A large proportion of breast cancer patients receive hormonal therapy as their adjuvant treatment options. For postmenopausal women, the initial choice for the hormonal therapy is aromatase inhibitor (AI), and tamoxifen (TM) is reserved for women experiencing severe side effects against AI or having low bone density. An important but unresolved clinical question regarding the use of AI in postmenopausal women is the safety of AI regarding the risk cardiovascular events. Studies have shown inconsistent results over the cardiovascular safety of AI and TM. In this study, we investigated the risk of developing cardiovascular and cerebrovascular events in women with breast cancer who receive hormonal therapy using AI, TM, or both. To this end, we used the National Health Insurance Sharing Service in Korea which is provided by National Health Insurance Service. The database provides anonymized insurance data for research purposes after the approval of the review committee. In the database, we identified 47,569 women with the age older than 55 who were diagnosed with breast cancer. Patients were classified as no hormonal treatment group (n=18,807), AI group (n=19,584), TM group (n=7,081), or Switch group (n=2,097). The Switch group was defined as the women with history of both AI and TM prescriptions. During the studied period, a total of 2,032 cardiovascular or cerebrovascular events (CVE) were recorded. Overall, the women prescribed with TM had significantly less hazard ratio for developing CVE when compared to the women who did not receive any hormonal treatment (HR 0.809 95% C.I. 0.706-0.928). However, this protective effect of tamoxifen was not observed in either AI or Switch group (HR 0.917 95% C.I. 0.833-1.010, and HR 0.856 95% C.I. 0.695-1.053, respectively). The protective effect of TM was also similar in women older than 60 (HR 0.808 95% C.I. 0.696-0.938). The cardiovascular and cerebrovascular protective effects of tamoxifen was also substantial in high risk women defined by their family history of cardiovascular diseases and the diagnosis of hypertension or diabetes. Our results suggest that the use of TM is associated with a substantial protective effect against developing cardiovascular or cerebrovascular events in women with breast cancer. However, the protective effect was not observed for women receiving AI. Our data suggest the potential tailored approach in hormonal treatment in breast cancer patients who are at high risk of cardiovascular of cerebrovascular events. Citation Format: Moon H-G, Choi SH, Park Y, Jung JG, Ju YW, Kim KE, Kim Y, Lee E, Lee H-B, Han W, Noh D-Y, Yoon H-J. A nationwide data on the cardiovascular protective effect of tamoxifen and aromatase inhibitor in postmenopausal women with breast cancer [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr P4-14-09.
Backgroud: Obesity, postdiagnosis weight gain, and presence of metabolic syndrome in breast cancer are reported to adversely affect survival among breast cancer survivors. Most of the studies on weight gain and metabolic syndrome in breast cancer are from Western countries and few information is available on Asian population. We designed this prospective observational study to characterize weight and metabolic changes during adjuvant treatment in women with early breast cancer and to identify factors associated with occurrence of metabolic syndrome, focusing on dietary pattern. Methods: Patients aged 18–75 who underwent curative surgery with stage I-III invasive breast cancer were enrolled from 2008 to 2010. We measured glucose (FBS), hemoglobin A1c (HbA1c), total cholesterol (TC), HDL cholesterol, and triglyceride (TG) level in fasting serum samples before starting adjuvant therapy, at 6 months and 12 months after enrollment. Body weight, body mass index (BMI), body fat mass, and percent body fat at baseline, 6 months, and 12 months were also measured. Dietary intake was assessed using valid semi-quantitative Food frequency questionnaire (FFQ). Results: Total of 63 patients were enrolled. Median age of the enrolled patients were 48 (range, 25–68), with premenopausal/postmenopausal 40 (63.5%)/ 23 (36.5%). Fifty (82.0%) and 10 (16.4%) received adjuvant chemotherapy followed by hormone therapy and hormone therapy alone. Hormone receptor positive (ER+/PR+) and HER2 positive cancer accounted for 52 (83.9%) and 7 (12.1%). Mean FBS, HbA1c, TC, HDL, and TG level was 99.9 mg/dL (range, 83–159), 5.59 mg/dL (range, 4.8−7.5), 197.4 mg/dL (125-298), 51.9 mg/dL (range, 30–90), and 119.7 mg/dL (42-371). Mean height, weight, and BMI was 158 cm (range, 149–169), 61.7kg (range, 46.2−96.0), and 24.7 kg/m2 (range, 18.7−35.7), respectively. According to the WHO and NTH guidelines for Asian, normal (BMI 18.5−22.9), overweight (BMI 23–24.9), and obesity (BMI≥25) was 18 (28.6%), 13 (20.6%), and 32 (50.8%), respectively. Number of patients with metabolic syndrome was 18 (34%). Mean BMI (26.1 vs 24.0, p=0.021) and TG (180.6 vs 92.0, p<0.001) was higher, HDL cholesterol was lower (42.2 vs 57.3, p<0.001) in patients with metabolic syndrome. Composition of daily calorie intake consisted of 13.5% (range 10.7−21.8) of protein, 6.7% (range, 3.3−22.1) of fat, and 70.1% (range, 28.1−79.5) of carbohydrate. The presence of metabolic syndrome was associated with a higher carbohydrate intake (carbohydrate intake per ideal body weight>6.0) (p=0.071). The TG level of patients who indigested high carbohydrate was significantly higher (143.8 vs 102.9, p=0.023). The HDL level of patients who took high fat diet (>20% of total calorie) was lower (45.3 vs 53.5, p=0.045). Conclusion: In our cohort of Korean breast cancer patients, 34% had metabolic syndrome at baseline. Those patients with metabolic syndrome consumed higher proportion of carbohydrate, which resulted in significantly higher level of TG. Our data suggest that composition of calorie intake is different in Asian population compared to Western countries, warranting for reappraisal on the recommendation on life style modification and diet. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P4-11-20.
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