Journal articles: 'Pubertal induction'

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Dunkel, Leo, and Richard Quinton. "TRANSITION IN ENDOCRINOLOGY: Induction of puberty." European Journal of Endocrinology 170, no. 6 (June 2014): R229—R239. http://dx.doi.org/10.1530/eje-13-0894.

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Puberty is the period during which we attain adult secondary sexual characteristics and reproductive capability. Its onset depends upon reactivation of pulsative GNRH, secretion from its relative quiescence during childhood, on the background of intact potential for pituitary–gonadal function. This review is intended: to highlight those current practices in diagnosis and management that are evidence based and those that are not; to help clinicians deal with areas of uncertainty with reference to physiologic first principles; by sign-posting relevant data arising from other patient groups with shared issues; to illustrate how recent scientific advances are (or should be) altering clinician perceptions of pubertal delay; and finally, to emphasise that the management of men and women presenting in advanced adult life with absent puberty cannot simply be extrapolated from paediatric practice. There is a broad spectrum of pubertal timing that varies among different populations, separated in time and space. Delayed puberty usually represents an extreme of the normal, a developmental pattern referred to as constitutional delay of growth and puberty (CDGP), but organic defects of the hypothalamo–pituitary–gonadal axis predisposing to hypogonadism may not always be initially distinguishable from it. CDGP and organic, or congenital hypogonadotrophic hypogonadism are both significantly more common in boys than girls. Moreover, around 1/3 of adults with organic hypogonadotrophic hypogonadism had evidence of partial puberty at presentation and, confusingly, some 5–10% of these subsequently may exhibit recovery of endogenous gonadotrophin secretion, including men with Kallmann syndrome. However, the distinction is crucial as expectative (‘watch-and-wait’) management is inappropriate in the context of hypogonadism. The probability of pubertal delay being caused by organic hypogonadism rises exponentially both with increasing age at presentation and the presence of associated ‘red flag’ clinical features. These ‘red flags’ comprise findings indicating lack of prior ‘mini-puberty’ (such as cryptorchidism or micropenis), or the presence of non-reproductive congenital defects known to be associated with specific hypogonadal syndromes, e.g. anosmia, deafness, mirror movements, renal agenesis, dental/digital anomalies, clefting or coloboma would be compatible with Kallmann (or perhaps CHARGE) syndrome. In children, interventions (whether in the form or treatment or simple reassurance) have been historically directed at maximising height potential and minimising psychosocial morbidity, though issues of future fertility and bone density potential are now increasingly ‘in the mix’. Apubertal adults almost invariably harbour organic hypogonadism, requiring sensitive acknowledgement of underlying personal issues and the timely introduction of sex hormone replacement therapy at more physiological doses.

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Alves, Márcia, Margarida Bastos, Teresa Almeida Santos, and Francisco Carrilho. "Função Gonadal na Síndrome de Turner." Acta Médica Portuguesa 26, no. 6 (December 20, 2013): 655. http://dx.doi.org/10.20344/amp.1316.

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Introduction: Turner syndrome is characterized by the absence, total or partial, of one X chromosome in females, being one of the most frequent chromosomal abnormalities. Diagnosis is made by karyotype. Turner syndrome manifestations include primary hypogonadism, before or after puberty (gonadal dysgenesis). The degree and extent of gonadal disfunction are variable.Objectives: We intended to assess clinical, karyotype, gonadal function and pelvic ultrasound characteristics in women with Turner syndrome.Material and Methods: Retrospective study of patients with Turner syndrome followed in Endocrinology and Human Reproduction Departments of Hospitais da Universidade de Coimbra - Centro Hospitalar e Universitário de Coimbra, E.P.E. We evaluated the entire sample and considered group 1 (with spontaneous puberty and menarche) and group 2 (without spontaneous puberty). Parameters assessed: age at initial study, puberty (Tanner stages), karyotype, FSH, pelvic ultrasound (initial and after puberty), diagnostic laparoscopy and pubertal induction. Statistical Program: SPSS (20.0).Results: Global sample: 79 patients, 14.7 ± 6.6 years. No pubertal signs in 57.1%; 67.1% with primary amenorrhea and 6.6% with secondary amenorrhea. Karyotype: X monosomy-37.2%, mosaicism-37.2%, X structural changes-25.6%. Median FSH of 59.5 mIU/ mL. Initial ultrasound: normal uterus 34.2%, atrophic uterus 65.8%; normal ovaries 21.6%, atrophic ovaries 78.4%, ovarian follicles in 5.1%. Post-puberty ultrasound: normal uterus 67.9%, atrophic uterus 32.1%; normal ovaries 36.4%, atrophic ovaries 63.6%. Laparoscopy was performed in 16 (20.3%) patients, confirming the sonographic findings. Only two women with induced puberty became pregnant: one spontaneously, interrupted; another by donated oocytes, normal outcome. Group 1 (with spontaneous puberty and menarche):20 (25.3%) patients, 16.1 ± 8.9 years. Tanner at baseline: M1-22.2%, M2-33.3%, M3-16.7%, M4-16.7%, M5-11.1%. Karyotype: mosaicism-65%, X structural changes-20%, X monosomy-15%. Median FSH of 7 mUI/mL. Initial ultrasound: normal uterus-72.2%,atrophic uterus 27.8%; normal ovaries 63.2%, atrophic ovaries 36.8%. Post-puberty ultrasound: normal uterus 100%; normal ovaries 72.7%, atrophic ovaries 27.3%. Group 2 (without spontaneous puberty): 59 (74.7%) patients, 14.0 ± 5.5 years. Tanner at baseline: M1-69.2%, M2-13.5%, M3-5.8%, M4-3.8%, M5-7.7%. Karyotype: X monosomy-43.9%, X structural changes-28.1% mosaicism-28.1%. Median FSH of 74 mUI/mL. Initial ultrasound: normal uterus 20.4%, atrophic uterus 79.6%; normal ovaries 7.4%, atrophic ovaries92.6%. Post-puberty ultrasound: normal uterus 60.0%, atrophic uterus 40.0%; normal ovaries 27.3%, atrophic ovaries 72.7%. Pubertal induction at 16.1 ± 4.1 years, with bone age of 12.7 ± 1.6 years. Groups 1 and 2 differ significantly in karyotype (p = 0.010), median FSH (p < 0.001), and uterine and ovarian dimensions (p < 0.001).Conclusions: Most patients had gonadal dysfunction and needed pubertal induction. Spontaneous puberty with menarche occurred in 25.3% of patients (predominantly mosaics). 43.9% of patients with pubertal induction had X monosomy. These patients fertility is compromised and, in some cases, we should refer to assisted reproductive specialist for pregnancy or fertility preservation.

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Carel, Jean-Claude, Caroline Elie, Emmanuel Ecosse, Maïthé Tauber, Juliane Léger, Sylvie Cabrol, Marc Nicolino, Raja Brauner, Jean-Louis Chaussain, and Joël Coste. "Self-Esteem and Social Adjustment in Young Women with Turner Syndrome—Influence of Pubertal Management and Sexuality: Population-Based Cohort Study." Journal of Clinical Endocrinology & Metabolism 91, no. 8 (August 1, 2006): 2972–79. http://dx.doi.org/10.1210/jc.2005-2652.

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Abstract Context: Pediatric management of patients with Turner syndrome focuses on height, frequently resulting in a delay of pubertal induction. The influence of pubertal management on psychosocial adjustment and sex life has not been evaluated in Turner syndrome patients. Objective: The objective of the study was to identify the determinants of self-esteem, social adjustment, and initiation of sex life in patients with Turner syndrome, particularly those related to pubertal management. Design: This was a prospective evaluation, the StaTur study. Setting: The study was conducted with a population-based registry of GH-treated patients. Participants: Participants included 566 young adult women with Turner syndrome, aged 22.6 ± 2.6 yr (range, 18.3–31.2). Main Outcome Measures: Measures used in the study were Coopersmith’s Self-Esteem Inventory, Social Adjustment Scale Self-Report, questions on sexual experience, and extensive data on pediatric management. Results: Low self-esteem was associated with otological involvement and limited sexual experience. Low social adjustment was associated with lower paternal socioeconomic class and an absence of sexual experience. Late age at first kiss or date was associated with cardiac involvement and a lack of spontaneous pubertal development. Age at first sexual intercourse was related to age at puberty and paternal socioeconomic class. Delayed induction of puberty had a long-lasting effect on sex life. Height and height gain due to GH treatment had no effect on outcomes. Conclusions: Puberty should be induced at a physiologically appropriate age in patients with Turner syndrome to optimize self-esteem, social adjustment, and initiation of the patient’s sex life. Therapeutic interventions altering normal pubertal development in other groups of patients should be reconsidered in light of these findings.

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Matthews, Debbie, Louise Bath, Wolfgang Högler, Avril Mason, Arlene Smyth, and Mars Skae. "Hormone supplementation for pubertal induction in girls." Archives of Disease in Childhood 102, no. 10 (April 26, 2017): 975–80. http://dx.doi.org/10.1136/archdischild-2016-311372.

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Wakai, Takuya, Hozumi Tanaka, Ken-ichi Yamanaka, Satoshi Sugimura, Hiroshi Sasada, Manabu Kawahara, Eiji Kobayashi, and Eimei Sato. "Induction of estrus in pubertal miniature gilts." Animal Reproduction Science 103, no. 1-2 (January 2008): 193–98. http://dx.doi.org/10.1016/j.anireprosci.2007.04.004.

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Federici, Silvia, Biagio Cangiano, Giovanni Goggi, Luca Persani, and Marco Bonomi. "A Clinical Experience of Pubertal Induction in Female Patients With Congenital Hypogonadotropic Hypogonadism (CHH) From an Endo-ERN Referral Center." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A665. http://dx.doi.org/10.1210/jendso/bvab048.1357.

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Abstract Female congenital hypogonadotropic hypogonadism (CHH) is a rare condition, with a strong genetic background, characterized by absent or incomplete pubertal development, for which inductive treatment with sex-hormone is required. Although the available data, mostly coming from studies in patients with Turner syndrome, indicate transdermal estradiol (TDE) as the first-choice formulation, no internationally validated therapeutic schemes are currently available. Furthermore, data on CHH patients are certainly lacking and there is no standard of care for pubertal induction in this specific population. The aim of our work was the retrospective analysis of the data from a collection of case reports of pubertal induction in CHH patients referred to our Center. Six patients underwent induction with transdermal estradiol (TDE) at the starting dose of 0.1µg/kg/day (night-time for the first 4-6 months), increased every 4-6 months up to the adult dose, for a mean period of 2.86 ± 0.45 ys. Micronized progesterone (200 mcg) was introduced at reaching of 50µg dose or if breakthrough bleeding occurred. Treatment was monitored through clinical and anthropometric evaluations at each dose modification. The average age of induction was 17.25 ± 1.41 ys, with each bone age> 13 ys. Three out of six patients already had a Tanner B2 stage at diagnosis. The mean times of pubertal advancement were respectively 1.3 ± 0.46 ys for the achievement of B3, 2.13 ± 0.29 ys for the B4 and 2.35 ± 0.77 ys for menarche; all the patients reached an adult breast conformation (B5) in 2.81 ± 0.28 ys. These data are consistent with physiological pubertal progress. All of them achieved adequate uterine development (medium longitudinal diameter 72.2 ± 3.37mm), except one patient with suboptimal development (54mm). The final height (FH) was adequate in all patients, with SDS FH +1.6 (-0.43 - +3.38), in spite of an average growth of 4.11 cm (2.5-6) during the induction period and a growth rate > 2cm/year only in 50% of patients. No side effects were reported, and individual compliance and satisfaction were quite high. This clinical experience suggests that the adopted regimen, consistent with current literature, guarantees excellent efficacy and safety. However, further studies are needed to identify the optimal treatment in adolescents with CHH, taking into account their higher age at the start of induction, the modest impact on growth and final stature, to focus on the specific clinical objectives in these patients

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Burnett, P. J., and N. Walker. "The effect of boar contact on the maintenance of cyclic activity in gilts after the hormonal induction of puberty." Proceedings of the British Society of Animal Production (1972) 1986 (March 1986): 122. http://dx.doi.org/10.1017/s0308229600016287.

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A single injection of 400 i.μ. pregnant mare's serum gonadotrophin (PMSG) plus 200 i.μ. human chorionic gonadotrophin (HCG) has been shown to induce puberty in a high proportion of gilts treated (Burnett and Walker, 198S). However, studies indicate that the hormone treatment may fail to initiate normal oestrous cycling after the pubertal ovulation. The work of Paterson and Lindsay (1981) has shown that housing gilts in contact with boars throughout the cycle after puberty induction will enhance the proportion of animals which maintain cyclic activity to a second ovulation. The purpose of the experiment reported here was to examine the effect of boar contact and the timing of the introduction of boar contact on the maintenance of cyclic activity after puberty induction by PMSG + HCG.

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Baggio, Marcelo, José Paulo P. R. Barroso, Leticia Carolina Bortolanza Soares, Josiane F. Lages, Joel G. Oliveira Junior, Mariana Jeronymo, Natasha B. Petrenko, Evandro Maia M. Ferreira, and Alexandre Vaz Pires. "PSV-B-18 Effect of Puberty Induction on Embryonic Loss in Precocious Nellore Heifers." Journal of Animal Science 100, Supplement_3 (September 21, 2022): 345–46. http://dx.doi.org/10.1093/jas/skac247.632.

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Abstract This study aimed to determine if heifers induced to puberty had damage in reproductive performance compared with heifers that reach puberty naturally. Nellore heifers (n = 210) were weaned at 8 ± 0.7 mo of age were assigned to 42 feedlot pens according to BW (184 ± 1 kg). The diet was compounded by Tifton-85 haylage (18% CP; 55% TDN) ad libitum and supplement (4g/kg of BW; 25% CP; 60% TDN). Puberty and growth were assessed weekly. At 14 mo of age, 46 heifers reached puberty naturally (precocious heifers; PH) and 164 non-pubertal heifers were submitted to puberty induction with progesterone (P4) insert for 10 days and estradiol cypionate (0.5 mg) at P4 removal (puberty induction; PI). After fourteen days, all heifers were submitted to TAI. Heifers were considered pregnant at 20 days (P20) after AI when CL had blood flow < 25% of area (Power-Doppler). Pregnancy rate was also determined at 30 (P30) and 60 (P60) days after AI by embryo detection. Early (P20 – P30) and late (P30 – P60) embryonic loss were determined. Reproductive data were analyzed by GLIMMIX, and BW was analyzed using repeated measures over time (MIXED; SAS 9.3). The PH was heavier than PI from 8 to 16 mo of age, which BW was 296 and 285 ± 3 kg at 14 mo of age, respectively. At beginning of TAI, 88% of PI heifers had a CL. Pregnancy rate was similar (P > 0.05) between treatments, in which pregnancy rate at 20, 30 or 60 days after AI was 65, 47 and 43% for PH and 61, 53 and 48% for PI, respectively. Early (26 vs 14%) and late (9 vs 9%) embryonic loss were similar (P > 0.05) in PH and PI, respectively. In summary, natural or induced pubertal heifers had similar reproductive performance.

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Rodari, Giulia, Sophie Guez, Simona Salera, Fabio Massimo Ulivieri, Gianluca Tadini, Michela Brena, Eriselda Profka, Federico Giacchetti, Maura Arosio, and Claudia Giavoli. "A single-centre study on predictors and determinants of pubertal delay and growth impairment in Epidermolysis Bullosa." PLOS ONE 17, no. 9 (September 6, 2022): e0274072. http://dx.doi.org/10.1371/journal.pone.0274072.

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Background Delayed puberty is a possible complication of Epidermolysis Bullosa (EB), though the actual incidence is still unknown. In chronic illnesses delayed puberty should be correctly managed since, if untreated, can have detrimental effects on adult height attainment, peak bone mass achievement and psychological health. Aims and methods This is a single-centre study on pubertal development, growth and bone status in EB. Auxological, densitometric (areal Bone Mineral Density-aBMD Z-score, Bone Mineral Apparent Density-BMAD Z-score, Trabecular Bone Score-TBS and Bone Strain Index-BSI at Lumbar spine) and body composition data (Total Body DXA scans) were collected. Disease severity was defined according to Birmingham Epidermolysis Bullosa Severity (BEBS) score. Results Twenty-one patients (12 Recessive Dystrophic EB-RDEB, 3 Dominant Dystrophic EB, 3 Junctional EB-JEB, 2 EB Simplex and one Kindler EB) aged 13 years (females) or 14 years (males) and above were enrolled (age 16.2±2.5 years, M/F 11/10). Short stature was highly prevalent (57%, mean height -2.12±2.05 SDS) with 55% patients with height <-2SD their mid-parental height. 7/21 patients (33%, 6 RDEB and 1 JEB) had delayed puberty with a median BEBS of 50 (range 29 to 63), a height SDS of -2.59 SDS (range -5.95 to -2.22) and a median lumbar BMAD Z-score of -4.0 SDS (range -5.42 to -0.63 SDS). Pubertal status was negatively associated with BEBS, skin involvement, inflammatory state and positively with height SDS and BMI SDS. Conclusions Pubertal delay is highly prevalent in EB, especially in patients with RDEB and JEB, high severity score and inflammatory state. Moreover, pubertal delay worsens growth impairment and bone health. A study on pubertal induction is ongoing to enlighten possible beneficial effects on adult height attainment and peak bone mass accrual.

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Donaldson, Malcolm, Berit Kriström, Carina Ankarberg-Lindgren, Siska Verlinde, Janiëlle van Alfen-van der Velden, Aneta Gawlik, Marleen M. H. J. van Gelder, and Theo Sas. "Optimal Pubertal Induction in Girls with Turner Syndrome Using Either Oral or Transdermal Estradiol: A Proposed Modern Strategy." Hormone Research in Paediatrics 91, no. 3 (2019): 153–63. http://dx.doi.org/10.1159/000500050.

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Background: Most girls with Turner syndrome (TS) require pubertal induction with estrogen, followed by long term replacement. However, no adequately powered prospective studies comparing transdermal with oral 17β-estradiol administration exist. This reflects the difficulty of securing funding to study a rare condition with relatively low morbidity/mortality when competing against conditions such as cancer and vascular disease. Protocol Consensus: The TS Working Group of the European Society for Paediatric Endocrinology (ESPE) has agreed to both a 3-year oral and a 3-year transdermal regimen for pubertal induction. Prerequisites include suitable 17β-estradiol tablets and matrix patches to allow the delivery of incremental doses based on body weight. Study Proposal: An international prospective cohort study with single centre analysis is proposed in which clinicians and families are invited to choose either of the agreed regimens, usually starting at 11 years. We hypothesise that pubertal induction with transdermal estradiol will result in better outcomes for some key parameters. The primary outcome measure chosen is height gain during the induction period. Analysis: Assessment of the demographics and drop-out rates of patients choosing either oral or transdermal preparations; and appropriate analysis of outcomes including pubertal height gain, final height, liver enzyme and lipid profile, adherence/acceptability, cardiovascular health, including systolic and diastolic blood pressure and aortic root diameter and bone health. Conclusion: The proposed model of prospective data collection according to internationally agreed protocols aims to break the current impasse in obtaining evidence-based management for TS and could be applied to other rare paediatric endocrine conditions.

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Kenigsberg, Lisa, Sadana Balachandar, Kris Prasad, and Bina Shah. "Exogenous Pubertal Induction by Oral versus Transdermal Estrogen Therapy." Journal of Pediatric and Adolescent Gynecology 26, no. 2 (April 2013): 71–79. http://dx.doi.org/10.1016/j.jpag.2011.09.012.

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Palmer, Elizabeth, Marcelo Vedovatto, Juliana Ranches, Rhaiza Oliveira, John Arthington, Joao Vendramini, and Philipe Moriel. "55 Effects of concentrate supplementation frequency and amount on growth and reproductive performance of Brangus heifers." Journal of Animal Science 98, Supplement_2 (November 1, 2020): 58–59. http://dx.doi.org/10.1093/jas/skz397.133.

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Abstract A 2-yr study evaluated the impacts of supplementation frequency and amount on growth and puberty attainment of Brangus heifers. On d 0 of each year, 64 Brangus heifers were stratified by BW and age (244 ± 4 kg; 311 ± 18 d) and assigned to 1 of 16 bahiagrass pastures (4 heifers/pasture). Treatments were randomly assigned to pasture (4 pastures/treatment) in a 2 × 2 factorial design and consisted of heifers offered a soybean hulls-based supplement DM at 1.25% or 1.75% of BW delivered either daily (7X) or 3 times weekly (3X; Monday, Wednesday, and Friday). On d 56, heifers were inserted with a CIDR device for 14 d, followed by administration of PGF2α and a timed-AI+GnRH protocol on d 89. Heifers were exposed to bulls from d 89 to 167. Data were analyzed using the SAS GLIMMIX procedure. No rate × frequency interactions were detected (P ≥ 0.20). Overall ADG was greater for 7X vs. 3X heifers (P = 0.007). Daily supplementation increased (P ≤ 0.03) the percentage of pubertal heifers prior to CIDR insertion and at AI compared to 3X supplementation; however, percentage of pregnant heifers did not differ (P = 0.70). Supplementation at 1.25% vs. 1.75% enhanced the overall ADG (P = 0.02) but did not impact (P = 0.18) the percentage of pubertal heifers before CIDR insertion. After the puberty induction protocol, heifers supplemented at 1.75% of BW achieved greater puberty attainment at time of AI (P = 0.05) and final pregnancy rates (P = 0.02) than heifers supplemented at 1.25% of BW. When a puberty induction protocol was included, the percentage of pregnant Brangus heifers were not affected by supplementation frequency (daily vs. 3 times weekly) but enhanced when the supplement dry matter amount was offered at 1.75 vs. 1.25% of body weight.

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Wei, Christina, and Elizabeth Clare Crowne. "Recent advances in the understanding and management of delayed puberty." Archives of Disease in Childhood 101, no. 5 (September 9, 2015): 481–88. http://dx.doi.org/10.1136/archdischild-2014-307963.

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Delayed puberty, especially in boys, is a common presentation in paediatrics. Recent advances have improved our understanding of the neuroendocrine, genetic and environmental factors controlling pubertal development, and hence inform the pathophysiology of delayed puberty. The discovery of kisspeptin signalling through its receptor identified neuroendocrine mechanisms controlling the gonadotrophin-releasing hormone (GnRH) pulse generator at the onset of puberty. Genetic mechanisms from single gene mutations to single nucleotide polymorphism associated with delayed puberty are being identified. Environmental factors, including nutritional factors and endocrine disruptors, have also been implicated in changes in secular trends and abnormal timing of puberty. Despite these advances, the key clinical question is to distinguish delayed puberty associated with an underlying pathology or hypogonadism from constitutional delay in growth and puberty, which remains challenging as biochemical tests are not always discriminatory. The diagnostic accuracies of newer investigations, including 36-hour luteinising hormone releasing hormone (LHRH) tests, GnRH-agonist tests, antimullerian hormone and inhibin-B, require further evaluation. Sex hormone replacement remains the main available treatment for delayed puberty, the choice of which is largely dictated by clinical practice and availability of the various sex steroid preparations. Spontaneous reversal of hypogonadism has been reported in boys with idiopathic hypogonadotrophic hypogonadism after a period of sex steroid treatment, highlighting the importance of reassessment at the end of pubertal induction. Novel therapies with a more physiological basis such as gonadotrophins or kisspeptin-agonist are being investigated for the management of hypogonadotrophic hypogonadism. Careful clinical assessment and appreciation of the normal physiology remain the key approach to patients with delayed puberty.

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Zacharin, Margaret. "Pubertal induction in hypogonadism: Current approaches including use of gonadotrophins." Best Practice & Research Clinical Endocrinology & Metabolism 29, no. 3 (June 2015): 367–83. http://dx.doi.org/10.1016/j.beem.2015.01.002.

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Vandewalle, Sara, Eva Van Caenegem, Margarita Craen, Youri Taes, Jean-Marc Kaufman, and Guy T’Sjoen. "Growth, sexual and bone development in a boy with bilateral anorchia under testosterone treatment guided by the development of his monozygotic twin." Journal of Pediatric Endocrinology and Metabolism 31, no. 3 (March 28, 2018): 361–67. http://dx.doi.org/10.1515/jpem-2017-0126.

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Abstract Background: Sex steroids are essential for sexual maturation, linear growth and bone development. However, there is no consensus on the optimal timing, dosage and dosage interval of testosterone therapy to induce pubertal development and achieve a normal adult height and bone mass in children with hypogonadism. Case presentation: A monozygotic monochorial male twin pair, of which one boy was diagnosed with anorchia at birth due to testicular regression syndrome was followed from the age of 3 until the age of 18 years. Low dose testosterone substitution (testosterone esters 25 mg/2 weeks) was initiated in the affected twin based on the start of pubertal development in the healthy twin and then gradually increased accordingly. Both boys were followed until age 18 and were compared as regards to linear growth, sexual maturation, bone maturation and bone development. Before puberty induction both boys had a similar weight and height. During puberty, a slightly faster weight and height gain was observed in the affected twin. Both boys ended up however, with a similar and normal (near) adult height and weight and experienced a normal development of secondary sex characteristics. At the age of 17 and 18 years, bone mineral density, body composition and volumetric bone parameters at the forearm and calf were evaluated in both boys. The affected boy had a higher lean mass and muscle cross-sectional area. The bone mineral density at the lumbar spine and whole body was similar. Trabecular and cortical volumetric bone parameters were comparable. At one cortical site (proximal radius), however, the affected twin had a smaller periosteal and endosteal circumference with a thicker cortex. Conclusions: In conclusion, a low dose testosterone substitution in bilateral anorchia led to a normal onset of pubertal development and (near) adult height. Furthermore, there was no difference in bone mineral density at the age of 17 and 18 years.

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Tsao, Jennie CI, Ning Li, Delana Parker, Laura C. Seidman, and Lonnie K. Zeltzer. "Pubertal Status Moderates the Association between Mother and Child Laboratory Pain Tolerance." Pain Research and Management 19, no. 1 (2014): 23–29. http://dx.doi.org/10.1155/2014/390368.

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BACKGROUND:There is limited information regarding the relationship between parent and child responses to laboratory pain induction in the absence of experimental manipulation.OBJECTIVES: To assess the association between responses to cold and pressure pain tasks in 133 nonclinical mothers and children (mean age 13.0 years; 70 girls), and the moderating effects of child sex and pubertal status on these mother-child relationships.METHODS: Mothers and children independently completed the cold and pressure pain tasks. Multiple linear regression analyses examined the association between mothers’ and children’s laboratory pain responses. The moderating effects of child sex and pubertal status were tested in the linear models by examining the interaction among mother laboratory pain responses, and child sex and pubertal status.RESULTS: Mothers’ cold pain anticipatory anxiety and pressure pain intensity were associated with children’s pressure pain anticipatory anxiety. Mothers’ pressure pain tolerance was associated with children’s pain tolerance for both the cold and pressure pain tasks. Mothers’ cold pain tolerance was associated with children’s pressure pain tolerance. Pubertal status moderated two of the three significant mother-child pain tolerance relationships, such that the associations held for early pubertal but not for late pubertal children. Sex did not moderate mother-child pain associations.CONCLUSIONS: The results indicate that mother-child pain relationships are centred primarily on pain avoidance behaviour, particularly among prepubertal children. These findings may inform interventions focused on pain behaviours, with a particular emphasis on mothers of prepubertal children, to reduce acute pain responses in their children.

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Cham, Grace, Brooke O'Brien, and Rebecca MN Kimble. "Idiopathic hypogonadotropic hypogonadism: a rare cause of primary amenorrhoea in adolescence—a review and update on diagnosis, management and advances in genetic understanding." BMJ Case Reports 14, no. 4 (April 2021): e239495. http://dx.doi.org/10.1136/bcr-2020-239495.

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Idiopathic hypogonadotropic hypogonadism (IHH) refers to a family of genetic disorders that affect the production and/or action of gonadotropic-releasing hormone, resulting in reduced serum levels of sex steroids. This condition has a prevalence of 1–10 cases/100 000 births and is characterised by the absence of spontaneous pubertal development. In women, the condition is characterised by the onset of normal adrenarche, with the absence of thelarche and menarche. Pubertal induction for breast development and uterine growth with oestradiol, and sequential maintenance of a normal menstrual cycle and adequate oestrogen for bone health, with an oestrogen and progesterone, is considered first-line treatment. Pregnancy can be achieved in patients who have received and responded to treatment with ovulation induction with exogenous gonadotrophins. Advances in genetic testing have led to increased research and understanding of the underlying genetics of IHH with gene mutations described in up to 50% of all IHH cases.

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Labarta, José I., Maria L. Moreno, Juan P. López-Siguero, Cristina Luzuriaga, Itxaso Rica, Jaime Sánchez-del Pozo, and Ricardo Gracia-Bouthelier. "Individualised vs fixed dose of oral 17β-oestradiol for induction of puberty in girls with Turner syndrome: an open-randomised parallel trial." European Journal of Endocrinology 167, no. 4 (October 2012): 523–29. http://dx.doi.org/10.1530/eje-12-0444.

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ContextOestrogen induction of pubertal changes in Turner girls may reinforce their psychological well-being and may also optimise final height; however, oestrogen type, dose, and route are not well established.ObjectiveTo induce normal pubertal development in Turner girls and ovarian insufficiency with oral 17β-oestradiol (E2), either as individualised dose (ID) or as fixed dose (FD), and to determine whether growth is affected.DesignOpen-label randomised, parallel groups, multicentre clinical trial in 48 GH-treated Turner girls. Oral E2was given in tablets, either as an ID of 5–15 μg/kg per day during 2 years or as a FD of 0.2 mg daily during the first year followed by 0.5 mg daily during the second year. Main outcome measures were the event of attaining a Tanner breast staging ≥4 (primary), FSH, and auxological variables (secondary).ResultsShorter median time to Tanner staging ≥ B4 in the FD group (733 days) compared with the ID group (818 days) (P=0.046). Higher proportion of girls with Tanner staging ≥ B4 (65%) in the FD group compared with the ID group (42%) (P=0.068). Bone age did not show inadequate acceleration and adult height prediction was maintained in both groups. No oestrogen-related adverse events were reported.ConclusionsTwo-year treatment with oral E2can progressively induce normal pubertal development in Turner syndrome. Low-dose oral E2given as a FD produces a satisfactory pubertal development not inferior to ID. Treatment was well tolerated and did not interfere with the growth-promoting effect of GH.

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Aupperlee, Mark D., Yong Zhao, Ying Siow Tan, Jeffrey R. Leipprandt, Jessica Bennett, Sandra Z. Haslam, and Richard C. Schwartz. "Epidermal Growth Factor Receptor (EGFR) Signaling Is a Key Mediator of Hormone-Induced Leukocyte Infiltration in the Pubertal Female Mammary Gland." Endocrinology 155, no. 6 (June 1, 2014): 2301–13. http://dx.doi.org/10.1210/en.2013-1933.

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It is well documented that macrophages and eosinophils play important roles in normal murine pubertal mammary gland development. Although it is accepted that estrogen (E) and progesterone (P) are key players in mammary gland development, the roles these hormones might play in regulating the actions of leukocytes in that process is an understudied area. We show here that P and E, respectively, induce unique, but overlapping, sets of proinflammatory and angiogenic cytokines and chemokines, in the pubertal female BALB/c mammary gland, as well as induce infiltration of macrophages and eosinophils to the mammary periepithelium. This extends earlier studies showing P induction of proinflammatory products in pubertal and adult mammary epithelial organoids and P-induced in vivo infiltration of leukocytes to the adult mammary periepithelium. Importantly, epidermal growth factor receptor-signaling, which is likely mediated by amphiregulin (Areg), a downstream mediator of E and P, is both necessary and sufficient for both E- and P-induced recruitment of macrophages and eosinophils to the pubertal mammary periepithelium. We further show that receptor activator of nuclear factor κB ligand (RANKL), although not sufficient of itself to cause macrophage and eosinophil recruitment, contributes to an optimal response to P. The potency of Areg is highlighted by the fact that it is sufficient to induce macrophage and eosinophil recruitment at levels equivalent to that induced by either E or P. Our finding of a dominant role for Areg in hormonally induced leukocyte recruitment to the pubertal mammary gland parallels its dominance in regulating ductal outgrowth and its role in P-induced proliferation in the pubertal gland.

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Biswas, Subrata K., and Jose B. Lopes de Faria. "Pre-pubertal induction of experimental diabetes protects against early renal macrophage infiltration." Pediatric Nephrology 22, no. 7 (July 2007): 1045–49. http://dx.doi.org/10.1007/s00467-007-0453-y.

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Martins, Thiago, Felipe A. C. C. da Silva, Mariana Sponchiado, Gabriela A. Soriano, Leonardo M. F. Pinto, Cecilia C. Rocha, Federico Podversich, et al. "PSIII-7 Determining the requirement of puberty induction to the reproductive performance of Bos indicus-influenced heifers submitted to AI." Journal of Animal Science 98, Supplement_4 (November 3, 2020): 231–32. http://dx.doi.org/10.1093/jas/skaa278.425.

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Abstract Induction of puberty by treating heifers with progesterone (P4) inserts may favor pregnancy/AI (P/AI) to a subsequent estrus synchronization program. However, it remains to be elucidated whether induction is required when the synchronization program contains P4 supplementation. To address this question, yearling, Brahman-influenced heifers (mostly 3/8 Brahman) classified as pubertal (PUB; n = 363) or prepubertal (PRE; n = 214) based on the presence of a CL, were assigned to receive no P4 supplementation (NoCIDR) or a CIDR for 10 days, starting on D-23. On D-13, all heifers received a dose of prostaglandin analogue and CIDRs were removed. On D-9, all heifers were enrolled in a 6-day CIDR & TAI protocol. Heifers were serviced based on heat between D-2 and D0 or were TAI on D0. Reproductive tract scores (RTS, 1 to 5 scale) were evaluated on D-23 and D-3. Induction increased the proportion of PRE heifers bearing a CL on D-3 (PRE|CIDR: 60.3% vs. PRE|NoCIDR: 42.7%). Among heifers with CL on D-3, P/AI of PRE heifers (42.5%) was similar to that PUB (47.7%). Conversely, for heifers without CL on D-3, P/AI of PRE (14.7%) was lower than PUB (37.3%). RTS increased between D-23 and D-3 from 2.3 to 4.0 (CIDR) and 2.3 to 3.6 (NoCIDR). For every 1-point increase in RTS, P/AI was 6–9% greater. Despite hastened puberty, P/AI of PRE heifers were less (PRE|NoCIDR: 29.2% and PRE|CIDR: 30.4%) than that of PUB (PUB|NoCIDR: 50.7% and PUB|CIDR: 42.2%). Less PRE (42.5%) than PUB animals (69.7%) were AI at estrus, and heifers showing estrus had a higher P/AI (52.8% vs. 18.7%). In conclusion, induction is not required when the subsequent synchronization protocol for AI contains progesterone. Induction hastened puberty attainment but failed to improve estrus response and fertility to the synchronization protocol.

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Bonavera, J. J., D. J. Tortonese, J. M. Doray, and F. Petraglia. "Endocrine response to superovulatory treatment in pre-pubertal beef heifers: its lack of ability to induce puberty." Animal Science 46, no. 2 (April 1988): 163–67. http://dx.doi.org/10.1017/s0003356100042215.

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AbstractThis study was carried out to investigate: (1) changes in plasma oestradiol-17β and progesterone concentrations in six pre-pubertal beef heifers, 9 months old, subjected to a superovulatory treatment, consisting of a single dose of PMSG followed 120 h later by a single injection of human chorionic gonadotrophin (HCG); and (2) the ability of this treatment to trigger cyclic gonadal activity. After PMSG administration, oestradiol-17β levels increased from 11·8 (s.d. 10·78) to 92·9 (s.d. 38·15) ng/1 just before HCG injection. The oestradiol-17β increase during the superovulatory treatment and numbe r of ovulations were correlated (r = 0·83; P < 0·05). After HCG injection, progesterone concentrations rose significantly reaching values which in some cases were higher than 60 [μg/1. The progesterone peak on days 9 and 10 post HCG was strongly correlated with the number of corpora lutea (r = 0·95; P < 0·01 and r = 0·92; P < 0·01, respectively). Progesterone determinations were performed for a period of 90 days after HCG administration. No evidence was found for the induction of permanent cyclic ovarian activity since all heifers returned, after the induced luteal phase, to their pre-pubertal condition.

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Ankarberg-Lindgren, Carina, Aneta Gawlik, Berit Kriström, Laura Mazzanti, Elisabeth J. Ruijgrok, and Theo C. J. Sas. "Estradiol matrix patches for pubertal induction: stability of cut pieces at different temperatures." Endocrine Connections 8, no. 4 (April 2019): 360–66. http://dx.doi.org/10.1530/ec-19-0025.

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Objective Transdermal estradiol patches are primarily designed for adult women. No low-dose patches are licensed for pubertal induction in hypogonadal girls. Low doses can be achieved by cutting a matrix patch into smaller pieces. However, the manufacturers do not guarantee stability or utility of cut estradiol patches. The aim of the study was to assess 1-month stability of cut estradiol patches from four different manufacturers in the laboratory at room temperature (+21°C) and at an elevated temperature (+35°C). Design and methods Estraderm MX 50 µg, Systen 50 µg and Oesclim 25 µg matrix patches were cut into eight pieces while Estradot 50 µg small patches were cut in half. The cut patches were stored in their respective pouches at +21°C or at +35°C for up to 1 month. The estradiol drug was extracted from the patch by ethyl acetate n-hexane and determined by radioimmunoassay. Results Storage at +21°C or +35°C up to 1 month did not reduce the estradiol concentration in Estraderm MX, Systen and Oesclim patches. However, although the estradiol in Estradot patches was not affected by storage at +21°C, at +35°C, estradiol decreased by 57% (±1%) in cut pieces. Conclusions Unused Estraderm MX, Systen and Oesclim patch pieces may be stored for at least 1 month at ≤+35°C. Where estradiol patches for children are not available, cut pieces of these or similar patches can be used for pubertal induction. The Estradot patch was too small to properly cut into low doses and not stable in elevated temperatures.

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Lee, Yi-Chen, Chi-Yu Huang, Chao-Hsu Lin, Bi-Wen Cheng, Shih-Kang Huang, Shu-Nin Yeh, Yann-Jinn Lee, and Wei-Hsin Ting. "The effects of estrogen induction therapy on pubertal presentations in turner syndrome patients." Taiwanese Journal of Obstetrics and Gynecology 61, no. 5 (September 2022): 788–93. http://dx.doi.org/10.1016/j.tjog.2022.05.014.

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Hamre, M. R., L. L. Robison, M. E. Nesbit, H. N. Sather, A. T. Meadows, J. A. Ortega, G. J. D'Angio, and G. D. Hammond. "Effects of radiation on ovarian function in long-term survivors of childhood acute lymphoblastic leukemia: a report from the Childrens Cancer Study Group." Journal of Clinical Oncology 5, no. 11 (November 1987): 1759–65. http://dx.doi.org/10.1200/jco.1987.5.11.1759.

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The Childrens Cancer Study Group has assessed serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), and pubertal development in 97 long-term female survivors of childhood acute lymphoblastic leukemia (ALL). All patients received identical induction and maintenance therapy with either 18 or 24 Gy of radiation therapy (RT) to one of the following fields: cranial, craniospinal, or craniospinal plus 12 Gy abdominal RT including the ovaries. Thirty-six percent (35 patients) were found to have above normal levels of FSH and/or LH. The percentages of elevated values for RT fields were 93% for craniospinal plus abdominal RT, 49% for craniospinal RT, and 9% for cranial RT (P less than .001). A dose-response relationship was observed between 18 Gy and 24 Gy in females receiving only craniospinal RT (P = .01). Craniospinal plus abdominal RT and abnormal FSH/LH levels were significantly associated with lack of pubertal development and delayed onset of menses. Duration of maintenance chemotherapy was not associated with abnormal gonadotropin levels or the development of secondary sexual characteristics. Additional follow-up of this cohort is needed to establish the ultimate pubertal development and fertility of these patients.

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Dupont-Lucas, Claire, Rachel Marion-Letellier, Mathilde Pala, Charlène Guerin, Christine Bôle-Feysot, Emmeline Salameh, Alexis Goichon, et al. "Magnetic resonance colonography assessment of acute trinitrobenzene sulfonic acid colitis in pre-pubertal rats." PLOS ONE 16, no. 11 (November 4, 2021): e0259135. http://dx.doi.org/10.1371/journal.pone.0259135.

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Pre-pubertal murine models of acute colitis are lacking. Magnetic resonance colonography (MRC) is a promising minimally invasive tool to assess colitis. We aimed to: 1/ Adapt a model of acute experimental colitis to pre-pubertal rats and determine whether MRC characteristics correlate with histological inflammation. 2/ Test this model by administering a diet supplemented in transforming growth factor β2 to reverse inflammation. Twenty-four rats were randomized at weaning to one of 3 groups: Trinitrobenzene Sulfonic Acid (TNBS) group (n = 8) fed a standard diet, that received an intra-rectal 60 mg/kg dose of TNBS-ethanol; Control group (n = 8) fed standard diet, that received a dose of intra-rectal PBS; TNBS+MODULEN group (n = 8) that received a dose of TNBS and were exclusively fed MODULEN-IBD® after induction of colitis. One week after induction of colitis, rats were assessed by MRC, colon histopathology and inflammation markers (Interleukin 1β, Tumor necrosis factor α, Nitric Oxide Synthase 2 and Cyclooxygenase 2). TNBS induced typical features of acute colitis on histopathology and MRC (increased colon wall thickness, increased colon intensity on T2-weighted images, target sign, ulcers). Treatment with MODULEN-IBD® did not reduce signs of colitis on MRC. Inflammatory marker expression did not differ among study groups.

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Das, Goutam Kumar, Sanjeev Mehrotra, Krishnaswamy Narayanan, Babu Lal Kumawat, Ujjal De Kumar, and Tanweer Ahmad Khan. "Estrus Induction Response and Fertility Performance in Delayed Pubertal Heifers Treated withAegle marmelosandMurraya koenigii." Journal of Animal Research 6, no. 1 (2016): 151. http://dx.doi.org/10.5958/2277-940x.2016.00025.5.

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Knox, Robert V., Ashley Daniel, Jenny Patterson, Lidia S. Arend, and George Foxcroft. "17 Effects of birth traits, physical or fenceline boar exposure and group size on pubertal measures and lifetime fertility of replacement gilts." Journal of Animal Science 97, Supplement_2 (July 2019): 12. http://dx.doi.org/10.1093/jas/skz122.021.

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Abstract In experiment 1, prepubertal gilts with (n = 264) and without (n = 43) birth records received Fenceline (FBE) or Physical (PBE) Boar Exposure (BE) in a Boar Exposure Area (BEAR). At 185 d of age, gilts (13/pen) received BE for 15 min/d for 3 wk. At the start of Week 3, anestrual gilts received PG600 or no-PG600 (Control). At estrus, females were moved into stalls and inseminated at 2nd heat. Gilts born in larger litters were lighter (r = -0.26) while heavier pigs grew faster to puberty (r = 0.25). PBE increased estrus in Week 1 (38%) over FBE (28%). In Week 3, PBE-PG600 increased estrus (79.9%) compared with PBE- Control (36.2%), while FBE-PG600 and Control did not differ (52.7 vs. 42.5%). By 6 wk, estrus tended to be greater (P < 0.08) for PBE (91.2%) than FBE (83.2%). Reduced fertility associated with: 1) small birth litter; 2) heaviest birthweight; 3) slower growth rate; 4) delayed puberty and age at 1st service; and 5) abnormal estrus interval. Experiment 2 tested the pubertal response to PBE or FBE with 10 or 20 gilts/pen. Gilts (n = 180) at 168 d with 1.8 m2 floor space received BE once/d for 15 min for 1–3 wk. At the start of Week 3, anestrual gilts received PG600. Estrus in Week 1 (7.3%) did not differ, but a BE x Pen effect occurred in Week 2 (estrus range: 15–34%). In Week 3, PG600 increased estrus (P < 0.03) in Pens of 10 (83.7%) compared to Pens of 20 (64.1%). BE method had no effect and Pens of 10 had greater estrus (P = 0.05) than Pens of 20 (88.3 vs 75.8%). These results indicated that use of PBE, a BEAR, smaller group size, and PG600 can be used in combinations to enhance puberty induction. Birth and pubertal measures influenced service and farrowing rate, litter size, and age at removal.

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Pazderska, Agnieszka, Yaasir Mamoojee, Satish Artham, Margaret Miller, Stephen G. Ball, Tim Cheetham, and Richard Quinton. "Safety and tolerability of one-year intramuscular testosterone regime to induce puberty in older men with CHH." Endocrine Connections 7, no. 1 (January 2018): 133–38. http://dx.doi.org/10.1530/ec-17-0241.

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We present herein our 20-year experience of pubertal induction in apubertal older (median age 56 years; range 38.4–69.5) men with congenital hypogonadotrophic hypogonadism (n = 7) using a simple fixed-dose and fixed-interval intramuscular testosterone that we originally pioneered in relation to achieving virilisation of natal female transgender men. This regime was effective and well tolerated, resulting in complete virilisation by around 1 year after treatment initiation. No physical or psychological adverse effects were encountered in this group of potentially vulnerable individuals. There were no abnormal excursions of laboratory parameters and extended follow-up beyond the first year of treatment revealed remarkable improvements in bone density. We highlight advantages to both patients and physicians of this regime in testosterone-naïve older men with congenital hypogonadism and discourage the over-rigid application to such patients of treatment algorithms derived from paediatric practice in relation to the evaluation and management in younger teenagers with delayed puberty of uncertain cause.

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Swee, Du Soon, and Richard Quinton. "Managing congenital hypogonadotrophic hypogonadism: a contemporary approach directed at optimizing fertility and long-term outcomes in males." Therapeutic Advances in Endocrinology and Metabolism 10 (January 2019): 204201881982688. http://dx.doi.org/10.1177/2042018819826889.

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Hormonal induction of spermatogenesis offers men with azoospermia due to hypogonadotrophic hypogonadism (HH) the promising prospect of fertility restoration. However, an important exception is the subset of individuals affected by congenital hypogonadotrophic hypogonadism (CHH), also known as Kallmann syndrome if associated with anosmia, who often display dismal responses to fertility induction, despite prolonged therapy. This primarily stems from the loss of minipuberty, which is a crucial phase of testicular maturation in early life that has a far-reaching impact on eventual spermatogenic capacity. Further exacerbating the compromised reproductive health is the failure to initiate timely pubertal induction in many CHH patients, resulting in suboptimal genital and psychosexual development. In this paper, the clinical implications and management of male HH across the lifespan is comprehensively reviewed, with a special focus on novel strategies that have the potential to modify disease severity and maximize fertility potential in CHH by addressing the inadequacies of conventional approaches.

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Chaudhari, C., B. Suthar, V. Sharma, V. Dabas, N. Chaudhari, and H. Panchasara. "Estrus induction and fertility response in delayed pubertal Kankrej heifers treated with norgestomet ear implant." Veterinary World 5, no. 8 (2012): 453. http://dx.doi.org/10.5455/vetworld.2012.453-458.

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Nagy, Von A., I. Szurop, and W. Jöchle. "Synchronized Induction of Pubertal Estrus in Gilts with Gonadotropins and Prostaglandin F2α Analogs: Clinical Observation." Reproduction in Domestic Animals 20, no. 2 (June 1985): 79–82. http://dx.doi.org/10.1111/j.1439-0531.1985.tb00402.x.

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Nagy, A., I. Szurop, and W. Jöchle. "Synchronized Induction of Pubertal Estrus in Gilts with Gonadotropins and Prostaglandin F2α Analogs: Clinical Observation." Reproduction in Domestic Animals 21, no. 2 (May 1986): 079–82. http://dx.doi.org/10.1111/j.1439-0531.1986.tb01222.x.

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Harvey, Susan, Susan M. O’Connell, and Jonathan O’B Hourihane. "Safety of intramuscular testosterone in arachis oil for boys with peanut allergy requiring pubertal induction." Annals of Allergy, Asthma & Immunology 124, no. 1 (January 2020): 94–95. http://dx.doi.org/10.1016/j.anai.2019.10.015.

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Singh, C., and M. L. Madan. "Plasma prolactin in relation to estrus induction during synchronization & superovulation among peri-pubertal buffaloes." Theriogenology 33, no. 1 (January 1990): 326. http://dx.doi.org/10.1016/0093-691x(90)90750-n.

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Wood, Claire L., Kieren G. Hollingsworth, Eric Hughes, Sadhanandham Punniyakodi, Robert Muni-Lofra, Anna Mayhew, Rod T. Mitchell, Michela Guglieri, Timothy D. Cheetham, and Volker Straub. "Pubertal induction in adolescents with DMD is associated with high satisfaction, gonadotropin release and increased muscle contractile surface area." European Journal of Endocrinology 184, no. 1 (January 2021): 67–79. http://dx.doi.org/10.1530/eje-20-0709.

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Background Pharmacological doses of glucocorticoids (GC) reduce inflammation and preserve muscle function in boys with Duchenne muscular dystrophy (DMD). Delayed puberty and bone fragility are consequences of GC treatment. The aim of this study was to determine the acceptability of a 2-year pubertal induction regimen using 4-weekly testosterone injections and examine changes in physique, bone integrity, muscle pathology (assessed by MRI) and muscle function. Methods Fifteen prepubertal males with DMD, aged 12–17 years and receiving GC, were treated with an incremental testosterone regimen for 2 years. Participants completed a Treatment Satisfaction Questionnaire (TSQM). Data on BMI, bone density, muscle pathology and function were collected at baseline and 2 years later. Results Testosterone injections were well tolerated, with high TSQM scores. Baseline BMI z-score was 2.16 (0.90) and 1.64 (1.35) 2 years later. Median testosterone levels were 9.7 nmol/L (IQR: 5.7–11.1) 6–9 months after the last injection with an associated increase in testicular volume. Lumbar spine z-score was 0.22 (s.d. 2.21) at baseline and 0.35 (s.d. 2.21) after 2 years. Upper and lower limb muscle contractile cross-sectional area increased in all participants during the trial (P = 0.05 and P < 0.01, respectively). There was a reduction in T2 relaxation times in most muscle groups with stable upper limb muscle function. Conclusion Incremental monthly testosterone injections were well tolerated, promoted endogenous testosterone production and had a positive impact on the skeleton and contractile muscle bulk with evidence suggesting a beneficial impact on the underlying disease process.

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Crawford, B. A., P. Dobbie, J. J. Bass, M. S. Lewitt, R. C. Baxter, and D. J. Handelsman. "Growth hormone (GH) regulation of circulating insulin-like growth factor-I levels during sexual maturation of the GH-deficient dwarf (dw/dw) male rat." Journal of Endocrinology 141, no. 3 (June 1994): 393–401. http://dx.doi.org/10.1677/joe.0.1410393.

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Abstract In many mammalian species, circulating levels of insulinlike growth factor-I (IGF-I) rise during puberty. Previous studies manipulating testosterone levels in rats with normal GH secretion suggested that the pubertal IGF-I rise is regulated by an interaction between GH and sex steroids. Therefore, in a reciprocal study, IGF-I levels were examined during sexual maturation of the GH-deficient dwarf (dw/dw) rat which has a selective genetic deficiency of GH but normal sex steroid levels. Male dw/dw rats were treated with daily injections of recombinant human GH (200 μg/100 g body weight) or saline vehicle, from 28 to 70 days of age. Sexual maturation was determined to occur primarily between 42 and 63 days of age based on testis and seminal vesicle growth and plasma testosterone levels. GH treatment had no effect on seminal vesicle weights, plasma testosterone or gonadotrophins. GH administration resulted in a 7% increase in absolute testes weight (P<0·05), but a 50% increase in body weight (P<0·0001). These results supported previous findings that the reproductive development of dw/dw rats is essentially normal. Untreated dw/dw rats had no rise in IGF-I levels during sexual maturation. In contrast, treatment with GH produced a marked sustained rise in IGF-I levels (P<0·0001). Ligand blots demonstrated GH induction of IGF-binding protein-3 (IGFBP-3) and an IGFBP cluster at 32 kDa. The initially high immunoreactive IGFBP-1 levels (>600 ng/ml) decreased by 49 days of age after which untreated dw/dw rats had significantly higher IGFBP-1 levels than GH-treated dw/dw rats (P<0·01). We conclude that GH secretion, rather than sex steroids, may be the predominant determinant of pubertal IGF-I levels in rats and that the rise in circulating IGF-I levels during puberty is not an indispensible event for normal reproductive development. Journal of Endocrinology (1994) 141, 393–401

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Agarwal, Swashti, Duong D. Tu, Paul F. Austin, Michael E. Scheurer, and Lefkothea P. Karaviti. "Testosterone versus hCG in Hypogonadotropic Hypogonadism – Comparing Clinical Effects and Evaluating Current Practice." Global Pediatric Health 7 (January 2020): 2333794X2095898. http://dx.doi.org/10.1177/2333794x20958980.

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Background. Gonadotropin therapy is not typically used for pubertal induction in hypogonadotropic hypogonadism (HH), however, represents a promising alternative to testosterone. It can potentially lead to the maintenance of future fertility in addition to testicular growth. We compared the pubertal effects of human chorionic gonadotropin (hCG) versus testosterone in adolescent males with HH. We evaluated the current practice, among pediatric endocrinologists, to identify barriers against gonadotropin use. Methods. In this retrospective review, we compared the effect of testosterone versus hCG therapy on mean testicular volume (MTV), penile length, growth velocity, and testosterone levels. We surveyed pediatric endocrinologists at our center, using RedCap. Results. Outcomes were assessed in 52 male patients with HH (hCG, n = 4; T, n = 48) after a mean treatment duration of 13.4 (testosterone) and 13.8 months (hCG; P = .79). Final MTV was higher with hCG (8.25 mL) than testosterone (3.4 mL; P < .001). The groups did not differ in penile length, growth velocity, or testosterone levels. Survey results showed that more than half the providers were aware of the benefits of gonadotropins, however, 91% were uncomfortable prescribing hCG. Commonly reported barriers to prescribing hCG were lack of experience (62%) and insurance coverage concerns (52%). Conclusions. Larger testicular volume predicts faster induction of spermatogenesis. Since hCG promoted better testicular growth, compared to testosterone, it may potentially improve future fertility outcomes in HH patients. Our results identify an opportunity to improve current practice among pediatric endocrinologists worldwide and reduce barriers to prescribing gonadotropins in the adolescent population.

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Lim, Angelina, Margaret Zacharin, Janne Pitkin, Katy de Valle, Monique M. Ryan, and Peter J. Simm. "Therapeutic Options to Improve Bone Health Outcomes in Duchenne Muscular Dystrophy: Zoledronic Acid and Pubertal Induction." Journal of Paediatrics and Child Health 53, no. 12 (December 2017): 1247–48. http://dx.doi.org/10.1111/jpc.13692.

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Pearce, G. P., and P. E. Hughes. "The influence of boar-component stimuli on puberty attainment in the gilt." Animal Science 44, no. 2 (April 1987): 293–302. http://dx.doi.org/10.1017/s0003356100018663.

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ABSTRACTTwo experiments employing 72 and 48 pre-pubertal Large White ♂ × (Large White ♂ × Landrace ♀) gilts respectively were carried out to investigate the involvement of various boar stimuli in the induction of precocious puberty in the gilt. Experiment 1 consisted of the following treatments commencing at 165 days of age: (1) contact with an androgenized, castrated male; (2) contact with an androgenized castrated male plus a recording of boar chants; (3) as treatment (2) plus exposure to a solution of 16-androstene steroids, 3α-androstenol (5α-androst-16-en-3α-ol) and 5α-androstenone (5α-androst-16-en-3-one); and (4) contact with an entire boar. In experiment 2, additional exposure to boar urine occurred in treatments (2) and (3).Exposure of gilts to tactile, visual and auditory cues from the boar had little effect on puberty attainment. The additional exposure to 16-androstene steroids did stimulate puberty but was not as efficacious as boar exposure. Additional exposure to boar urine improved the puberty-stimulating effect of the castrated males, and further additional exposure to 16-androstenes produced a response approaching that obtained by boar exposure.These results confirm the involvement of olfactory cues from the boar in stimulating puberty in the gilt. The olfactory cues appear to be 16-androstene steroids present in boar saliva and some undefined compound(s) present in boar urine. These experiments suggest that olfactory stimuli from the boar require the simultaneous exposure to tactile and possibly also visual and auditory cues from the boar in order to stimulate the onset of puberty in the gilt.cues from the mature boar are also involved in mediating the stimulation of puberty. Exposure of gilts to isolated sources of androstene pheromones was ineffective in stimulating puberty (Kirkwood et al., 1983), whereas exposure to contact with a sialectomized boar order to stimulate the onset of puberty in the gilt.

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Raivio, Taneli, Anne M. Wikström, and Leo Dunkel. "Treatment of gonadotropin-deficient boys with recombinant human FSH: long-term observation and outcome." European Journal of Endocrinology 156, no. 1 (January 2007): 105–11. http://dx.doi.org/10.1530/eje.1.02315.

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Background: Boys with prepubertal onset of hypogonadotropic hypogonadism (HH) are at a risk of poor testis growth and impaired spermatogenesis. One potential cause for this is deficient proliferation of immature Sertoli cells before and during puberty due to the absence of FSH. Objective: To evaluate the effects of recombinant human FSH (r-hFSH) and human chorionicgonadotropin (hCG) on testicular function and pubertal development in boys with prepubertal onset of HH. Design: Retrospective clinical study. Setting: Two university central hospitals, pediatric referral endocrinology outpatient clinics. Patients: Fourteen boys (aged, 9.9–17.7 years) with prepubertal (testicular volume (TV) <3 ml) onset of HH (idiopathic HH, n=2; Kallman syndrome, n=2; idiopathic panhypopituitarism, n=4; organic panhypopituitarism, n=6). Intervention: Treatment with r-hFSH alone (2 mo–2.8 years) prior to induction of puberty with the combination of FSH and hCG. Main outcome measures: Progression of puberty, change in serum inhibin B, spermatogenesis. Results: r-hFSH alone increased testicular volume twofold, from 0.9±0.6 ml (mean±s.d.) to 1.8 ± 1.1 ml (P<0.005), and serum inhibin B threefold, from 27±14 to 80±57 pg/ml (P<0.01). Three boys with an apparent absence of postnatal hypothalamic–pituitary–testicular axis activation displayed attenuated inhibin B responses to long-term (≥1 year) r-hFSH (P<0.01). Further significant increase in both TVand inhibin B occurred with induction of puberty with FSH and hCG (P<0.001). Seven boys provided semen samples: one had azoospermia, and others displayed a maximal sperm count range from 2.9 to 92 million/ml (median 8.5 million/ml). Conclusions: (i) r-hFSH induces prepubertal testis growth and increases circulating inhibin B levels, findings suggesting proliferation of immature Sertoli cells. (ii) Puberty was successfully induced with hCG and r-hFSH following r-hFSH priming. (iii) Inhibin B appears useful for monitoring spermatogenetic activity in boys treated with hCG. (iv) Despite the extremely small initial testis volume, six out of seven patients (86%) primed with r-hFSH displayed sperm in the ejaculate suggesting beneficial effect of r-hFSH priming on testicular function later in life.

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42

Hull, KL, and S. Harvey. "Growth hormone: roles in female reproduction." Journal of Endocrinology 168, no. 1 (January 1, 2001): 1–23. http://dx.doi.org/10.1677/joe.0.1680001.

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GH, as its name suggests, is obligatory for growth and development. It is, however, also involved in the processes of sexual differentiation and pubertal maturation and it participates in gonadal steroidogenesis, gametogenesis and ovulation. It also has additional roles in pregnancy and lactation. These actions may reflect direct endocrine actions of pituitary GH or be mediated by its induction of hepatic or local IGF-I production. However, as GH is also produced in gonadal, placental and mammary tissues, it may act in paracrine or autocrine ways to regulate local processes that are strategically regulated by pituitary GH. The concept that GH is an important modulator of female reproduction is the focus of this review.

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43

Bergendahl, M., and I. Huhtaniemi. "Acute fasting is ineffective in suppressing pituitary-gonadal function of pubertal male rats." American Journal of Physiology-Endocrinology and Metabolism 264, no. 5 (May 1, 1993): E717—E722. http://dx.doi.org/10.1152/ajpendo.1993.264.5.e717.

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Effects of short-term fasting (3–4 days) on pituitary-testicular functions were studied during sexual maturation in male rats at 25, 35, 45, 55, and 65 days of age. Among the main findings, testicular testosterone decreased by 41–68% at all ages (P < 0.01–0.05). The pituitary steady-state mRNA levels of the common alpha-subunit (28–55%) and follicle-stimulating hormone (FSH) beta-subunit (25–50%) decreased (P < 0.01–0.05) at 25, 55, and 65 days of age but not at 35 and 45 days; the luteinizing hormone (LH) beta-subunit did not respond at any age. Fasting decreased serum LH (P < 0.01) at 25, 55, and 65 days of age but not at 35 and 45 days. Likewise, fasting decreased pituitary and/or serum FSH only in the 25- and 65-day-old rats (P < 0.01–0.05). In conclusion, LH and FSH secretion, and the gene expression of common alpha- and FSH beta-subunits, decreased consistently during short-term fasting only in prepubertal (25 days) and adult (65 days) but not in peripubertal animals (35 and 45 days). Hence, the pubertal rise in gonadotropins represents such a strong positive induction that it largely overrides the antigonadotropic effect of fasting.

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Benchimol, Gabriela da Costa, Josye Bianca Santos, Ana Sophia da Costa Lopes, Karol Guimarães Oliveira, Eviny Sayuri Trindade Okada, Bianca Nascimento de Alcantara, Washington Luiz Assunção Pereira, et al. "Zika Virus Infection Damages the Testes in Pubertal Common Squirrel Monkeys (Saimiri collinsi)." Viruses 15, no. 3 (February 23, 2023): 615. http://dx.doi.org/10.3390/v15030615.

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During the Zika virus (ZIKV) outbreak and after evidence of its sexual transmission was obtained, concerns arose about the impact of the adverse effects of ZIKV infection on human fertility. In this study, we evaluated the clinical-laboratory aspects and testicular histopathological patterns of pubertal squirrel monkeys (Saimiri collinsi) infected with ZIKV, analyzing the effects at different stages of infection. The susceptibility of S. collinsi to ZIKV infection was confirmed by laboratory tests, which detected viremia (mean 1.63 × 106 RNA copies/µL) and IgM antibody induction. Reduced fecal testosterone levels, severe testicular atrophy and prolonged orchitis were observed throughout the experiment by ultrasound. At 21 dpi, testicular damage associated with ZIKV was confirmed by histopathological and immunohistochemical (IHC) analyses. Tubular retraction, the degeneration and necrosis of somatic and germ cells in the seminiferous tubules, the proliferation of interstitial cells and an inflammatory infiltrate were observed. ZIKV antigen was identified in the same cells where tissue injuries were observed. In conclusion, squirrel monkeys were found to be susceptible to the Asian variant of ZIKV, and this model enabled the identification of multifocal lesions in the seminiferous tubules of the infected group evaluated. These findings may suggest an impact of ZIKV infection on male fertility.

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Borges, J. B. S., D. S. V. Luiz, P. R. L. Aguiar, C. G. B. Berlitz, G. S. Velho, C. R. Oliveira, B. M. Guerreiro, B. G. Freitas, and A. G. C. Dalto. "8 Evaluation of puberty induction protocol in peripubertal beef heifers prior to fixed-time AI programs." Reproduction, Fertility and Development 31, no. 1 (2019): 129. http://dx.doi.org/10.1071/rdv31n1ab8.

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Beef heifers that conceive early during their first breeding season calve earlier, wean heavier calves, and tend to continue doing so throughout the rest of their reproductive lives. Otherwise, under extensively managed systems in Southern Brazil, only a variable proportion of 2-year-old beef heifers reach puberty before the start of the breeding season. The aim of this study was to evaluate a protocol to induce puberty in peripubertal beef heifers using injectable progesterone (P4) and oestradiol cypionate (EC) to improve pregnancy per AI (P/AI) in fixed-time AI (FTAI) programs. A total of 311 Angus heifers, 24±3 months of age, 3.1±0.3 body condition score (1=emaciated; 5=obese), and 328±41kg of body weight (BW), were examined before FTAI protocol (Day −24) by transrectal ultrasonography to determine reproductive tract score (RTS; 1=prepubertal; 5=pubertal). Prepubertal heifers (RTS 1; 12.8%, 40/311) were excluded from the study. Heifers with RTS=2 (n=271) were assigned to 2 groups: P4 (RTS 2 or 3, n=100) and cyclic (RTS 4 and 5, n=171). Peripubertal heifers were treated on Day −24 with 150mg of injectable P4 IM (Sincrogest® injectable, Ourofino Animal Health, Cravinhos, Brazil) and on Day −12 received 1mg of EC IM (Sincro CP®, Ourofino Animal Health). Cyclic heifers received no hormonal treatment before FTAI protocol. On Day 0, heifers in the P4 group were evaluated again to determine RTS, body condition score, and BW. Induction of puberty was defined by the presence of a follicle >8.5mm (RTS=4) or a corpus luteum (RTS=5). All heifers received an FTAI protocol consisting of 2mg of oestradiol benzoate IM (Sincrodiol®, Ourofino Animal Health) and an intravaginal progesterone implant (1 g; Sincrogest®, Ourofino Animal Health). On Day 8, heifers had implants removed and were injected with 1mg of EC and 500µg of sodium cloprostenol IM (Sincrocio®, Ourofino Animal Health). After 48h, all heifers received an FTAI. Thirty days after AI, the diagnosis of gestation was performed by ultrasonography. Statistics included chi-square and linear regression with coefficients analysed as independent variables, considering a significant P-value of 0.05. On Day 0, percentages of RTS 5, 4, and 3 in the P4 heifers were 37, 27, and 36%, respectively, resulting in 64% of puberty induction. The P/AI was similar (P=0.14) in P4-treated and cyclic heifers (59v. 50.3%, respectively). The regression analysis presented a linear and positive effect of BW on P/AI (P<0.001) in cyclic heifers and a positive influence of BW on RTS (P=0.05) and RTS on P/AI (P=0.008) in P4-treated heifers. The application of RTS system associated with P4 treatment of peripubertal heifers before FTAI protocol improved ovarian activity and might have contributed to higher P/AI, comparable with that achieved in cyclic heifers.

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Ubaid-Ur-Rehman, Shujait Ali, Nazir Ahmad, Shanaz Adeeb Khanum, and Muhammad Zubair. "Ovulation induction in pre-pubertal Sahiwal-Friesian cross bred heifers by the use of clomiphene citrate and hCG." Animal Reproduction Science 149, no. 3-4 (October 2014): 141–44. http://dx.doi.org/10.1016/j.anireprosci.2014.07.019.

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Eastham, Philippa R., and D. J. A. Cole. "Reproduction in the gilt 7. Exposure of young gilts to the same mature boar and relocation: effects on the attainment of puberty." Animal Science 44, no. 3 (June 1987): 435–41. http://dx.doi.org/10.1017/s000335610001237x.

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ABSTRACTTwenty-four Landrace × (Landrace × Large White) gilts were randomly allocated at a mean age of 70 days to each of two rearing treatments which were: (1) housing gilts with other gilts but in complete isolation from other pigs; or (2) housing gilts with fence-line contact with a mature boar. At 160 days of age all gilts were relocated, treatment 1 gilts being adjacent to a mature boar for the first time while treatment 2 gilts were adjacent to the same mature boar with which they had had contact during rearing. In addition, the gilts on each treatment were exposed to full contact with this boar for 30 min/day. There were no significant differences between the treatments in age (176 and 185 days) or weight at puberty (81·9 and 82·6 kg), in the interval from relocation and full boar contact to puberty (11 and 16 days) and in ovulation rate at the pubertal oestrus (11·6 and 11·5).In a second experiment, 72 gilts were reared with fence-line contact with a mature boar and at 160 days of age, half were relocated adjacent to a novel mature boar and the other half remained in the rearing house next to a novel boar with all gilts receiving full boar contact for 30 min/day. Significantly more relocated gilts reached puberty during the experimental period (25/32) than gilts which were only exposed to contact with a novel boar and not relocated (12/31) (P < 0·001) and those relocated gilts were significantly younger (187 v. 225 days; P < 0·001) and lighter (75·4 v. 93·9 kg; P < 0·001) at puberty and the induction interval was significantly shorter (20 v. 89 days; P < 0·001) compared with gilts on the second treatment.

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Patel, Shailendra B., and Srujana Kamala Yada. "Adult Onset Isolated Hypogonadotropic Hypogonadism- a Cause of Secondary Amenorrhea." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A777. http://dx.doi.org/10.1210/jendso/bvab048.1581.

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Abstract A 23-year-old African American female was referred for secondary amenorrhea evaluation. She attained menarche at 12 years and had regular menses. At 18 years, she used OCPs for few months, and used plan B, after which her menses stopped. She had hot flashes and sweating. She was placed on progesterone, but never had withdrawal bleeding. Review of systems was positive for intentional weight loss after her menses stopped, hair loss and nipple discharge. She denied any loss of sensation of smell. She has a PMH of asthma, anxiety and OSA. Family history was not significant for any fertility issues. She smoked cannabis after menses stopped. On physical examination, vitals were stable, BMI of 35 kg/meter2, well-developed secondary sexual characteristics, no thyromegaly, acne or hirsutism. Upon work up, CBC, CMP were normal, Urine pregnancy test was negative, gonadotropins were undetectable (FSH- <0.7mIU/ml, LH- <0.2mIU/ml), anti-mullerian hormone was 3.82ng/ml (WNL), Estradiol was also absent (<15pg/ml), with a low Total testosterone (11ng/dl), TSH was 1.17uIU/ml, Free T4 was 1.1ng/dl, ACTH was 9.58pg/ml, Cortisol was 14.8mcg/dl, and Prolactin was 1.5ng/ml. MRI brain was normal with normal pituitary gland, no focal lesion visualized. Pelvic ultrasound showed ovaries 5.9mL and 4.6mL with multiple follicles present bilaterally. Diagnosis of adult-onset isolated hypogonadotropic hypogonadism (IHH) was made. Patient was started on estradiol patches and progesterone. IHH is a genetic disorder of defective production or action of GnRH. IHH when associated with anosmia is called Kallmann syndrome. It was first described by German American geneticist Joseph Kallmann in 1944. GnRH is a decapeptide, produced in arcuate nucleus and pre-optic nucleus of hypothalamus. GnRH stimulates anterior pituitary to secrete FSH and LH. IHH is caused due to impaired migration of GnRH neurons to brain during embryogenesis. It is inherited as autosomal or X-linked dominant or recessive. Gene mutations associated are ANOS-1, FGFR, PROK-2. It is rare in females. IHH has a broad spectrum of clinical presentation from complete absence of sexual development to partial completion of puberty. It presents with microphallus, cryptorchidism, cleft lip/palate, syndactyly, renal aplasia. In childhood presents with anosmia, hearing deficits, dental agenesis, mirror movements, short stature. During puberty, absent pubertal growth spurt, amenorrhea, lack of virilization, no secondary sexual characteristics, infertility. In partial forms, known as Adult onset or acquired form of IHH, patients have slight testicular growth, thelarche, menarche. Goals of treatment are- pubertal induction, maintenance of sexual maturation and restoration of fertility. In females, pre-puberty only estrogen is given, after puberty both estrogen and progesterone are used, for fertility, pulsatile gonadotropins or GnRH analogues are used.

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Liu, Peter Y., H. W. Gordon Baker, Veena Jayadev, Margaret Zacharin, Ann J. Conway, and David J. Handelsman. "Induction of Spermatogenesis and Fertility during Gonadotropin Treatment of Gonadotropin-Deficient Infertile Men: Predictors of Fertility Outcome." Journal of Clinical Endocrinology & Metabolism 94, no. 3 (March 1, 2009): 801–8. http://dx.doi.org/10.1210/jc.2008-1648.

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Abstract Background: The induction of spermatogenesis and fertility with gonadotropin therapy in gonadotropin-deficient men varies in rate and extent. Understanding the predictors of response would inform clinical practice but requires multivariate analyses in sufficiently large clinical cohorts that are suitably detailed and frequently assessed. Design, Setting, and Participants: A total of 75 men, with 72 desiring fertility, was treated at two academic andrology centers for a total of 116 courses of therapy from 1981–2008. Outcomes: Semen analysis and testicular examination were performed every 3 months. Results: A total of 38 men became fathers, including five through assisted reproduction. The median time to achieve first sperm was 7.1 months [95% confidence interval (CI) 6.3–10.1]) and for conception was 28.2 months (95% CI 21.6–38.5). The median sperm concentration at conception for unassisted pregnancies was 8.0 m/ml (95% CI 0.2–59.5). Multivariate correlated time-to-event analyses show that larger testis volume, previous treatment with gonadotropins, and no previous androgen use each independently predicts faster induction of spermatogenesis and unassisted pregnancy. Conclusions: Larger testis volume is a useful prognostic indicator of response. The association of slower responses after prior androgen therapy suggests that faster pregnancy rates might be achieved by substituting gonadotropin for androgen therapy for pubertal induction, although a prospective randomized trial will be required to prove this.

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Katsagoni, Christina N. "Malnutrition in Inflammatory Bowel Diseases. What do we know today?" Kompass Nutrition & Dietetics 1, no. 2 (2021): 46–48. http://dx.doi.org/10.1159/000516279.

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Growth delay with height and weight impairment is a common feature of pediatric inflammatory bowel diseases (PIBD). Up to 2/3 of Crohn Disease patients have impaired weight at diagnosis, and up to 1/3 have impaired height. Ulcerative colitis usually manifests earlier with less impaired growth, though patients can be affected. Ultimately, growth delay, if not corrected, can reduce final adult height. Weight loss, reduced bone mass, and pubertal delay are also concerns associated with growth delay in newly diagnosed PIBD patients. The mechanisms for growth delay in IBD are multifactorial and include reduced nutrient intake, poor absorption, increased fecal losses, as well as direct effects from inflammation and treatment modalities. Management of growth delay requires optimal disease control. Exclusive enteral nutrition (EEN), biologic therapy, and corticosteroids are the primary induction strategies used in PIBD, and both EEN and biologics positively impact growth and bone development. Beyond adequate disease control, growth delay and pubertal delay require a multidisciplinary approach, dependent on diligent monitoring and identification, nutritional rehabilitation, and involvement of endocrinology and psychiatry services as needed. Pitfalls that clinicians may encounter when managing growth delay include refeeding syndrome, obesity (even in the setting of malnutrition), and restrictive diets. Although treatment of PIBD has improved substantially in the last several decades with the era of biologic therapies and EEN, there is still much to be learned about growth delay in PIBD in order to improve outcomes.

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Journal articles on the topic 'Pubertal induction'

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