scholarly journals OR11-01 Using Kisspeptin to Predict Pubertal Outcomes for Youth With Pubertal Delay

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Yee-Ming Chan ◽  
Margaret Flynn Lippincott ◽  
Priscila Sales Barroso ◽  
Cielo Alleyn ◽  
Jill Brodsky ◽  
...  
Keyword(s):  
Inhibin B ◽  
Stimulation Test ◽  
Delayed Puberty ◽  
Laboratory Studies ◽  
Pubertal Delay ◽  
Gnrh Release ◽  
Reproductive Endocrine ◽  
Physical Examinations ◽  
Outcomes For Children ◽  
Endocrine Axis

Abstract Background: The management of youth presenting with delayed puberty is challenging because it can be difficult to predict which children will eventually progress through puberty and which children will not. We have previously shown that exogenous administration of the neuropeptide kisspeptin, which stimulates GnRH release, can be used to probe the integrity of the reproductive endocrine axis. We hypothesized that responses to kisspeptin could predict outcomes for individuals with pubertal delay. Methods: We conducted a longitudinal study of 16 children (3 girls and 13 boys) with delayed or stalled puberty who had undergone stimulation testing with kisspeptin and GnRH. Participants were followed with serial physical examinations and laboratory studies every six months for evidence of progression through puberty. Inhibin B was measured in boys. A subset of participants underwent exome sequencing. Results: “Kisspeptin responders” who had responded to kisspeptin with a rise in LH of 0.8 mIU/mL or greater all subsequently progressed through puberty (n = 8). In contrast, “kisspeptin nonresponders” who had exhibited LH responses to kisspeptin ≤0.4 mIU/mL all reached age 18 years without developing physical signs of puberty (n = 8). Thus, responses to kisspeptin accurately predicted later pubertal outcomes (p = 0.0002), with sensitivity and specificity of 100% (95% CI 74-100%). Moreover, the kisspeptin-stimulation test outperformed overnight LH measurements, GnRH-stimulated LH, inhibin B, and genetic testing in predicting pubertal outcomes. Conclusion: The kisspeptin-stimulation test can be used to reveal future reproductive endocrine potential in prepubertal children and is a promising novel tool for predicting pubertal outcomes for children with delayed puberty. Trial registration: ClinicalTrials.gov NCT01438034

scholarly journals Using Kisspeptin to Predict Pubertal Outcomes for Youth With Pubertal Delay

2020 ◽  
Vol 105 (8) ◽  
pp. e2717-e2725 ◽  
Author(s):  
Yee-Ming Chan ◽  
Margaret F Lippincott ◽  
Priscila Sales Barroso ◽  
Cielo Alleyn ◽  
Jill Brodsky ◽  
...  
Keyword(s):  
Medical Center ◽  
Academic Medical Center ◽  
Inhibin B ◽  
Endocrine Function ◽  
Delayed Puberty ◽  
Pubertal Delay ◽  
Gnrh Release ◽  
Stimulation Tests ◽  
Reproductive Endocrine ◽  
Outcomes For Children

Abstract Context The management of youth with delayed puberty is hampered by difficulty in predicting who will eventually progress through puberty and who will fail to attain adult reproductive endocrine function. The neuropeptide kisspeptin, which stimulates gonadotropin-releasing hormone (GnRH) release, can be used to probe the integrity of the reproductive endocrine axis. Objective We sought to determine whether responses to kisspeptin can predict outcomes for individuals with pubertal delay. Design, Setting, and Participants We conducted a longitudinal cohort study in an academic medical center of 16 children (3 girls and 13 boys) with delayed or stalled puberty. Intervention and Outcome Measures Children who had undergone kisspeptin- and GnRH-stimulation tests were followed every 6 months for clinical evidence of progression through puberty. Inhibin B was measured in boys. A subset of participants underwent exome sequencing. Results All participants who had responded to kisspeptin with a rise in luteinizing hormone (LH) of 0.8 mIU/mL or greater subsequently progressed through puberty (n = 8). In contrast, all participants who had exhibited LH responses to kisspeptin ≤ 0.4 mIU/mL reached age 18 years without developing physical signs of puberty (n = 8). Thus, responses to kisspeptin accurately predicted later pubertal outcomes (P = .0002). Moreover, the kisspeptin-stimulation test outperformed GnRH-stimulated LH, inhibin B, and genetic testing in predicting pubertal outcomes. Conclusion The kisspeptin-stimulation can assess future reproductive endocrine potential in prepubertal children and is a promising novel tool for predicting pubertal outcomes for children with delayed puberty.

scholarly journals FSH stimulated inhibin B (FSH-iB): A novel marker for the accurate prediction of pubertal outcome in delayed puberty

2021 ◽  
Author(s):  
Shakun Chaudhary ◽  
Rama Walia ◽  
Anil Bhansali ◽  
Devi Dayal ◽  
Naresh Sachdeva ◽  
...  
Keyword(s):  
Validation Cohort ◽  
Hypogonadotropic Hypogonadism ◽  
Inhibin B ◽  
Stimulation Test ◽  
Delayed Puberty ◽  
P Value ◽  
Healthy Children ◽  
Group 2 ◽  
Group 1

Abstract Background Clinicians have long been struggling to find an effective tool to predict onset of puberty. Objective To explore stimulability of inhibin B after exogenous FSH and it’s potential role for prediction of onset of puberty. Design and participants Study subjects were enrolled into “exploratory cohort”(n=42) and “validation cohort”(n=19). “Exploratory cohort” was further divided into Group-1(Healthy children with spontaneous puberty: SP, n=26) and Group-2 (Patients of hypogonadotropic hypogonadism: HH, n=16). “Validation cohort” included children who presented with complaints of delayed puberty. Intervention and outcome Participants were subjected to FSH stimulation test and GnRHa stimulation test. Cut-offs derived from “exploratory cohort” for basal and FSH stimulated inhibin B(FSH-iB) were applied on “validation cohort” .Basal LH, GnRHa stimulated LH, basal inhibin B and FSH-iB were compared with clinical outcome on prospective follow-up for prediction of onset of puberty. Results There was statistically significant increment in inhibin B after exogenous FSH in Group 1(SP) in both male(188.8 pg/ml;p-value-0.002) and female (1065 pg/ml;p-value-0.023) subjects. The increment was not statistically significant in Group 2(HH) in both genders. FSH-iB at a cut-off of 116.14 pg/ml in male and 116.50 pg/ml in female had 100% sensitivity and specificity for labelling entry into puberty. On application of these cut-offs on “validation cohort”, FSH-iB had 100% PPV, NPV and diagnostic accuracy for prediction of onset of puberty. Conclusion Inhibin B was stimulable in both male and female subjects. FSH-iB can be considered as novel and promising investigation for prediction of onset of puberty. Future studies are required for further validation.

scholarly journals Redundancy in the central tachykinin systems safeguards puberty onset and fertility

2018 ◽  
Author(s):  
Silvia León ◽  
Chrysanthi Fergani ◽  
Rajae Talbi ◽  
Serap Simavli ◽  
Caroline A. Maguire ◽  
...  
Keyword(s):  
Substance P ◽  
Reproductive Success ◽  
Sex Steroids ◽  
Delayed Puberty ◽  
Neurokinin A ◽  
Neurokinin B ◽  
Female Mice ◽  
Gnrh Release ◽  
Lh Release ◽  
Puberty Onset

ABSTRACTThe tachykinin neurokinin B (NKB, Tac2) is critical for GnRH release. NKB signaling deficiency leads to infertility in humans. However, some patients reverse this hypogonadism resembling the fertile phenotype of Tac2KO and Tacr3KO (encoding NKB receptor, NK3R) mice despite the absence of NKB signaling. Here, we demonstrate that in the absence of NKB signaling, other tachykinins (substance P and neurokinin A [NKA], encoded by Tac1) may take over to preserve fertility. The complete absence of tachykinins in Tac1/Tac2KO mice leads to delayed puberty onset in both sexes and infertility in 80% of females (but not males), in contrast to the 100% fertile phenotype of Tac1KO and Tac2KO mice separately. Furthermore, we demonstrate that NKA controls puberty onset and LH release through NKB-independent mechanisms in the presence of sex steroids and NKB-dependent mechanisms in their absence. In summary, tachykinins interact in a coordinated manner to ensure reproductive success in female mice.

Delayed Puberty

2020 ◽  
Author(s):  
Amanda French
Keyword(s):  
Pubertal Timing ◽  
Hormone Replacement ◽  
Hypogonadotropic Hypogonadism ◽  
Disease Process ◽  
Optimal Growth ◽  
Underlying Disease ◽  
Delayed Puberty ◽  
Hypergonadotropic Hypogonadism ◽  
Pubertal Delay ◽  
Constitutional Delay

Although common, delayed puberty can be distressing to patients and families.   Careful assessment is necessary to ensure appropriate physical and social development in patients that require intervention to reach pubertal milestones and achieve optimal growth.  Most pubertal delay is from lack of activation of the hypothalamic-pituitary-gonadal axis which then results in a functional or physiologic GnRH deficiency.  The delay may be temporary or permanent.  Constitutional delay (CDGP), also referred to as self-limited delayed puberty (DP), describes children on the extreme end of normal pubertal timing and is the most common cause of delayed puberty, representing about one third of cases.  Hypergonadotropic hypogonadism (primary hypogonadism) results from a failure of the gonad itself, and hypogonadotropic hypogonadism (secondary hypogonadism) results from a failure of the hypothalamic-pituitary axis, which is usually caused by another process, often systemic.  Diagnosis is based on history and examination.  Treatment is based on the underlying cause of pubertal delay and may include hormone replacement.  Involving a pediatric endocrinologist should be considered.  Appropriate counseling and ongoing support are important for all patients and families, regardless of underlying disease process.   This review contains 4 figures, 4 tables, and 32 references. Keywords: puberty, delayed puberty, hypogonadism, hypogonadotropic hypogonadism, hypergonadotropic hypogonadism, menarche, thelarche, constitutional delay and growth in puberty, Turner syndrome

Effects of global warming on fish reproductive endocrine axis, with special emphasis in pejerrey Odontesthes bonariensis

2013 ◽  
Vol 192 ◽  
pp. 45-54 ◽  
Author(s):  
Leandro Andrés Miranda ◽  
Tomás Chalde ◽  
Mariano Elisio ◽  
Carlos Augusto Strüssmann
Keyword(s):  
Global Warming ◽  
Odontesthes Bonariensis ◽  
Reproductive Endocrine ◽  
Endocrine Axis

SERUM INHIBIN B LEVELS AND THE RESPONSE TO GONADOTROPIN STIMULATION TEST IN PUBERTAL BOYS WITH VARICOCELE

1999 ◽  
Vol 162 (3 Part 1) ◽  
pp. 875-877 ◽  
Author(s):  
ADRIANA CARRILLO ◽  
ABBEY GERSHBEIN ◽  
KENNETH I. GLASSBERG ◽  
MARCO DANON
Keyword(s):  
Inhibin B ◽  
Stimulation Test ◽  
Gonadotropin Stimulation ◽  
Pubertal Boys

scholarly journals PACAP neurons in the ventral premammillary nucleus regulate reproductive function in the female mouse

2018 ◽  
Author(s):  
Rachel A. Ross ◽  
Silvia León ◽  
Joseph C. Madara ◽  
Danielle Schafer ◽  
Chrysanthi Fergani ◽  
...  
Keyword(s):  
Reproductive Function ◽  
Delayed Puberty ◽  
Targeted Deletion ◽  
Pituitary Adenylate Cyclase ◽  
Genetic Cross ◽  
Gnrh Release ◽  
Lh Release ◽  
Puberty Onset ◽  
Disclosure Statement ◽  
Hypothalamic Level

AbstractPituitary adenylate cyclase activating polypeptide (PACAP) is a neuromodulator implicated in anxiety, metabolism and reproductive behavior. PACAP global knockout mice have decreased fertility and PACAP modulates LH release. However, its source and role at the hypothalamic level remain unknown. We demonstrate that PACAP-expressing neurons of the ventral premamillary nucleus of the hypothalamus (PMVPACAP) project to, and make direct contact with, kisspeptin neurons in the arcuate and AVPV/PeN nuclei and a subset of these neurons respond to PACAP exposure. Targeted deletion of PACAP from the PMV through stereotaxic virally mediated cre- injection or genetic cross to LepR-i-cre mice with PACAPfl/flmice led to delayed puberty onset and impaired reproductive function in female, but not male, mice. We propose a new, sex-specific role for PACAP-expressing neurons in the PMV in the relay of nutritional state information to regulate GnRH release by modulating the activity of kisspeptin neurons, thereby regulating reproduction.Disclosure statementThe authors have nothing to disclose.

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