83 (Group B), 5.47 (Group C), and 3.31 (Group D) in comparison with Group A.Conclusion.: Hyperuricemia is prevalent in the Taiwan population. Hyperuricemia is only weakly associated with renal function, but is strongly associated with metabolic syndrome with or without a low eGFR.