Association between antidepressants and venous thromboembolism in Taiwan.

OBJECTIVE: To investigate the association between venous thromboembolism (VTE) and antidepressant use in an Asian population. METHODS: The authors conducted a nested case-control study of 1888 patients with VTE and 11,222 matched controls enrolled in the National Health Insurance Research Database in Taiwan from 2001 to 2009. The antidepressant exposure status and potential confounding factors were measured and included in the analyses. Conditional logistic regressions were applied to determine the effect of antidepressant use on VTE. RESULTS: We found a significant association of current antidepressant use with VTE in the total study sample (adjusted odds ratio [aOR], 1.59; 95% confidence interval (CI), 1.27-2.00). With regard to antidepressant classes and potency, we found that tricyclic antidepressants (aOR, 1.56; 95% CI, 1.11-2.18), serotonin 5-HT2A receptor blockers (aOR, 2.03; 95% CI, 1.27-3.24), and antidepressants with a low potency of serotonin reuptake inhibition (aOR, 1.57; 95% CI, 1.18-2.08) were associated with a significantly increased risk of VTE. When further stratifying by age, sex, and comorbid conditions, the VTE risk with antidepressant use was elevated among young and middle-aged adults, but not among the elderly. In addition, an elevated risk of VTE was observed in women and subjects without severe comorbid conditions, but not in men and subjects with severe comorbid conditions. CONCLUSIONS: There was a small increase in VTE risk with antidepressant use. The prescription of antidepressant drugs should be cautious, and especially, should be based on clinical evaluations of benefits and risks. The underlying mechanisms of the interaction between antidepressants and VTE warrant further investigation.

Is high serum uric acid a risk marker or a target for treatment? Examination of its independent effect in a large cohort with low cardiovascular risk.

BACKGROUND: Cohort studies evaluating increased uric acid level as a cardiovascular disease (CVD) risk factor have shown variable results; studies are particularly lacking in lower risk populations. STUDY DESIGN: Prospective cohort study. SETTING & PARTICIPANTS: 484,568 adults participating in a medical screening program in Taiwan since 1994 were followed up for a median of 8.5 years. Two subgroups were constructed: the first (n = 246,697; 51%) excluded participants with either overt CVD or overt CVD risk factors (including hypertension, diabetes, obesity, and hypertriglyceridemia) and the second (n = 157,238; 32%) further excluded individuals with early-stage CVD risk factors (including prehypertension, prediabetes, overweight, and borderline hypertriglyceridemia). PREDICTOR: Serum uric acid. OUTCOMES & MEASUREMENTS: All-cause and CVD mortality risk assessed using Cox proportional hazards models for categorical and continuous serum uric acid levels. As applicable, models adjusted for 14 variables. Population-attributable fraction was applied to compare contributions to mortality between high uric acid level and other CVD risk factors. RESULTS: In the total cohort, mean age was 41.4 +/- 14.0 years and 26.2% had serum uric acid levels >or=7 mg/dL. Through 2007, there were 16,246 deaths (3.4% of all participants), with 35.2% of deaths occurring in individuals with hyperuricemia. Adjusted HRs associated with serum uric acid levels >or=7 mg/dL for all-cause and CVD mortality were 1.10 (95% CI, 1.04-1.17) and 1.38 (95% CI, 1.20-1.58), respectively. In individuals with hyperuricemia, 64.3% had overt CVD risk factors and 82.5% had either overt or early-stage CVD risk factors. Individuals with serum uric acid levels >or=8 mg/dL without overt CVD risk factors constituted 13.5% of the total study population with hyperuricemia; in analyses excluding those with overt CVD risk factors, serum uric acid level >or=8 mg/dL was significantly associated with all-cause and CVD mortality, with HRs of 1.37 (95% CI, 1.18-1.60) and 2.30 (95% CI, 1.51-3.49), respectively. In the subgroup of those with serum uric acid levels >or=8 mg/dL but who lacked both overt and early-stage CVD risk factors, the HRs for all-cause and CVD mortality were also significant and were 1.39 (95% CI, 1.08-1.78) and 2.38 (95% CI, 1.24-4.54), respectively. HRs for individuals with the same risk profiles but with serum uric acid of 7.0-7.9 mg/dL were not significant. In all groups, inclusion of proteinuria and glomerular filtration rate in models substantially attenuated the association between uric acid level and outcomes. High uric acid levels contributed a relatively insignificant portion to mortality (1.2%) and CVD deaths (4.5%) in this population. LIMITATIONS: A single measurement of uric acid was used. CONCLUSION: Increased serum uric acid level is a minor, but significant, risk factor for all-cause and CVD mortality. However, except for a small proportion (13.5%), increased serum uric acid level is more a risk marker than a target for treatment and is not an independent risk. Determining appropriate groups to target in clinical trials for uric acid-lowering therapy is critical.

Cancer risks from betel quid chewing beyond oral cancer: a multiple-site carcinogen when acting with smoking.

OBJECTIVES: This cohort study is to assess the extent of cancer risks of betel quid chewing (without tobacco added) beyond oral cancer, as such information was limited from case-control studies. METHODS: The cohort, selected from participants in a medical screening program since 1994, consisted of 177,271 adult men with 19.2% chewers of betel quid. As of 2006, out of 4,840 deaths, 1,901 cancer deaths were identified. Mortality hazard ratios (HR) were estimated by Cox proportional hazard model. Life expectancy was calculated by life table method. RESULTS: One-third of smokers chewed (33%) but most of chewers smoked (90%). Risk for all cancer doubled among chewers (HR = 2.00). Risks of at least six cancer sites were increased among chewers: oral cavity (HR = 12.52), esophagus (HR = 5.64), liver (HR = 2.27), pancreas (HR = 2.67), larynx (HR = 6.24), and lung (HR = 2.43) with risks increased with increasing betel quid amount consumed. All-cancer age-adjusted mortality rates in Taiwan increased 25%, including 223% increase in oral cancer, during the last 20 years when chewing rate increased five- to tenfolds. Chewing on top of smoking increased the risks synergistically, and these two were responsible for at least half (50%) of all cancer deaths among 2 million chewers in Taiwan. Life expectancy of chewers was shorter than non-chewers by 5.93 years at age 20 and 5.55 years at age 40. CONCLUSION: In addition to oral cancer, significant increases were seen among chewers for cancer of the esophagus, liver, pancreas, larynx, lung, and all cancer. Chewing and smoking, as combined by most chewers, interacted synergistically and was responsible for half of all cancer deaths in this group. They were responsible for the recent increases in oral, esophageal, pancreatic, and liver cancer in Taiwan. Chewing and smoking shortened their life span by nearly 6 years.

A 10-year experience with universal health insurance in Taiwan: measuring changes in health and health disparity.

BACKGROUND: Universal national health insurance, financed jointly by payroll taxes, subsidies, and individual premiums, commenced in Taiwan in 1995. Coverage expanded from 57% of the population (before the introduction of national health insurance) to 98%. OBJECTIVE: To assess the role of national health insurance in improving life expectancy and reducing health disparities in Taiwan. DESIGN: A before-and-after comparison of the decade before the introduction of national health insurance (1982-1984 to 1992-1994) with the decade after (1992-1994 to 2002-2004). SETTING: Taiwan. PATIENTS: All townships (n = 358) in Taiwan were ranked according to overall mortality rates before the introduction of national health insurance and then ranked into 10 health class groups in descending order of health (groups 1 [healthiest] to 10 [least healthy]). MEASUREMENTS: Health improvement (change in life expectancy after the introduction of national health insurance) and health disparity (reduction in the difference in life expectancy between the highest- and lowest-ranked health class groups). RESULTS: After the introduction of national health insurance, life expectancy increased more in health class groups that had higher mortality rates before the introduction of national health insurance and health disparity narrowed, reversing an earlier trend toward widening disparity. The major contributors to the reduction in disparity were relatively larger reductions in death from cardiovascular diseases, ill-defined conditions, infectious diseases, and accidents in the lower-ranked health class groups. However, death from cancer increased more in the lower-ranked health class groups. Utilization of medical services increased, whereas cost remained at 5% to 6% of the gross domestic product. The per capita average annual number of visits to the physician's office was 14. LIMITATION: The interpretation of comparisons before and after the introduction of national health insurance assumes that the changes were entirely due to the effect of national health insurance rather than secular trends. CONCLUSION: Life expectancy after the introduction of national health insurance improved more for lower-ranked health classes, resulting in narrowed health disparity. The magnitude of the reduced disparity was small compared with the size of the remaining gaps. Relying on universal insurance alone to eliminate health disparity does not seem realistic. To further reduce health disparity, universal insurance programs should incorporate primary prevention, focusing on lifestyle risk reductions.

Bridging the gap in life expectancy of the aborigines in Taiwan.

BACKGROUND: Similar to the general population in Taiwan, the health of aborigines has steadily improved over the last 30 years, but the gap remains wide, especially in males, despite an infusion of substantial medical resources. The objectives of this study are to quantify the contribution of major causes of death to the gap in life expectancy and to propose initiatives to bridge the health gap between aborigines and the general population. METHODS: This study included residents (slightly over 200000) from 30 'aboriginal townships' in Taiwan. The gap in life expectancy between aborigines and the general population was analysed by decomposing these gaps according to major causes of deaths. This analysis quantifies the contribution of different causes of deaths to the gap in life expectancy between the two populations. RESULTS: The overall mortality of aborigines in these townships was approximately 70% higher than the respective male and female general populations over the past 30 years. Mortality from infectious disease, cirrhosis of the liver, accidents, and suicide are substantially higher than the general population. The gap in life expectancy at birth in males was 8.5 years during 1971-1973, increasing to 13.5 years by 1998-2000, however, the gap in females remained relatively stable (8.0 years and 8.4 years, respectively). Of the 13.5-year difference in life expectancy in males, the differential mortality from diseases of the digestive system (mainly due to cirrhosis of the liver), accidents (from both motor vehicle and non-motor vehicle accidents), and infectious and parasitic disease contributed half (50%) of the gap in life expectancy. In females, the above primarily preventable causes of deaths accounted for 41% of the life expectancy gap. CONCLUSIONS: Based on the findings of this study, we suggest that future focus should be in the area of primary prevention in order to reduce the incidence of infectious and parasitic diseases, liver cirrhosis, and accidents.