OBJECTIVE -Polychlorinated biphenyls (PCBs) and polychlorinated dibenzofurans (PCDFs) are important and persistent organic pollutants (POPs) in humans. Recent cross-sectional studies have detected increased concentrations of serum POPs in diabetic patients. We aimed to examine the association between previous high exposures to PCBs and PCDFs and the cumulative incidence of type 2 diabetes and hypertension.RESEARCH DESIGN AND METHODS -During the late 1970s, the consumption of rice-bran oil laced with PCBs poisoned thousands of Taiwanese. Between 1993 and 2003, we examined 1,054 Yucheng ("oil disease") victims against neighborhood reference subjects using a protocol blinded for POP exposure. Here, we report the results derived from 378 Yucheng subjects and 370 matched references.RESULTS -The diabetes risk to members of the Yucheng cohort relative to their reference subjects was significantly increased for women (odds ratio [OR] 2.1 [95% CI 1.1-4.5]) but not for men after considering age, BMI, cigarette smoking, and alcohol intake. Yucheng women diagnosed with chloracne had adjusted ORs of 5.5 (95% CI 2.3-13.4) for diabetes and 3.5 (1.7-7.2) for hypertension compared with those who were chloracne free.CONCLUSIONS -Yucheng women, who had endured previous exposure to PCBs and PCDFs, suffered from increased incidences of diabetes, particularly those who had retained significant levels of pollutant as evident from chloracne. When planning treatments against diabetes, the body burden of PCBs and dioxins should be carefully considered, especially for women.
INTRODUCTION:
It is unclear whether entecavir (ETV) and tenofovir disoproxil fumarate (TDF) differ in their effectiveness for preventing hepatocellular carcinoma (HCC) in patients with chronic hepatitis B (CHB).
METHODS:
This retrospective cohort study analyzed an international consortium that encompassed 19 centers from 6 countries or regions composed of previously untreated CHB patients then treated with either ETV or TDF monotherapy. Those who developed HCC before antiviral treatment or within 1 year of therapy were excluded. The association between antiviral regimen and HCC risk was evaluated using competing-risk survival regression. We also applied propensity score matching (PSM) to 1:1 balance the 2 treatment cohorts. A total of 5,537 patients were eligible (n = 4,837 received ETV and n = 700 received TDF) and observed for HCC occurrence until December 23, 2018. Before PSM, the TDF cohort was significantly younger and had generally less advanced diseases.
RESULTS:
In the unadjusted analysis, TDF was associated with a lower risk of HCC (subdistribution hazard ratio [SHR], 0.45; 95% confidence interval [CI], 0.26–0.79; P = 0.005). The multivariable analysis, however, found that the association between TDF and HCC no longer existed (SHR, 0.81; 95% CI, 0.42–1.56; P = 0.52) after adjustment for age, sex, country, albumin, platelet, α-fetoprotein, cirrhosis, and diabetes mellitus. Furthermore, the PSM analysis (n = 1,040) found no between-cohort differences in HCC incidences (P = 0.51) and no association between regimens (TDF or ETV) and HCC risk in the multivariable-adjusted analysis (adjusted SHR, 0.89; 95% CI, 0.41–1.92; P = 0.77).
DISCUSSION:
TDF and ETV did not significantly differ in the prevention of HCC in patients with CHB.
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