Objective To determine whether measures of ovarian reserve differ between females exposed to cancer therapies in a dose-dependent manner as compared to healthy controls of similar age and late-reproductive age. Design Cross-sectional analysis of data from a prospective cohort study Setting University Medical Center Patients 71 cancer survivors age 15-39; 67 healthy, similarly aged unexposed subjects; 69 regularly menstruating women of late-reproductive age (40-52 years). Interventions: None Main Outcome measures Early follicular phase hormones (FSH, Estradiol, Inhibin B, AMH) and ovarian ultrasound measurements (ovarian volume and Antral Follicle Counts) were compared using multivariable linear regression. Results In adjusted models, FSH, AMH and AFC differed between exposed vs. unexposed (FSH 11.12mIU/ml vs. 7.25mIU/ml, p=0.001; AMH 0.81ng/ml vs. 2.85ng/ml, p<0.001; AFC: 14.55 vs. 27.20, p<0.001. In participants with an FSH<10, survivors had lower levels of AMH and AFC compared to controls. Alkylating agent dose score was associated with increased levels of FSH (p= 0.016) and decreased levels of AMH (p=0.003). Exposure to pelvic radiation was associated with impairment in FSH, AMH, AFC and ovarian volume. AMH was similar in women previously exposed to high-dose cancer therapy and 40-42 year old controls. Conclusions Measures of ovarian reserve are impaired in a dose-dependent manner among cancer survivors compared to unexposed females of similar age. Reproductive hormone levels in menstruating survivors exposed to high-dose therapy are similar to late-reproductive women. The predictive value of measures for pregnancy and menopause must be studied.
Objective To identify factors associated with ovarian reserve (OR) impairment during and immediately after chemotherapy. Design Prospective cohort study. Setting Four university hospitals. Patients Adolescent and young adult females with a new diagnosis of cancer requiring chemotherapy. Interventions None. Main Outcome Measures Participants were followed to assess measures of OR (serum follicle-stimulating hormone, luteinizing hormone, estradiol, inhibin B, anti-mullerian hormone (AMH), and antral follicle counts and mean ovarian volume) at 3 month intervals. Changes in OR were quantified for both the acute impact of treatment using linear regression and the longitudinal recovery after therapy using mixed effects models adjusted for baseline OR, use of alkylating agent, and hormone use. Results 46 women with at least 1 pretreatment and 2 post-treatment study visits were included (mean follow-up 12 months). All measures of OR demonstrated significant changes during chemotherapy. Alkylating agent exposure and baseline OR were associated with the magnitude of impairment acutely, and pretreatment AMH levels were associated with the rate of recovery of AMH post-treatment. In adjusted models, participants with a pretreatment AMH level >2 ng/mL recovered at a rate of 11.9% per month after chemotherapy, whereas participants with pretreatment AMH levels ≤2 ng/mL recovered at a rate of 2.6% per month after therapy (p=0.003). Conclusion Baseline OR and alkylating agent exposure effect the magnitude of acute changes in OR from chemotherapy. The rate of recovery of AMH is impacted by pretreatment levels. This should be considered during pretreatment fertility preservation counseling.
Objective To determine the exact nature and timing of alterations in thyroid function throughout controlled ovarian hyperstimulation (COH). Design Prospective cohort study. Setting University fertility clinic. Patient(s) Fifty-seven women undergoing COH as part of planned in vitro fertilization. Intervention(s) None. Main Outcome Measure(s) Timing and magnitude of change in serum thyroid hormones, including TSH, total and free T4, E2, and thyroxine-binding globulin (TBG), measured at six time points from before stimulation to 2 weeks after serum pregnancy test. Result(s) Geometric mean serum TSH increased during stimulation, peaking 1 week after hCG administration compared with baseline (2.44 vs. 1.42 mIU/L), as did free T4 (1.52 vs. 1.38 ng/dL) and TBG (32.86 vs. 21.52 μg/mL). Estradiol levels increased, peaking at hCG administration (1743.21 vs. 71.37 pg/mL). Of 50 women with baseline TSH ≤2.5 mIU/L, 22 (44.0%) had a subsequent rise in TSH to >2.5 during or after COH. The pattern of change over time in TSH concentrations was significantly influenced by baseline hypothyroidism and whether pregnancy was achieved. Conclusion(s) COH led to significant elevations in TSH, often above pregnancy appropriate targets. These findings were particularly evident in women with preexisting hypothyroidism and may have important clinical implications for screening and thyroid hormone supplementation.
Objective To compare Anti-Mullerian Hormone (AMH) levels in women at high risk for hereditary breast and ovarian cancer compared to healthy, low-risk controls. Design Prospective cohort Setting Ambulatory Patient(s) Reproductive age women with a uterus and both ovaries were analyzed in four groups: BRCA1 carriers, BRCA2 carriers, BRCA negative, and low-risk controls Intervention(s) Self-collected dried blood spot (DBS) Main Outcome Measure(s) AMH levels Result(s) One hundred ninety-five women were included: 55 BRCA1 carriers, 50 BRCA2 carriers, 26 BRCA negative, and 64 low-risk controls. After adjusting for confounders, BRCA2 carriers had AMH levels that were 33% lower than controls (Geometric Mean Ratio(GMR)=0.67, 95% CI 0.47–0.94) and an increased odds of having AMH<1 ng/mL (OR 3.69, 95% CI 1.34–10.19). BRCA1 carriers and BRCA negative women had similar AMH levels to controls. When analysis was restricted to regularly menstruating women younger than 40, BRCA2 carriers continued to demonstrate significantly lower AMH levels and increased likelihood of low AMH. Also, in this restricted group, BRCA negative women demonstrated AMH levels that were 42% lower than controls (GMR=0.58; 95%CI 0.35–0.95). No difference in AMH was observed among BRCA1 carriers. Conclusion(s) We observed significantly lower AMH levels among BRCA2 carriers compared to low-risk controls. These results were stable across all models. BRCA negative women also had lower AMH values, but only in models restricted to young, regularly menstruating women. In contrast to previous analyses, BRCA1 carriers had AMH values that were similar to low-risk controls, but this may be due to differences in the population studied.
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