ESPE Abstracts

Aim: Although genetic factors are primarily responsible for the etiology of puberty, nutrition and environmental factors are also known to be effective. Obesity is associated with various metabolic complications and affects many aspects of pubertal development such as changes in pubertal hormones and onset of puberty. However, the relationships between these factors are still unclear. It has been reported that overweight and obese children generally have advanced bone age with accelerated growth and sexual maturation. We aimed to investigate whether there is a difference in terms of clinical, laboratory and radiological findings between obese and non-obese girls who presented with breast development and were examined for early puberty.

Methods: Fifty overweight and obese and fifty normal weight girls (between 3-8 years of age) who were admitted to the pediatric endocrinology clinic for breast development and investigated for early puberty were included in the study. Cases with genetic or hormonal obesity, chronic disease and drug use, laboratory or radiologically diagnosed as central precocious puberty (CPP) due to pituitary or intracranial pathologies and peripheral precocious puberty due to liver, renal, thyroid, adrenal pathologies were excluded from the study. Chronological age (CA), body weight standard deviation score (SDS), height SDS, body mass index (BMI) SDS, bone age (BA), BA-CA difference (ΔBA-CA), basal and stimulated follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2) and peak LH / FSH ratio were recorded. Uterine long diameter, uterine and ovarian volumes were evaluated by pelvic ultrasound. CPP was diagnosed when the peak LH levels after gonadorelin stimulation was > 5.0 U/L.

Results: Height SDS and ΔBA-CA values of obese subjects were found to be statistically higher than normal weight controls (P = 0.001, P = 0.02 respectively). Baseline FSH levels were higher in non-obese subjects than in obese subjects (P = 0.03). There was no statistically difference between the two groups in LH-RH test responses. Eight (16%) of the obese and 13 (26%) of the non-obese subjects were diagnosed as CPP.

Conclusion: It was shown that height SDS and ΔBA-CA values were higher in obese subjects. Despite advanced bone age, rate of CPP diagnosis was low in the obese group. In obese girls, underlying biological mechanisms such as compensatory hyperinsulinemia, insulin resistance, endocrine disruptors, and androgens may be contributing to bone age progression and pubertal characteristic changes. Consequently those can be misleading for CPP predicting.

Keywords: Early puberty, Girl, Obesity, Advanced bone age