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BACKGROUND: Prior literatures have shown inflammatory bowel disease (IBD) could increase fibromyalgia (FM) risk. However, studies about gender and age distributions of FM risk among patients with IBD are rare. With large study samples, this study aimed to evaluate the FM risk among IBD patients with different gender and different age. OBJECTIVE: We aim to estimate the FM risk among male and younger IBD patients with a large patient sample. STUDY DESIGN: A retrospective cohort study was arranged in this research. SETTING: The data used in this research were selected from the Taiwan National Health Insurance Research Database (NHIRD). METHODS: From the Taiwan NHIRD, we selected 4,510 patients with IBD and 18,040 randomly gender- and age-matched patients without a history of IBD from the beginning of 2000 to the end of 2005 to analyze the development of FM over a 12-year follow-up period (2000-2011). The Cox regression model was used to assess the effects of IBD on the risk of FM by adjusting for gender, age, and comorbidities, including hypertension, diabetes, hyperlipidemia, depression, anxiety, and sleep disorder. RESULTS: After adjusting suitable covariates, the IBD patients had a greater FM risk (adjusted hazard ratio [aHR] 1.70, 95% confidence interval [CI] 1.59-1.83) than the controls. Male IBD patients had a higher FM risk than female IBD patients did (aHR 2.00, 95% CI 1.79-2.23 and aHR 1.52, 95% CI 1.38-1.67, respectively). The greatest age-specific FM risk occurred in the youngest IBD subgroup (= 39 years old) (aHR 1.92, 95% CI 1.68-2.19). LIMITATIONS: The information about personal behaviors was unobtainable in the Taiwan NHIRD. Other risk factors for cardiovascular disease that might augment FM cannot be excluded entirely in this study. CONCLUSION: IBD is disclosed to be correlated with an enhanced risk to develop FM, particularly in male and younger IBD patients. For preventing FM, it is necessary to pay more attention to the management of the IBD patients. Future researches are needed to further confirm the findings in this study. KEY WORDS: Inflammation, inflammatory bowel disease, fibromyalgia, Taiwan National Health Insurance Research Database.
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Fibromialgia/epidemiologia , Doenças Inflamatórias Intestinais/complicações , Adulto , Distribuição por Idade , Idoso , Estudos de Coortes , Comorbidade , Bases de Dados Factuais , Feminino , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Fatores de Risco , Caracteres Sexuais , Taiwan/epidemiologia , Adulto JovemRESUMO
Biologics has been widely used in the treatment of rheumatoid arthritis. We aimed to determine whether etanercept, a TNF-α inhibitor (TNFi) that is used to treat patients with rheumatoid arthritis (RA), affects cancer risk.This retrospective matched cohort study used data in the Registry of Catastrophic Illness Database in Taiwan from January 1, 1996 to December 31, 2010. RA, all-cancer, and solid cancer were defined using International Classification of Disease codes (ICD-9-CM 714.X, 140-208, and 140-199, respectively). Cox proportional hazard modeling was used to estimate the hazard ratio (HR) of cancer in all TNFi-treated RA patients, with a focus on the risk in the etanercept-treated patients, after adjusting for comorbidities and concomitant medication.In this Taiwanese dataset, there were 1111 TNFi-treated RA patients and 16,812 RA patients who were naive to all biologics identified. Among the 1002 pairs of etanercept-treated and biologic-naive patients who were matched 1-to-1 for age, gender, RA duration, methotrexate-use, and index date of TNFi prescription, the mean age was 48.9â±â15.0 years. The highest proportion of patients was in the age subgroup of 30 to 60 years (63.8%). Most patients (77.2%) were women. The mean RA duration before etanercept treatment was 2.0â±â1.5 years. During a mean 2.1 years of observation, etanercept was associated with significant risk reduction for all-cancer (HR 0.59, 0.36-0.98) and solid cancer (HR 0.46, 0.27-0.79) relative to the matched biologic-naive patients.The current study explored the safety profile of TNFi and identified a potential benefit of etanercept on the incidence of all-cancer and solid cancer in RA patients.
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Antirreumáticos/uso terapêutico , Artrite Reumatoide/tratamento farmacológico , Etanercepte/uso terapêutico , Neoplasias/prevenção & controle , Adulto , Artrite Reumatoide/complicações , Feminino , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Neoplasias/epidemiologia , Neoplasias/etiologia , Estudos Retrospectivos , Taiwan/epidemiologiaRESUMO
Chronic inflammation, which changes the neurotransmitter metabolism and kindles neuroendocrine system dysfunction in the central nervous system, might cause fibromyalgia (FM) formation. In FM patients without traditional FM risk factors, such as hypertension, hyperlipidemia, diabetes, sleep disorder, depression, and anxiety, the chronic inflammatory process is a possible risk factor for FM. Thus, we investigated whether chronic osteomyelitis (COM), a disease characterized by chronic inflammation, increases FM risk. Including data for 1 million enrollees, the Longitudinal Health Insurance Database was used, and 1,244 COM patients without FM history and 4,976 randomly selected sex- and age-matched control subjects without COM or FM history were extracted. The development of FM over a 13-year follow-up period from 1999 to 2011 was evaluated, and FM risk was estimated using the Cox proportional regression model. The aforementioned FM risk factors were more common in COM patients, who had a significantly greater FM risk than did the control subjects. Compared with those who had no associated risk factors, patients with COM had a greater FM risk than did the control subjects (adjusted hazard ratio [aHR] = 1.32, 95% confidence interval [CI], .99-1.75). Younger people had an even greater risk (age younger than 35 years: aHR = 1.58, 95% CI, 1.03-2.44; age 60 years or older: aHR = 1.03, 95% CI, .78-1.36). To our knowledge, this is the first study to link COM to an enhanced risk of FM development. The results imply that COM is a predictor of FM, suggesting that close follow-up for patients with COM is required to prevent FM, especially in younger populations. PERSPECTIVE: COM is associated with the augmented risk of developing FM, and rigorous treatments for COM patients might decrease the future risk of FM formation, especially in those with relatively younger ages.
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Fibromialgia/epidemiologia , Osteomielite/epidemiologia , Adulto , Fatores Etários , Idoso , Distribuição de Qui-Quadrado , Doença Crônica , Estudos de Coortes , Feminino , Fibromialgia/etiologia , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Osteomielite/complicações , Modelos de Riscos Proporcionais , Risco , Medição de Risco , Taiwan/epidemiologiaRESUMO
An increased risk of suicide ideation and death has been reported in patients with fibromyalgia. This study aimed to evaluate the risk of a suicide event in patients with primary fibromyalgia and in fibromyalgia patients with comorbidities. We used the Longitudinal Health Insurance Database, a subset of the national insurance claim dataset, which enrolled 1 million Taiwanese people from 2000 to 2005, to identify 95,150 patients with incident fibromyalgia (ICD-9-CM 729.0-729.1) and 190,299 reference subjects matched by sex, age, and index date of diagnosis, with a mean of 8.46â±â2.37 years of follow-up until 2011. The risk of a suicide event (ICD-9-CM, External-Cause Codes 950-959) was analyzed with a Cox proportional hazards model. Stratification analysis was performed by separating fibromyalgia patients and reference subjects with respect to each comorbidity to determine the risk of suicide in fibromyalgia patients with or without comorbidity relative to subjects who had neither fibromyalgia nor comorbidity. In this Taiwanese dataset, there were 347 suicide events in patients with fibromyalgia (4.16 per 10 person-years) and 424 in matched reference subjects (2.63 per 10 person-years) with a significant crude hazard ratio (HR) of 1.58 (95% confidence interval [CI] 1.38-1.83) and an adjusted HR of 1.38 (95% CI 1.17-1.71) for fibromyalgia patients relative to the matched reference subjects. According to the 2â×â2 stratification analysis, we found that fibromyalgia patients without comorbidity had an independent but mild risk of a suicide event with adjusted HRs ranging from 1.33 to 1.69 relative to subjects with neither fibromyalgia nor comorbidity. Meanwhile, fibromyalgia patients with comorbidity led to a markedly enhanced risk of a suicide event relative to the matched reference subjects, with adjusted HRs ranging from 1.51 to 8.23. Our analysis confirmed a mild-to-moderate risk of a suicide event in patients with primary fibromyalgia. Attention should be paid to the prevention of suicide in fibromyalgia patients with concomitant comorbidities.
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Fibromialgia/complicações , Suicídio/estatística & dados numéricos , Adulto , Idoso , Estudos de Coortes , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Medição de Risco , TaiwanRESUMO
Neuropsychiatric diseases might enhance stroke development, possibly through inflammation and atherosclerosis. Approximately 25% to 40% of patients with stroke, largely younger patients, are not associated with any conventional stroke risk factors. In this research, we explored whether fibromyalgia (FM), a neuropsychosomatic disorder, increases stroke risk.From a claims dataset with one million enrollees sourced of the Taiwan National Health Insurance database, we selected 47,279 patients with FM and randomly selected 189,112 age- and sex-matched controls within a 3-year period from January 1, 2000 to December 31, 2002. Stroke risk was assessed using Cox proportional hazards regression.Comorbidities associated with increased stroke risk, such as hypertension, diabetes, hyperlipidemia, coronary heart disease, irritable bowel syndrome, and interstitial cystitis, were more prevalent in patients with FM and high stroke risk than in the controls. The overall stroke risk was 1.25-fold (95% confidence interval [CI]: 1.21-1.30) higher in the FM group than in the non-FM group. Even without comorbidities, stroke risk was higher in patients with FM than in the controls (adjusted hazard ratio [aHR]â=â1.44, 95% CI: 1.35-1.53, Pâ<â0.001). The relative risk of stroke was 2.26-fold between FM and non-FM groups in younger patients (age <35 years, 95% CI: 1.86-2.75).This is the first investigation associating FM with an increased risk of stroke development. The outcomes imply that FM is a significant risk factor for stroke and that patients with FM, particularly younger patients, require close attention and rigorous measures for preventing stroke.
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Fibromialgia/complicações , Acidente Vascular Cerebral/etiologia , Adulto , Idoso , Estudos de Coortes , Feminino , Fibromialgia/epidemiologia , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Medição de Risco , Fatores de Risco , Acidente Vascular Cerebral/epidemiologia , Taiwan/epidemiologiaRESUMO
OBJECTIVES: Fibromyalgia has seldom been associated with coronary heart disease (CHD). The aim of this study was to evaluate the risk of CHD in patients with fibromyalgia. METHODS: We used a dataset of one million participants, systemically scrambled from the Taiwanese national insurance beneficiaries, to identify 61,612 patients with incident fibromyalgia (ICD-9-CM 729.0-729.1) and 184,834 reference subjects matched by sex, age and index date of diagnosis in a 1:3 ratio from 2000 to 2005, with a mean 8.86 ± 2.68 years of follow-up until 2011. Risk of CHD was analyzed by Cox proportional hazard modeling. RESULTS: Patients with fibromyalgia had a mean age of 44.1 ± 16.5 years. CHD events developed in fibromyalgia patients (n = 8,280; 15.2 per 103 person-years) and reference subjects (n = 15,162; 9.26 per 103 person-years) with a significant incidence rate ratio of 1.64 (95% confidence interval: 1.61-1.68). The adjusted hazard ratio for CHD in fibromyalgia patients relative to reference subjects was 1.47 (1.43-1.51), after adjusting for age, gender, occupation, monthly income, traditional cardiovascular comorbidities, depression and anxiety. We noted that fibromyalgia and cardiovascular comorbidities had a significant interaction effect on CHD risk (p for interaction <0.01), which was markedly enhanced in fibromyalgia patients with concomitant comorbidities relative to patients with primary fibromyalgia and reference subjects (no fibromyalgia, no comorbidity). CONCLUSIONS: Our report shows that fibromyalgia patients have an independent risk for CHD development. Fibromyalgia patients with concomitant comorbidities have markedly increased CHD risk relative to those with primary fibromyalgia.
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Doença das Coronárias/epidemiologia , Doença das Coronárias/etiologia , Fibromialgia/complicações , Fibromialgia/epidemiologia , Adulto , Estudos de Coortes , Comorbidade , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Taiwan/epidemiologiaRESUMO
INTRODUCTION: Transglutaminase 2 (TG2), a protein crosslinking enzyme with multiple biochemical functions, has been connected to various inflammatory processes. In this study, the involvement of TG2 in monosodium urate (MSU) crystal-induced inflammation was studied. METHODS: Immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR) were performed to detect TG2 expression in synovial fluid mononuclear cells (SFMCs) and synovial tissue from patients with gouty arthritis. MSU crystal-exposed RAW264.7 mouse macrophages were analyzed for interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), transforming growth factor ß1 (TGF-ß1) and TG2 expression by RT-PCR and enzyme-linked immunosorbent assay (ELISA). TG2 small interfering (si)-RNA-mediated silencing and overexpression in RAW264.7 cells were used to evaluate the involvement of TG2 in resolving MSU crystal-induced inflammation. The role of metastatic tumor antigen 1 (MTA1), a master chromatin modifier, was investigated by MTA1 si-RNA-mediated knockdown. In addition, the inflammatory responses were followed in wild type and TG2 null mice after being challenged with MSU crystals in an in vivo peritonitis model. RESULTS: TG2 expression was up-regulated in the synovium tissue and SFMCs from patients with gouty arthritis. The levels of MTA1, TG2, TGF-ß1, IL-1ß and TNF-α mRNAs were consistently increased in MSU crystal-stimulated RAW264.7 cells. si-MTA1 impaired the basal, as well as the MSU crystal-induced expression of TG2 and TGF-ß1, but increased that of IL-1ß and TNF-α. TG2 overexpression dramatically suppressed MSU crystal-induced IL-1ß and TNF-α, but significantly enhanced the TGF-ß1 production. Neutralizing TGF-ß antibodies or inhibition of the crosslinking activity of TG2 attenuated these effects. On the contrary, loss of TG2 resulted in a reduced TGF-ß, but in an increased IL-1ß and TNF-α production in MSU crystal-stimulated RAW264.7 cells and mouse embryonic fibroblasts (MEFs). MSU crystal-stimulated IL-1ß production was Janus kinase 2 (JAK2)-signaling dependent and TG2-induced TGF-ß suppressed the activity of it. Finally, TG2-deficient mice exhibited hyper inflammatory responses after being challenged with MSU crystals in an in vivo peritonitis model. CONCLUSIONS: These findings reveal an inherent regulatory role of the MTA1-TG2 pathway in the self-limitation of MSU crystal-induced inflammation via positively regulating the levels of active TGF-ß1 in macrophages that opposes the MSU crystal-induced JAK2-dependent pro-inflammatory cytokine formation.
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Artrite Gotosa/metabolismo , Proteínas de Ligação ao GTP/biossíntese , Histona Desacetilases/biossíntese , Proteínas Repressoras/biossíntese , Fator de Crescimento Transformador beta1/biossíntese , Transglutaminases/biossíntese , Regulação para Cima/fisiologia , Ácido Úrico/toxicidade , Animais , Artrite Gotosa/patologia , Linhagem Celular , Humanos , Inflamação/metabolismo , Inflamação/patologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Proteína 2 Glutamina gama-Glutamiltransferase , Transativadores , Regulação para Cima/efeitos dos fármacosRESUMO
OBJECTIVE: To determine which clinical, laboratory, and imaging features most accurately distinguished gout from non-gout. METHODS: We performed a cross-sectional study of consecutive rheumatology clinic patients with ≥1 swollen joint or subcutaneous tophus. Gout was defined by synovial fluid or tophus aspirate microscopy by certified examiners in all patients. The sample was randomly divided into a model development (two-thirds) and test sample (one-third). Univariate and multivariate association between clinical features and monosodium urate-defined gout was determined using logistic regression modeling. Shrinkage of regression weights was performed to prevent overfitting of the final model. Latent class analysis was conducted to identify patterns of joint involvement. RESULTS: In total, 983 patients were included. Gout was present in 509 (52%). In the development sample (n = 653), the following features were selected for the final model: joint erythema (multivariate odds ratio [OR] 2.13), difficulty walking (multivariate OR 7.34), time to maximal pain <24 hours (multivariate OR 1.32), resolution by 2 weeks (multivariate OR 3.58), tophus (multivariate OR 7.29), first metatarsophalangeal (MTP1) joint ever involved (multivariate OR 2.30), location of currently tender joints in other foot/ankle (multivariate OR 2.28) or MTP1 joint (multivariate OR 2.82), serum urate level >6 mg/dl (0.36 mmoles/liter; multivariate OR 3.35), ultrasound double contour sign (multivariate OR 7.23), and radiograph erosion or cyst (multivariate OR 2.49). The final model performed adequately in the test set, with no evidence of misfit, high discrimination, and predictive ability. MTP1 joint involvement was the most common joint pattern (39.4%) in gout cases. CONCLUSION: Ten key discriminating features have been identified for further evaluation for new gout classification criteria. Ultrasound findings and degree of uricemia add discriminating value, and will significantly contribute to more accurate classification criteria.
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Gota/classificação , Adulto , Idoso , Estudos Transversais , Feminino , Gota/diagnóstico , Humanos , Masculino , Pessoa de Meia-Idade , Análise MultivariadaRESUMO
BACKGROUND: High serum uric acid (sUA) has been associated with increased mortality risks, but its clinical treatment varied with potential side effects. The role of physical activity has received limited attention. METHODS: A cohort, consisting of 467â 976 adults, who went through a standard health screening programme, with questionnaire and fasting blood samples, was successively recruited between 1996 and 2008. High sUA is defined as uric acid above 7.0â mg/dL. Leisure time physical activity level was self-reported, with fully active defined as those with 30â min per day for at least 5â days a week. National death file identified 12â 228 deaths with a median follow-up of 8.5â years. Cox proportional model was used to analyse HRs, and 12 variables were controlled, including medical history, life style and risk factors. FINDINGS: High sUA constituted one quarter of the cohort (25.6%). Their all-cause mortality was significantly increased [HR: 1.22 (1.15-1.29)], with much of the increase contributed to by the inactive (HR: 1.27 (1.17-1.37)), relative to the reference group with sUA level of 5-6â mg/dL. When they were fully active, mortality risks did not increase, but decreased by 11% (HR: 0.89 (0.82-0.97)), reflecting the benefits of being active was able to overcome the adverse effects of high sUA. Given the same high sUA, a 4-6â years difference in life expectancy was found between the active and the inactive. CONCLUSIONS: Physical activity is a valuable alternative to pharmacotherapy in its ability to reduce the increases in mortality risks from high sUA. By being fully active, exercise can extend life span by 4-6â years, a level greater than the 1-4â years of life-shortening effect from high sUA.
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Exercício Físico , Hiperuricemia/epidemiologia , Mortalidade , Atividade Motora , Ácido Úrico/sangue , Adulto , Idoso , Doenças Assintomáticas , Causas de Morte , Estudos de Coortes , Diabetes Mellitus/epidemiologia , Feminino , Seguimentos , Humanos , Hiperlipidemias/epidemiologia , Hipertensão/epidemiologia , Atividades de Lazer , Masculino , Pessoa de Meia-Idade , Estado Pré-Diabético/epidemiologia , Modelos de Riscos Proporcionais , Insuficiência Renal Crônica/epidemiologia , Fatores de Risco , Comportamento de Redução do Risco , Comportamento Sedentário , Fumar/epidemiologia , Taiwan/epidemiologia , Adulto JovemRESUMO
AIMS: There is an ongoing discussion on whether serum uric acid (SUA) predicts ischemic heart disease (IHD) independently of other metabolic factors, which, if confirmed, would signify a role for uric acid in the pathogenesis of cardiovascular disease. We investigated whether such a relation exists for ethnic Chinese with low CVD risk. METHODS AND RESULTS: Enrolled, between 1994 and 1996, were 128,569 adults ≥ 20 years from four 'MJ' Health Check-up Clinics in Taiwan. Excluded were those with heart disease, previous stroke(s), renal disease, and/or cancer. Physical examinations, biospecimen collections, and structured questionnaires were executed according to standardised protocols. We identified IHD events according to the ICD-9-CM codes 410-414 using hospitalisation records obtained from the National Health Insurance and the Death Certification Registry databases. The Cox proportional hazard model was used to estimate the hazard ratios (HRs) between SUA and IHD events. A total of 2049 subjects (1239 men, 810 women) developed IHD from baseline to Dec. 31, 2002. Men had a higher IHD incidence than did women (2.84 vs. 1.61 1/1000 person-years; p < 0.0001). The risk-factor-adjusted HRs (95% confidence-interval [CI]) for hyperuricemiae (SUA ≥ 7.0/≥ 6.0mg/dL) were 1.25 (1.11-1.40) for men and 1.19 (1.02-1.38) for women. In the low-risk population (lacking the NCEP-ATPIII metabolic syndrome components), a significant association was still observed (adjusted HR: 1.54 [1.09-2.17]). CONCLUSION: The hyperuricemia was independently associated with the development of IHD not only in the general population but also in those without any metabolic risk factor for NCEP ATPIII. Hyperuricemia may be considered as a potential risk factor for IHD.
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Hiperuricemia/complicações , Isquemia Miocárdica/etiologia , Adulto , Povo Asiático , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Isquemia Miocárdica/epidemiologia , Estudos Prospectivos , Fatores de Risco , TaiwanRESUMO
Human osteoclast formation from mononuclear phagocyte precursors involves interactions between lectins and their receptors. A type-2 ribosome inactivating protein consists of an A chain and a B chain. The glycosylated B chain binds specifically to galactose moieties of sugar molecules. In this study we showed that the recombinant ribosome inactivating protein B-chain (rRBC) could induce osteoclast formation from human monocytes and murine RAW264.7 macrophages. Tartrate-resistant acid phosphatase (TRAP) staining and bone resorption assays demonstrated that differentiation of osteoclast-like cells was induced in the presence of rRBC in a dose-dependent manner. The rRBC-induced osteoclast differentiation was independent of caspase activation and apoptosis induction activity; however, rRBC-induced osteoclastogenesis was dependent on activation of NF-κB, ERK1/2, and p38 MAP kinase. Thus, our data demonstrated that rRBC induced osteoclast differentiation through a non-apoptotic signaling pathway. In addition to triggering apoptosis, the rRBC also induced osteoclast differentiation. According to this study, a novel role is proposed for rRBC in regulating osteoclast differentiation and in osteoimmunology.
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Diferenciação Celular/fisiologia , Macrófagos/citologia , Osteoclastos/citologia , Proteínas Inativadoras de Ribossomos/fisiologia , Animais , Western Blotting , Linhagem Celular , Linhagem da Célula , Ativação Enzimática , Humanos , Sistema de Sinalização das MAP Quinases , Camundongos , Reação em Cadeia da Polimerase Via Transcriptase ReversaRESUMO
OBJECTIVE: The association between hyperuricemia and cardiovascular events has been documented in high-risk groups, but is still undetermined in general populations, especially Chinese. This study assessed the temporal association between serum uric acid level, hyperuricemia, and cardiovascular mortality. METHODS: A prospective cohort study of 41,879 men and 48,514 women ages > or = 35 years was conducted using data from the MJ Health Screening Centers in Taiwan. Mortality from all causes, total cardiovascular disease (CVD), ischemic stroke, congestive heart failure, hypertensive disease, and coronary heart disease were compared according to increasing serum uric acid levels. RESULTS: A total of 1,151 (21.2%) events of 5,427 total deaths were ascribed to CVD (mean followup 8.2 years). Hazard ratios (HRs) for hyperuricemia (serum uric acid level >7 mg/dl) were estimated with Cox regression model after adjusting for age, sex, body mass index, cholesterol, triglycerides, diabetes, hypertension, heavy cigarette smoking, and frequent alcohol consumption. In all patients, HRs were 1.16 (P < 0.001) for all-cause mortality, 1.39 (P < 0.001) for total CVD, and 1.35 (P = 0.02) for ischemic stroke. In subgroup analysis, the HRs for cardiovascular risk remained significant in patients with hypertension (1.44, P < 0.001) and in patients with diabetes (1.64, P < 0.001). In addition, in a low metabolic risk subgroup, the HRs for all-cause mortality and total cardiovascular morbidity were 1.24 (P = 0.02) and 1.48 (P = 0.16), respectively. CONCLUSION: Hyperuricemia was an independent risk factor of mortality from all causes, total CVD, and ischemic stroke in the Taiwanese general population, in high-risk groups, and potentially in low-risk groups.