Asma Javed1, Aida N Lteif2, Seema Kumar1, Patricia S Simmons3, Alice Y Chang4. 1. Division of Pediatric Endocrinology, Department of Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, Minnesota. 2. Division of Pediatric Endocrinology, Department of Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, Minnesota. Electronic address: Lteif.aida@mayo.edu. 3. Division of Pediatric and Adolescent Gynecology, Department of Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, Minnesota. 4. Division of Endocrinology, Department of Internal Medicine, Diabetes, Metabolism and Nutrition, Mayo Clinic, Rochester, Minnesota.
Abstract
STUDY OBJECTIVE: To compare changes in fasting glucose among adolescents with polycystic ovary syndrome (PCOS) with those in obese adolescents without PCOS. DESIGN, SETTING, AND PARTICIPANTS: Retrospective cohort study of 310 adolescents with PCOS and 250 obese adolescents (age range 13 to 18 years) seen at Mayo Clinic, Rochester, MN, from 1996 to 2012. METHODS: Included for analysis were 98 adolescents with PCOS and 150 obese adolescents who had 2 or more fasting glucose measurements separated by at least 6 months. Adolescents with impaired fasting glucose (IFG) or diabetes were excluded. Multivariate models were used to assess predictors of change in fasting glucose. RESULTS: At diagnosis, adolescents with PCOS had lower body mass index (BMI) (kg/m(2)) and older age than obese adolescents (P < .001). Adolescents with PCOS had shorter follow-up (P = .02). Baseline fasting glucose was not different between groups. Mean change in fasting glucose was 2.4 ± 9.4 mg/dL per year for PCOS and 2.2 ± 6.2 mg/dL per year for obese adolescents (P = .83). Significant predictors for change in fasting glucose were BMI and fasting glucose at diagnosis (P < .01). Within the PCOS cohort, BMI was a significant predictor for development of IFG (P = .003). Prevalence of hypertension increased in the PCOS cohort from baseline to follow-up (P = .02). PCOS and BMI were significantly associated with development of HTN in the entire cohort. CONCLUSION: Adolescent girls with PCOS do not show a significant change in fasting glucose or an increased risk for the development of IFG compared with obese adolescents. BMI, not PCOS status, was the strongest predictor for changes in fasting glucose and development of IFG over time.
STUDY OBJECTIVE: To compare changes in fasting glucose among adolescents with polycystic ovary syndrome (PCOS) with those in obese adolescents without PCOS. DESIGN, SETTING, AND PARTICIPANTS: Retrospective cohort study of 310 adolescents with PCOS and 250 obese adolescents (age range 13 to 18 years) seen at Mayo Clinic, Rochester, MN, from 1996 to 2012. METHODS: Included for analysis were 98 adolescents with PCOS and 150 obese adolescents who had 2 or more fasting glucose measurements separated by at least 6 months. Adolescents with impaired fasting glucose (IFG) or diabetes were excluded. Multivariate models were used to assess predictors of change in fasting glucose. RESULTS: At diagnosis, adolescents with PCOS had lower body mass index (BMI) (kg/m(2)) and older age than obese adolescents (P < .001). Adolescents with PCOS had shorter follow-up (P = .02). Baseline fasting glucose was not different between groups. Mean change in fasting glucose was 2.4 ± 9.4 mg/dL per year for PCOS and 2.2 ± 6.2 mg/dL per year for obese adolescents (P = .83). Significant predictors for change in fasting glucose were BMI and fasting glucose at diagnosis (P < .01). Within the PCOS cohort, BMI was a significant predictor for development of IFG (P = .003). Prevalence of hypertension increased in the PCOS cohort from baseline to follow-up (P = .02). PCOS and BMI were significantly associated with development of HTN in the entire cohort. CONCLUSION: Adolescent girls with PCOS do not show a significant change in fasting glucose or an increased risk for the development of IFG compared with obese adolescents. BMI, not PCOS status, was the strongest predictor for changes in fasting glucose and development of IFG over time.
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