Hyperandrogenaemia in adolescent girls: origins of abnormal gonadotropin-releasing hormone secretion - PubMed (original) (raw)
Hyperandrogenaemia in adolescent girls: origins of abnormal gonadotropin-releasing hormone secretion
C M Burt Solorzano et al. BJOG. 2010 Jan.
Abstract
Polycystic ovarian syndrome is a common disorder characterized by ovulatory dysfunction and hyperandrogenemia (HA). Its origins begin peripubertally, as adolescent HA commonly leads to adult HA and decreased fertility. HA reduces inhibition of gonadotropin releasing hormone pulse frequency by progesterone, causing rapid LH pulse secretion and further increasing ovarian androgen production. Obese girls are at risk for HA and develop increased LH pulse frequency with elevated mean LH by late puberty. Many girls with HA do not exhibit normal LH pulse sensitivity to progesterone inhibition. Thus, HA may adversely affect LH pulse regulation during pubertal maturation leading to persistent HA.
Conflict of interest statement
Disclosure of Interests: There are no relevant or significant financial, personal, political, intellectual, or religious conflicts of interest to disclose.
Figures
Fig. 1
Early morning hormone levels in nonobese (open squares) and obese (solid squares) peripubertal girls by breast Tanner stage. Data are presented as mean ± SEM. Differences were assessed with Wilcoxon rank sum tests before Bonferroni correction: * p < 0.05, ** p ≤ 0.01, *** p ≤ 0.001, *** p ≤ 0.0001. Conversion from conventional to SI units: total T × 3.47 (nmol/L). (McCartney et al, 2007, adapted with permission from The Endocrine Society.)
Fig. 2
Schematic diagram of hormonal patterns during an ovulatory menstrual cycle. (Marshall JC and Eagleson CA, 1999, with permission from Elsevier.)
Fig. 3
Late evening and overnight LH characteristics in nonobese (open squares) and obese (solid circles) peripubertal girls by breast Tanner stage. Data are presented as mean ± SEM. The numbers of subjects are below the Tanner stage labels: NO = nonobese, OB = obese. The last column shows obese Tanner 5 girls only with PCOS (solid triangles) and without PCOS (open triangles). Due to blood volume constraints, time point 1900–2300 (subject awake) is used as a surrogate for daytime hormone levels. (McCartney et al, 2009, with permission from The Endocrine Society.)
Fig. 4
Percent change in LH pulse frequency during 11 hr following 7 days of oral E2 and P plotted as a function of mean plasma P on day 7 in control (A) and HA (B) adolescent girls. Shaded circles represent girls with breast Tanner stage 1–2; open circles represent girls with Tanner stage 3–5. The shaded background areas represent range of response to a similar protocol in adult control women (A) and women with PCOS (B). The outlined area in B represents the range of responses in control adolescent girls. Conversion from conventional to SI units: P × 3.18 (pmol/L). (Blank et al, 2009, with permission from The Endocrine Society.)
Fig. 5
Late evening and overnight sex steroid concentrations in nonobese (open squares) and obese (solid circles) peripubertal girls by breast Tanner stage. Data are presented as mean ± SEM. The numbers of subjects are below the Tanner stage labels: NO = nonobese, OB = obese. The last column shows obese Tanner 5 girls only with PCOS (solid triangles) and without PCOS (open triangles). Conversion from conventional to SI units: P × 3.18 (pmol/L); free T (pmol/L); E2 × 3.671 (pmol/L). (McCartney et al, 2009, with permission from The Endocrine Society.)
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