Abstract
Background: Problems with hormonal changes and the related variations in bone turnover in adolescents with polycystic ovarian syndrome (PCOS) have been of interest in terms of providing these patients with an opportunity to receive a prophylactic and precision-based treatment aiming to prevent early onset of osteoporosis. Materials and methods: Prospective comparative clinical trial—‘case-control’ type in Bulgarian populace of 36 female patients with PCOS and 42 healthy controls aged 12 to 18. The study protocol included a general section of anthropometric patient data, clinical section–including general and Ob/Gyn Medical History, ultrasound exam of the lesser pelvis and a lab section examining the serum levels of Follicle-stimulating hormone (FSH), Luteinizing hormone (LH), estradiol, Anti-Müllerian hormone (AMH) and bone turnover markers–osteocalcin and β-CrossLaps (bCTX), as well as Vitamin D. Results: A statistically significant high serum levels of the gonadotropic hormones were observed (LH — p < 0.001 и FSH — p = 0.017), AMH (p < 0.001) in patients with PCOS compared to the controls, while the estradiol (p = 0.043) and osteocalcin (p < 0.001) levels displayed a statistically significant lower values in patients with PCOS compared to the control group. AMH can be utilized as a surrogate marker for diagnosing patients with PCOS where the marker shows sensitivity — 94% and specificity — 69% with threshold value (cut-off) at ≥5.95 ng/mL (area under the curve 0.854, p < 0.001). Significant variance in Vitamin D serum levels between the two groups was not detected. Conclusion: Despite the hormonal characteristic of normogonadotropic normogonadism in adolescent patients with PCOS, the significantly lower values of osteocalcin demonstrated suppressed bone metabolism–bone formation, in particular–compared to the healthy controls, which can be interpreted as increased risk of insufficient bone accretion and risk of early onset of osteoporosis later in life.
Highlights
polycystic ovarian syndrome (PCOS) is a heterogenic endocrine disorder that affects 1 in 15 women worldwide [1]
The high diagnostic reliability of Anti-Müllerian hormone (AMH) as a surrogate marker complementary to the Rotterdam Criteria in diagnosing PCOS patients has been confirmed in multiple trials [7,8,9,10,11,12]
Follicle-stimulating hormone (FSH — Reference Range Female, Follicular phase: FSH — 1–10 IU/L), Luteinizing hormone (LH — Reference Range Female, Follicular phase: LH — 2–10 IU/L) were measured in a serum of highly sensitive immunoradiometric assays (IRMA) using two monoclonal antibodies with kits from Immunotech, France
Summary
PCOS is a heterogenic endocrine disorder that affects 1 in 15 women worldwide [1]. Usually the onset of the condition is during adolescence and the clinical presentation is characterized by anovulatory cycles (amenorrhea, opsomenorrhea, irregular menstrual cycles) combined with hyperandrogenism symptoms (hirsutism, acne, alopecia).Due to the varied expressions of the syndrome, the European Society for Human Reproduction and Embryology (ESHRE) and the American Society for Reproductive Medicine (ASRM) have established that the diagnosis requires the presence of at least two of the “Rotterdam Criteria”.- Polycystic ovaries on ultrasound. - Anovulatory menstrual cycles. - Clinical or biochemical evidence of excess androgen [2,3]. The estradiol serum levels are similar to those of the healthy controls but still of lower values and they remain constant along the duration of the whole menstrual cycle. The study protocol included a general section of anthropometric patient data, clinical section–including general and Ob/Gyn Medical History, ultrasound exam of the lesser pelvis and a lab section examining the serum levels of Follicle-stimulating hormone (FSH), Luteinizing hormone (LH), estradiol, Anti-Müllerian hormone (AMH) and bone turnover markers–osteocalcin and β-CrossLaps (bCTX), as well as Vitamin D. Conclusion: Despite the hormonal characteristic of normogonadotropic normogonadism in adolescent patients with PCOS, the significantly lower values of osteocalcin demonstrated suppressed bone metabolism–bone formation, in particular–compared to the healthy controls, which can be interpreted as increased risk of insufficient bone accretion and risk of early onset of osteoporosis later in life
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