Assessment of Contraceptive Counseling and Contraceptive Use in Women After Bariatric Surgery

BACKGROUND: Reproductive-aged women are, according to American and European guidelines, recommended to avoid pregnancy for 12-24 months after bariatric surgery. Oral contraceptives may have suboptimal efficacy after malabsorptive bariatric procedures. AIM: The aim of this study was to assess contraceptive use pre- and postoperatively in women who underwent bariatric surgery in two obesity clinics in The Netherlands. Also, the recall of contraceptive and pregnancy counseling was investigated. METHODS: A validated questionnaire was performed among women aged 18-45 years who underwent bariatric surgery from October 2017 through August 2018. RESULTS: In total, 230 women were eligible for final analysis. Postoperatively, 60% used safe contraception, 16.1% unsafe contraception, and 23.9% no contraception. In this study, 43.7% of women using a potential unsafe contraceptive method preoperatively switched to a safe method of contraception postoperatively (p < 0.0001). Only 62.6% of women confirmed to have received contraceptive counseling, mainly preoperatively. The odds ratio for receiving contraceptive counseling and using safe contraceptive methods compared with not receiving contraceptive counseling was 2.20 (95% CI, 1.27-3.79; p = 0.005). Eighty-three percent confirmed that they have received counseling regarding delaying a pregnancy, and 52.6% were familiar with the recommendation to avoid a pregnancy for 24 months postoperatively. CONCLUSIONS: In our study, 60% of women are using safe contraception postoperatively. Contraceptive counseling is suboptimal as 62.6% recall receiving counseling. Those who confirmed receiving counseling were more likely to use safe contraception after bariatric surgery. More counseling and monitoring in the postoperative and in the outpatient setting is recommended

Statin use is not associated with improved progression free survival in cetuximab treated KRAS mutant metastatic colorectal cancer patients: results from the CAIRO2 study.

Statins may inhibit the expression of the mutant KRAS phenotype by preventing the prenylation and thus the activation of the KRAS protein. This study was aimed at retrospectively evaluating the effect of statin use on outcome in KRAS mutant metastatic colorectal cancer patients (mCRC) treated with cetuximab. Treatment data were obtained from patients who were treated with capecitabine, oxaliplatin bevacizumab ± cetuximab in the phase III CAIRO2 study. A total of 529 patients were included in this study, of whom 78 patients were on statin therapy. In patients with a KRAS wild type tumor (n = 321) the median PFS was 10.3 vs. 11.4 months for non-users compared to statin users and in patients with a KRAS mutant tumor (n = 208) this was 7.6 vs. 6.2 months, respectively. The hazard ratio (HR) for PFS for statin users was 1.12 (95% confidence interval 0.78-1.61) and was not influenced by treatment arm, KRAS mutation status or the KRAS*statin interaction. Statin use adjusted for covariates was not associated with increased PFS (HR = 1.01, 95% confidence interval 0.71-1.54). In patients with a KRAS wild type tumor the median OS for non-users compared to statin users was 22.4 vs. 19.8 months and in the KRAS mutant tumor group the OS was 18.1 vs. 14.5 months. OS was significantly shorter in statin users versus non-users (HR = 1.54; 95% confidence interval 1.06-2.22). However, statin use, adjusted for covariates was not associated with increased OS (HR = 1.41, 95% confidence interval 0.95-2.10). In conclusion, the use of statins at time of diagnosis was not associated with an improved PFS in KRAS mutant mCRC patients treated with chemotherapy and bevacizumab plus cetuximab

Kaplan-Meier plots for progression free survival for patients with KRAS wild type (19 statin-users and 145 nonusers) and KRAS mutant (16 statin-users and 83 nonusers) tumors treated with capecitabine, oxaliplatin, bevacizumab and cetuximab.

<p>Kaplan-Meier plots for progression free survival for patients with KRAS wild type (19 statin-users and 145 nonusers) and KRAS mutant (16 statin-users and 83 nonusers) tumors treated with capecitabine, oxaliplatin, bevacizumab and cetuximab.</p

Patient Characteristics.

<p>Patient Characteristics.</p

Overview of the mevalonate pathway and the inhibition of HMG-CoA by statins.

<p><i>Mevalonate pathway causes prenylation of ras, N-glycosylation of EGFR and membrane and steroidsynthesis. Statins have inhibitory effects on the mevalonate pathway and thus on prenylation of k-ras. Abbreviations: Acetyl-CoA, Acetyl coenzyme A; EGFR, epidermal growth factor receptor; FTase, farnesyltransferase; GTase, geranylgeranyltransferase; HMG-CoA (reductase), 3-hydroxy-3-methyl-glutaryl-CoA reductase; -PP, -pyrophosphate.</i></p

Statin Use Is Not Associated with Improved Progression Free Survival in Cetuximab Treated KRAS Mutant Metastatic Colorectal Cancer Patients: Results from the CAIRO2 Study

Statins may inhibit the expression of the mutant KRAS phenotype by preventing the prenylation and thus the activation of the KRAS protein. This study was aimed at retrospectively evaluating the effect of statin use on outcome in KRAS mutant metastatic colorectal cancer patients (mCRC) treated with cetuximab. Treatment data were obtained from patients who were treated with capecitabine, oxaliplatin bevacizumab ± cetuximab in the phase III CAIRO2 study. A total of 529 patients were included in this study, of whom 78 patients were on statin therapy. In patients with a KRAS wild type tumor (n = 321) the median PFS was 10.3 vs. 11.4 months for non-users compared to statin users and in patients with a KRAS mutant tumor (n = 208) this was 7.6 vs. 6.2 months, respectively. The hazard ratio (HR) for PFS for statin users was 1.12 (95% confidence interval 0.78-1.61) and was not influenced by treatment arm, KRAS mutation status or the KRAS*statin interaction. Statin use adjusted for covariates was not associated with increased PFS (HR = 1.01, 95% confidence interval 0.71-1.54). In patients with a KRAS wild type tumor the median OS for non-users compared to statin users was 22.4 vs. 19.8 months and in the KRAS mutant tumor group the OS was 18.1 vs. 14.5 months. OS was significantly shorter in statin users versus non-users (HR = 1.54; 95% confidence interval 1.06-2.22). However, statin use, adjusted for covariates was not associated with increased OS (HR = 1.41, 95% confidence interval 0.95-2.10). In conclusion, the use of statins at time of diagnosis was not associated with an improved PFS in KRAS mutant mCRC patients treated with chemotherapy and bevacizumab plus cetuximab