Journal articles on the topic 'Puberty'
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Dira, I. Komang Prayoga Ariguna, I. Made Arimbawa, and I. Made Darma Yuda. "Hubungan status nutrisi dengan gangguan pubertas pada remaja panti asuhan di Kota Denpasar." Intisari Sains Medis 14, no. 3 (October 31, 2023): 1016–22. http://dx.doi.org/10.15562/ism.v14i3.1829.
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Background: Puberty is a transition period between childhood and adulthood influenced by various complex factors. Nutrition is one of the most important factors affecting pubertal development. Overweight or obese children are more likely to enter puberty earlier. Severe primary or secondary malnutrition can also delay the onset and progression of puberty. This study aims to determine the relationship between nutritional status and pubertal disorders in Denpasar city orphanage children. Methods: This study was conducted using an analytic research design with a cross-sectional design to determine the relationship between nutritional status and pubertal disorders in Denpasar city orphanage children. This study involved all children in Denpasar city orphanages, Bali, between November and December 2022. Subjects who met the inclusion and exclusion criteria were included in the study. Data were analyzed using SPSS version 25.0 for Windows. Results: This study involved 160 adolescents who had reached the age of puberty in an orphanage in Denpasar City. The sample was classified as having normal puberty, 93.75%, and as many as 10 research samples were found to have puberty disorders (6.25%). The samples were classified as well-nourished (75.00%) and malnutrition (25.00%). This study shows that nutritional status has a significant relationship with pubertal disorders, with a p-value of 0.003 and a prevalence ratio of 7.00 and CI95% (1.90-25.79). Conclusion: This study found that there is a significant relationship between nutritional status and the occurrence of puberty disorders. Adolescents with malnutrition nutritional status have a seven times greater risk of experiencing puberty disorders compared to adolescents with good nutritional status. Latar Belakang: Pubertas merupakan masa transisi antara masa anak-anak dengan dewasa yang di pengeruhi oleh berbagai faktor kompleks. Nutrisi merupakan salah satu faktor terpenting yang mempengaruhi perkembangan pubertas. Anak yang kelebihan berat badan atau obesitas lebih cenderung memasuki masa pubertas lebih awal. Malnutrisi primer atau sekunder yang parah juga dapat menunda permulaan dan perkembangan pubertas. Penelitian ini bertujuan untuk mengetahui hubungan antara status nutrisi dengan gangguan pubertas pada anak panti asuhan kota Denpasar. Metode: Penelitian ini dilakukan menggunakan rancangan penelitian analitik dengan desain potong lintang untuk mengetahui hubungan antara status nutrisi dengan gangguan pubertas pada anak panti asuhan kota Denpasar. Penelitian ini melibatkan semua anak pada panti asuhan kota Denpasar, Bali, diantara periode penelitian November hingga Desember 2022. Subjek yang memenuhi kriteria inklusi dan eksklusi dimasukkan ke dalam penelitian. Hasil: Penelitian ini melibatkan 160 remaja yang telah mencapai usia pubertas di Panti Asuhan yang terletak di Kota Denpasar. Sampel tergolong memiliki pubertas normal 93,75%, sebanyak 10 sampel penelitian ditemukan mengalami gangguan pubertas (6,25%). Sampel tergolong memiliki gizi baik (75,00%) dan malnutrisi (25,00%). Penelitian ini menunjukkan status nutrisi memiliki hubungan signifikan dengan gangguan pubertas dengan nilai p sebesar 0,003 dan prevalence ratio sebesar 7,00 dan IK95% (1,90-25,79). Simpulan: Penelitian ini menemukan bahwa terdapat hubungan yang signifikan antara status nutrisi dengan terjadinya gangguan pubertas. Remaja dengan status nutrisi malnutrisi memiliki risiko tujuh kali lebih besar untuk mengalami gangguan pubertas dibandingkan dengan remaja dengan status nutrisi baik.
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Begum, Poly, Dipti Rani Saha, and Md Kamrul Hassan. "Precocious Puberty A Case Report." Bangladesh Journal of Obstetrics & Gynaecology 30, no. 2 (December 30, 2016): 109–12. http://dx.doi.org/10.3329/bjog.v30i2.30906.
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The parents of a 04-year-old girl bring her to a Gynaecologist because of breast development, appearance of pubic hair and periodic per vaginal bleeding. Her medical history is unremarkable. The parents are of average height, and the mother reports first menstruating when she was 11 years old. At physical examination, the girl is 100 cm tall , weighs 17 kg, and has a bodymass index of 17. Her pubertal development is classified as Tanner stage 3 breast development and Tanner stage 2 pubic hair development. She was diagnosed as a case of precocious puberity. Appearance of secondary sexual development before the age of 9 in a male child and before the age of 8 in a female child is called precocious puberty. When the cause of precocious puberty is premature activation of the hypothalamic-pituitary axis, it is called central or complete precocious puberty and she was a case of central precocious puberty. After proper consult she was treated by GnRHa suppressor of pituitary till 11 years of age.Bangladesh J Obstet Gynaecol, 2015; Vol. 30(2) : 109-112
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Klump, K. L., K. M. Culbert, J. D. Slane, S. A. Burt, C. L. Sisk, and J. T. Nigg. "The effects of puberty on genetic risk for disordered eating: evidence for a sex difference." Psychological Medicine 42, no. 3 (August 22, 2011): 627–37. http://dx.doi.org/10.1017/s0033291711001541.
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BackgroundDifferences in genetic influences on disordered eating are present across puberty in girls. Heritability is 0% before puberty, but over 50% during and after puberty. Emerging data suggest that these developmental differences may be due to pubertal increases in ovarian hormones. However, a critical piece of evidence is lacking, namely, knowledge of genetic influences on disordered eating across puberty in boys. Boys do not experience increases in ovarian hormones during puberty. Thus, if pubertal increases in genetic effects are present in boys, then factors in addition to ovarian hormones may drive increases in heritability in girls. The current study was the first to examine this possibility in a sample of 1006 male and female twins from the Michigan State University Twin Registry.MethodDisordered eating was assessed with the Minnesota Eating Behavior Survey. Pubertal development was assessed with the Pubertal Development Scale.ResultsNo significant differences in genetic influences on disordered eating were observed in males across any developmental stage. Heritability was 51% in boys during pre-puberty, puberty and young adulthood. By contrast, in girls, genetic factors accounted for 0% of the variance in pre-puberty, but 51% of the variance during puberty and beyond. Sex differences in genetic effects were only significant during pre-puberty, as the best-fitting models constrained heritability to be equal across all males, pubertal females and young adult females.ConclusionsThe results highlight sex-specific effects of puberty on genetic risk for disordered eating and provide indirect evidence of a role for ovarian hormones and/or other female-specific factors.
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Sánchez-Garrido, M. A., J. M. Castellano, F. Ruiz-Pino, D. Garcia-Galiano, M. Manfredi-Lozano, S. Leon, A. Romero-Ruiz, C. Diéguez, L. Pinilla, and M. Tena-Sempere. "Metabolic Programming of Puberty: Sexually Dimorphic Responses to Early Nutritional Challenges." Endocrinology 154, no. 9 (June 10, 2013): 3387–400. http://dx.doi.org/10.1210/en.2012-2157.
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Body energy stores and metabolic cues influence the onset of puberty. However, the pubertal impact of early nutritional challenges has been only fragmentarily addressed. We evaluated here the consequences, in terms of pubertal timing and hormonal markers, of various nutritional manipulations during pre- or postnatal maturation in rats of both sexes. Males and females were submitted to gestational undernutrition (UNG) or peripubertal (SUB) subnutrition or were raised in large (LL; underfeeding) or small (SL; overfeeding) litters. In addition, groups of UNG, LL, and SL rats were fed on a high-fat diet (HFD) after weaning. Postnatal overfeeding resulted in higher body weights (BWs) during pubertal transition in both sexes, but only SL males displayed overtly advanced external signs of puberty. Postnatal underfeeding persistently decreased BW gain during puberty, yet the magnitude of pubertal delay was greater in LL males. In contrast, regardless of postnatal nutrition, HFD tended to advance the onset of puberty in females but did not alter pubertal timing in males. Likewise, SUB females displayed a marked delay in BW gain and puberty onset, whereas despite similar reduction in BW, SUB males showed normal timing of puberty. These sex divergences were also detected in various hormonal and metabolic indices so that postnatal overnutrition consistently increased LH, FSH, leptin, and insulin levels only in pubertal females, whereas HFD decreased gonadotropin levels in SL females but increased them in SL males. Notably, UNG rats did not show signs of delayed puberty but displayed a striking sex dimorphism in serum insulin/glucose levels, regardless of the diet, so that only UNG males had signs of presumable insulin resistance. Our data disclose important sex differences in the impact of various early nutritional challenges on the timing of puberty, which may help to explain the different trends of altered puberty and related comorbidities between sexes.
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Lindhardt Johansen, Marie, Casper P. Hagen, Mikkel G. Mieritz, Ole D. Wolthers, Carsten Heuck, Jørgen Holm Petersen, and Anders Juul. "Pubertal Progression and Reproductive Hormones in Healthy Girls With Transient Thelarche." Journal of Clinical Endocrinology & Metabolism 102, no. 3 (December 23, 2016): 1001–8. http://dx.doi.org/10.1210/jc.2016-2871.
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Abstract Context: Detailed evaluation of pubertal progression in girls from longitudinal studies is sparse, and the phenomenon of transient thelarche (TT), defined as the appearance, regression, and subsequent reappearance of breast buds, in healthy girls remains undescribed. Objective: To describe TT in terms of pubertal progression, growth, genotypes, and reproductive hormones and to apply new puberty nomograms for breast stages, pubic hair, and menarche. Design: A prospective, longitudinal population-based study. Patients or Other Participants: Ninety-eight healthy Danish schoolchildren (Caucasian girls) followed longitudinally as part of the COPENHAGEN Puberty Study were included in the evaluation of TT. A total of 1466 girls from 2 cross-sectional studies were included in the creation of the puberty nomograms. Intervention(s): None. Main Outcome Measure(s): Pubertal progression, specifically thelarche, reproductive hormones, genotype, and growth. Results: Twelve of 98 (12%) girls experienced TT. A larger proportion of girls with TT entered puberty by the pubarche pathway (50%) compared with girls with normal progression (15.4%), P = 0.014. Girls with TT progressed through puberty normally when evaluated using puberty nomograms. Reproductive hormones and growth velocity were lower at the first (transient) thelarche than the second (permanent) thelarche. Conclusion: TT is a frequent phenomenon that appears to be a peripheral occurrence independent of central puberty. It does not appear to affect subsequent pubertal progression as evaluated by our new puberty nomograms.
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Manotas, María Carolina, Daniel Mauricio González, Camila Céspedes, Catalina Forero, and Adriana Patricia Rojas Moreno. "Genetic and Epigenetic Control of Puberty." Sexual Development 16, no. 1 (October 14, 2021): 1–10. http://dx.doi.org/10.1159/000519039.
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Puberty is a complex transitional phase in which reproductive capacity is achieved. There is a very wide variation in the age range of the onset of puberty, which follows a familial, ethnic, and sex pattern. The hypothalamic-pituitary-gonadal axis and several genetic, environmental, and nutritional factors play an important role in the onset of and throughout puberty. Recently, there has been significant progress in identifying factors that affect normal pubertal timing. Different studies have identified single nucleotide polymorphisms (SNPs) that affect pubertal timing in both sexes and across ethnic groups. Single genes are implicated in both precocious and delayed puberty, and epigenetic mechanisms have been suggested to affect the development and function of the GnRH neuronal network and responsiveness of end organs. All these factors can influence normal puberty timing, precocious puberty, and delayed puberty. The objective of this review is to describe recent findings related to the genetic and epigenetic control of puberty and highlight the need to deepen the knowledge of the regulatory mechanisms of this process in the normal and abnormal context.
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Manotas, María Carolina, Daniel Mauricio González, Camila Céspedes, Catalina Forero, and Adriana Patricia Rojas Moreno. "Genetic and Epigenetic Control of Puberty." Sexual Development 16, no. 1 (October 14, 2021): 1–10. http://dx.doi.org/10.1159/000519039.
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Puberty is a complex transitional phase in which reproductive capacity is achieved. There is a very wide variation in the age range of the onset of puberty, which follows a familial, ethnic, and sex pattern. The hypothalamic-pituitary-gonadal axis and several genetic, environmental, and nutritional factors play an important role in the onset of and throughout puberty. Recently, there has been significant progress in identifying factors that affect normal pubertal timing. Different studies have identified single nucleotide polymorphisms (SNPs) that affect pubertal timing in both sexes and across ethnic groups. Single genes are implicated in both precocious and delayed puberty, and epigenetic mechanisms have been suggested to affect the development and function of the GnRH neuronal network and responsiveness of end organs. All these factors can influence normal puberty timing, precocious puberty, and delayed puberty. The objective of this review is to describe recent findings related to the genetic and epigenetic control of puberty and highlight the need to deepen the knowledge of the regulatory mechanisms of this process in the normal and abnormal context.
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Xu, Lu, Ming Li, Jinhua Yin, Hong Cheng, Miao Yu, Xiaoyuan Zhao, Xinhua Xiao, and Jie Mi. "Change of Body Composition and Adipokines and Their Relationship with Insulin Resistance across Pubertal Development in Obese and Nonobese Chinese Children: The BCAMS Study." International Journal of Endocrinology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/389108.
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A transient increase in insulin resistance (IR) is a component of puberty. We investigated the impact of body composition and adipokines on IR during puberty in Chinese children. This study included 3223 schoolchildren aged 6–18 years. IR was calculated using homeostasis model assessment (HOMA-IR). We revealed that body mass index (BMI) and waist circumference increased gradually during puberty in both genders, while fat-mass percentage (FAT%) increased steadily only in girls. Change of leptin showed striking sexual dimorphisms: in girls leptin increased steadily during puberty, whereas in boys, after a transient rise at the beginning of puberty, leptin declined by Tanner staging even in those overweight or obese. Inversely, adiponectin level decreased significantly during puberty. In both genders, HOMA-IR started to increase at the beginning of puberty, peaked in the middle, and revised at late puberty in overweight/obesity boys while it stayed high till the end of puberty in girls and normal weight boys. Multivariate regression analysis revealed that leptin presented a stronger indicator of HOMA-IR than anthropometric measures during puberty. Our results demonstrated that gender-specific FAT% and leptin changed with pubertal development. Leptin emerged as a stronger predictor of IR than traditional anthropometric indices, suggesting a prominent role in the development of pubertal IR.
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Vazquez, M. J., I. Velasco, and M. Tena-Sempere. "Novel mechanisms for the metabolic control of puberty: implications for pubertal alterations in early-onset obesity and malnutrition." Journal of Endocrinology 242, no. 2 (August 2019): R51—R65. http://dx.doi.org/10.1530/joe-19-0223.
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Puberty is driven by sophisticated neuroendocrine networks that timely activate the brain centers governing the reproductive axis. The timing of puberty is genetically determined; yet, puberty is also sensitive to numerous internal and external cues, among which metabolic/nutritional signals are especially prominent. Compelling epidemiological evidence suggests that alterations of the age of puberty are becoming more frequent; the underlying mechanisms remain largely unknown, but the escalating prevalence of obesity and other metabolic/feeding disorders is possibly a major contributing factor. This phenomenon may have clinical implications, since alterations in pubertal timing have been associated to adverse health outcomes, including higher risk of earlier all-cause mortality. This urges for a better understanding of the neurohormonal basis of normal puberty and its deviations. Compelling evidence has recently documented the master role of hypothalamic neurons producing kisspeptins, encoded by Kiss1, in the neuroendocrine pathways controlling puberty. Kiss1 neurons seemingly participate in transmitting the regulatory actions of metabolic cues on pubertal maturation. Key cellular metabolic sensors, as the mammalian target of rapamycin (mTOR), AMP-activated protein kinase (AMPK) and the fuel-sensing deacetylase, SIRT1, have been recently shown to participate also in the metabolic modulation of puberty. Recently, we have documented that AMPK and SIRT1 operate as major molecular effectors for the metabolic control of Kiss1 neurons and, thereby, puberty onset. Alterations of these molecular pathways may contribute to the perturbation of pubertal timing linked to conditions of metabolic stress in humans, such as subnutrition or obesity and might become druggable targets for better management of pubertal disorders.
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Voordouw, Jasper J., Mirjam M. van Weissenbruch, and Henriette A. Delemarre-van de Waal. "Intrauterine Growth Retardation and Puberty in Girls." Twin Research 4, no. 5 (October 1, 2001): 299–306. http://dx.doi.org/10.1375/twin.4.5.299.
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AbstractSome, albeit not all studies on the relationship between intrauterine growth retardation (IUGR) and female pubertal development have found an earlier and rapidly progressing puberty as well as concomitant disorders of related functional systems such as polycystic ovary syndrome and short stature. These pubertal changes are part of a growing list of IUGR-related diseases, which includes non-insulin dependent diabetes mellitus and coronary heart disease. A pulsatile release of gonadotropin releasing hormone is thought to be a conditio-sinne-qua-non for the initiation of puberty. In the absence of prospective studies on gonadotropin releasing hormone pulse patterns in IUGR-children other markers of pubertal development such as age at menarche have been deployed. From these studies it is not clear, however, whether the findings of an earlier onset of puberty in IUGR-girls merely reflect a more rapid progression of puberty. Both the role for IUGR and the mechanisms behind the onset of puberty are still elusive. Assuming a connection between IUGR and pubertal development, parallels can be drawn between hypotheses on the longterm consequences of IUGR and hypotheses on the initiation of puberty. For example, the somatometer concept proposes a role for fat mass in the initiation of puberty, which is compatible with the hypothesis on non-skeletal catch-up growth after IUGR. The debate on the origins of puberty and the role of IUGR mainly focuses on nature and nurture. Judgmentally, studies in mono- and dizygotic twins discordant for birth weight may be of particular help.
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van der Steen, Manouk, Annemieke J. Lem, Danielle C. M. van der Kaay, and Anita C. S. Hokken-Koèelega. "Puberty and Pubertal Growth in GH-treated SGA Children: Effects of 2 Years of GnRHa Versus No GnRHa." Journal of Clinical Endocrinology & Metabolism 101, no. 5 (May 1, 2016): 2005–12. http://dx.doi.org/10.1210/jc.2016-1317.
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Abstract Context: Most studies on puberty in children born small for gestational age (SGA) report height and age at onset of puberty. GH-treated SGA children with an adult height (AH) expectation below −2.5 SDS at onset of puberty can benefit from an additional 2 years of GnRH analog (GnRHa) treatment. There are no data on puberty and growth after discontinuation of GnRHa treatment in GH-treated SGA children. Objective: This study aimed to investigate the effects on puberty and pubertal growth of 2 years GnRHa vs no GnRHa in GH-treated SGA children. Methods: This was a GH trial involving 76 prepubertal short SGA children (36 girls) treated with GH. Thirty-two children received additional GnRHa for 2 years. Pubertal stages were 3-monthly assessed according to Tanner. Results: Age, bone age, and median height at pubertal onset were lower in girls and boys in the GH/GnRHa group compared with the GH group. In girls and boys treated with GH/GnRHa, pubertal duration after stop of GnRHa treatment was shorter than pubertal duration in those with GH only (40.9 vs 46.7 mo; P = .044; 50.8 vs 57.5 months; P = .006; respectively). Height gain from onset of puberty until AH, including height gain during 2 years of GnRHa treatment, was 25.4 cm in girls and 33.0 cm in boys, which was 6.6 cm more than girls and boys treated with GH only. AH was similar in children treated with GH/GnRHa compared with those with GH only. Conclusions: GH-treated SGA children who start puberty with an AH expectation below −2.5 SDS and are treated with 2 years of GnRHa have a shorter pubertal duration after discontinuation of GnRHa compared with pubertal duration in children treated with GH only. Height gain from onset of puberty until AH is, however, more due to adequate growth during 2 years of GnRHa treatment resulting in a similar AH as children treated with GH only.
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Jonsdottir-Lewis, Elfa, Amalia Feld, Ryan Ciarlo, Erica Denhoff, Henry A. Feldman, and Yee-Ming Chan. "Timing of Pubertal Onset in Girls and Boys With Constitutional Delay." Journal of Clinical Endocrinology & Metabolism 106, no. 9 (April 23, 2021): e3693-e3703. http://dx.doi.org/10.1210/clinem/dgab270.
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Abstract Context The decision whether to treat a child with delayed puberty with sex steroids is primarily based on patient, family, and provider preference. Knowing when children with constitutional delay eventually enter puberty would inform this decision. Objective, Design, Setting, Participants, and Outcome Measures To estimate and compare rates of pubertal entry, we conducted a retrospective cohort study by reviewing medical records of children evaluated for delayed puberty at a large academic medical center between 2000 and 2015, extracting data on pubertal status for all clinical visits, then conducting time-to-event analyses. Results Of 392 girls and 683 boys with delayed puberty, constitutional delay was the most common cause, found in 32% of girls and 70% of boys. In a subcohort of 97 girls and 243 boys who were prepubertal at one or more visits, we observed a broad age range for pubertal entry, up to >16 years for girls and >17 years for boys. The probability of entering puberty within the next year for 12- to 15.5-year-old girls and 13.5- to 16.5-year-old boys with delayed puberty ranged between 38% and 74%. No differences in the rates of pubertal entry were seen between girls and boys after data harmonization. Conclusion The broad range of ages at pubertal entry for children with constitutional delay challenges the concept that constitutional delay is merely an extreme of normal variation. Discussions with patients and families about management should consider the possibility that some children may need to wait years after presentation until puberty starts.
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German, A., M. Shmoish, J. Belsky, and Z. Hochberg. "Outcomes of pubertal development in girls as a function of pubertal onset age." European Journal of Endocrinology 179, no. 5 (November 2018): 279–85. http://dx.doi.org/10.1530/eje-17-1025.
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Background The relationship between pubertal onset and tempo and pubertal growth is controversial. We hypothesized that the age at onset of girls’ puberty predicts pubertal tempo and the rate of pubertal progression. Methods We analyzed the data of 380 girls from the prospective Study of Early Child Care and Youth Development (SECCYD) who were recruited in the USA from 1991 to 2006 and followed from birth to age 15.5 years. We used the following indicators: thelarche age (Tanner stage B2), pubarche age (P2), menarche age (M), the age when breast (B5) and pubic hair (P5) became fully mature, pubertal growth, pubertal duration (time from B2 to B5) and pubertal progression (time from B2 to M). We clustered the girls according to B2 age into early onset (EO; <9.4 years), intermediate (IO; 9.4–10.5 years), late onset (LO; >10.5 years). Results All indicators of pubertal onset and conclusion occurred earlier in the EOs than in the LOs; yet, the differences in the age at main pubertal milestones lessened as puberty progressed: 2 years for B2; −1.4 years for M; −1 year for B5. In EOs, puberty was 1 year (average) longer than in LOs. Although EOs grew 7 cm (average) more than LOs, their heights at B5 were comparable. There was a significant relationship between the thelarche age and puberty tempo (r = 0.23, P < 0.0001). Conclusions The study highlights the predictive nature of variation in the onset age of puberty on its progression and duration. These results are reassuring in this context and will add to clinicians’ and parental understanding of the expected milestones of puberty.
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Chan, Yee-Ming, Margaret F. Lippincott, Priscila Sales Barroso, Cielo Alleyn, Jill Brodsky, Hector Granados, Stephanie A. Roberts, Courtney Sandler, Abhinash Srivatsa, and Stephanie B. Seminara. "Using Kisspeptin to Predict Pubertal Outcomes for Youth With Pubertal Delay." Journal of Clinical Endocrinology & Metabolism 105, no. 8 (March 31, 2020): e2717-e2725. http://dx.doi.org/10.1210/clinem/dgaa162.
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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.
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Carpini, Stela, Annelise Barreto Carvalho, Gil Guerra-Júnior, Maria Tereza Matias Baptista, Sofia Helena Valente Lemos-Marini, and Andréa Trevas Maciel-Guerra. "Spontaneous puberty in girls with early diagnosis of Turner syndrome." Arquivos Brasileiros de Endocrinologia & Metabologia 56, no. 9 (December 2012): 653–57. http://dx.doi.org/10.1590/s0004-27302012000900009.
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OBJECTIVE: To verify if the frequency of spontaneous pubertal development among girls with Turner syndrome (TS) diagnosed in infancy and childhood is greater than that of patients diagnosed later. SUBJECTS AND METHODS: Thirty three girls aged < 10 years at the time of diagnosis were evaluated regarding pubertal development. The frequency of spontaneous puberty was compared with that of girls aged > 13 years diagnosed at the same service. RESULTS: Sixteen of 32 informative patients had signs of spontaneous puberty, a frequency greater than that of patients diagnosed later. In six patients, there was no progression of puberty; menarche occurred in six, and one became pregnant, but the fetus was a stillborn. Spontaneous puberty was absent in all cases with 45,X karyotype. CONCLUSIONS: The greater prevalence of spontaneous puberty in girls whose diagnosis was not based on pubertal delay suggests that, among those diagnosed later, there is a bias towards patients with hypogonadism. Arq Bras Endocrinol Metab. 2012;56(9):653-7
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Najafianpour, B. "The Sources of Pubertal Information and their Impact on Stress and Anxiety Among Adolescents." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70769-2.
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Adolescence is known as a period of major hormonal, physical, and psychological changes. Stress and anxiety during adolescence are associated with different factors. The aim of this study is to investigate and examine the associations between stress and anxiety and different sources of information received by adolescent students regarding puberty, as well as evaluating the intensity and degree of puberty's stress and anxiety. Using a cross-sectional method, two groups of students belonging to two different economic family levels were chosen randomly. Spillberger's test for anxiety and stress was applied utilizing a personal-familial data questionnaire. In this research, parents, teachers, friends, and media (books, TV, radio, magazines, internet, and so on) were considered as the major sources for information regarding puberty for the subjects in the groups under investigation. The obtained results have shown a meaningful impact of the pubertal information sources on the intensity and degree of stress and anxiety experienced by the individuals of each investigated group (p=< 0/001). Hence, characteristics and the types of sources used by adolescents to obtain pubertal information have a significant impact on controlling puberty's stress and anxiety in adolescents.
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Deeb, Asma, Mariette Akle, Abrar Al Zaabi, Zohra Siwji, Salima Attia, Hana Al Suwaidi, Nabras Al Qahtani, and Sarah Ehtisham. "Maternal attitude towards delaying puberty in girls with and without a disability: a questionnaire-based study from the United Arab Emirates." BMJ Paediatrics Open 2, no. 1 (October 2018): e000306. http://dx.doi.org/10.1136/bmjpo-2018-000306.
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BackgroundParental anxiety about the impact of puberty/menses, particularly in girls with severe disability leads to seeking therapeutic pubertal suppression. We aim to explore maternal attitudes and reasons for seeking pubertal suppression.MethodsMothers of girls receiving gonadotropin -releasing hormone analogue therapy in Mafraq hospital, Abu Dhabi were enrolled in the study. A semistructured interview was conducted to ascertain possible reasons for delaying puberty. The study group was divided into girls with a disability with central precocious puberty (CPP) or normal puberty and girls without a disability presenting with CPP.Results42 mother–daughter pairs were enrolled and divided into two groups; group A: 15 girls with CPP with no disability; group B: 27 girls with disability (10 had CPP (group B1) and 17 had normal pubertal timing (group B2)). Mothers in group A aimed to delay puberty, while in group B, 13 (48%) mothers desired to halt puberty and 7 (26%) requested permanent surgical intervention. Fear of short stature (15, 100%), inability to cope psychologically (10, 67%) and fear of peer rejection (9, 60%) were the main concerns in group A. In group B, mothers were concerned about menstrual hygiene management (25, 92.5%), fear of child abuse or unwanted pregnancy (15, 55%) and fear of inability to express pain/discomfort with menstruation (8, 30%).ConclusionMothers of girls with a disability commonly seek medical help to delay/halt puberty due to concerns about menstrual hygiene. Short final height was the main concern for girls without a disability. Culture and religion play an important role in puberty management in girls with a disability.
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K, Dao, A. Koné, Drago AA, Doumbia AA, Dollo I, Kamissoko CO, Maiga A, et al. "Pubertal Delay Secondary to Hashimoto's Disease in the Hypothyroid Phase: About a Case in the Internal Medicine Department of the Gabriel Touré University Hospital in Bamako, Mali." Scholars Journal of Medical Case Reports 12, no. 06 (June 1, 2024): 991–96. http://dx.doi.org/10.36347/sjmcr.2024.v12i06.003.
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Introduction: Pubertal delay is defined by the absence of development of secondary sexual characteristics beyond the age of 13 in girls or 14 years in boys. In children of puberty age, delayed puberty is common in long-standing, untreated hypothyroidism. We report a case of delayed puberty revealed by Hashimoto's disease in the hypothyroid phase diagnosed in the Internal Medicine department of the Gabriel Touré University Hospital in Bamako, Mali. Observation: This was a female patient, aged 20 years old, without any particular medico-surgical ATCD or notion of taking medication, who had consulted at the end of 2021, in the Internal Medicine department of the University Hospital Gabriel Touré from Bamako for primary amenorrhea and delayed puberty. At the end of the clinical and paraclinical examination, a hypometabolism syndrome and pubertal delay were noted. On an evolutionary level, development of secondary sexual characteristics (From T1 to T3, and appearance of menstruation) after one year of treatment. Conclusion: Delayed puberty may be the consequence of hypothyroidism. Opotherapy with L Thyroxine helps restore normal pubertal development.
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Guerriero, Kathryn A., Kim L. Keen, and Ei Terasawa. "Developmental Increase in Kisspeptin-54 Release in Vivo Is Independent of the Pubertal Increase in Estradiol in Female Rhesus Monkeys (Macaca mulatta)." Endocrinology 153, no. 4 (February 7, 2012): 1887–97. http://dx.doi.org/10.1210/en.2011-1701.
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Kisspeptin (KP) signaling has been proposed as an important regulator in the mechanism of puberty. In this study, to determine the role of KP in puberty, we assessed the in vivo release pattern of KP-54 from the basal hypothalamus/stalk-median eminence in prepubertal and pubertal ovarian-intact female rhesus monkeys. We found that there was a developmental increase in mean KP-54 release, pulse frequency, and pulse amplitude, which is parallel to the developmental changes in GnRH release that we previously reported. Moreover, a nocturnal increase in KP-54 release becomes prominent after the onset of puberty. Because the pubertal increase in GnRH release occurs independent of the pubertal increase in circulating gonadal steroids, we further examined whether ovariectomy (OVX) modifies the release pattern of KP-54. Results show that OVX in pubertal monkeys enhanced mean KP-54 release and pulse amplitude but not pulse frequency, whereas OVX did not alter the release pattern of KP-54 in prepubertal monkeys. Estradiol replacement in OVX pubertal monkeys suppressed mean KP-54 release and pulse amplitude but not pulse frequency. Estradiol replacement in OVX prepubertal monkeys did not alter the KP-54 release pattern. Collectively these results suggest that the pubertal increase in KP release occurs independent of the pubertal increase in circulating estradiol. Nevertheless, the pubertal increase in KP release is not likely responsible for the initiation of the pubertal increase in GnRH release. Rather, after puberty onset, the increase in KP release contributes to further increase GnRH release during the progression of puberty.
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Fidora, Irma, Silvia Adi Putri, and Ropika Ningsih. "Efektifitas Pemberian Paket Belajar Kesehatan Reproduksi Terhadap Kesiapan Remaja Aisyiyah Menghadapi Masa Pubertas." Jurnal Smart Keperawatan 7, no. 2 (December 22, 2020): 77. http://dx.doi.org/10.34310/jskp.v7i2.377.
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Masa remaja adalah masa terjadinya perubahan fisik dan mental yang dikenal dengan pubertas. Menarch merupakan salah satu tanda bahwa mereka sudah memasuki masa pubertas. Remaja yang tinggal di panti asuhan cenderung memiliki pengalaman yang berbeda ketika menghadapi masa pubertas terutama menjelang menarch dibandingkan remaja yang tinggal bersama orang tua. Informasi yang diperoleh mengenai pubertas terbatas. Perubahan pada masa pubertas bisa menyebabkan kecemasan dan ketakutan. Pemberian paket belajar kesehatan perlu sebagai upaya meningkatkan kesiapan remaja menghadapi masa pubertas. Panti Asuhan Aisyiyah Bukittinggi merupakan panti sosial dengan jumlah anak asuh yang terbanyak dan belum mendapatkan informasi mengenai kesehatan reproduksi. Penelitian ini bertujuan untuk mengetahui efektivitas pemberian paket belajar kesehatan reproduksi terhadap kesiapan remaja menghadapi masa pubertas. Metode quasy experimental digunakan dengan pendekatan pre-test dan post-test. Pengumpulan data menggunakan kuesioner kesiapan menghadapi perubahan fisik dan psikologis serta menstruasi. Analisa bivariat menggunakan paired t test. Sampel terdiri dari 40 remaja putri. Hasil penelitian mendapatkan responden penelitian memiliki usia antara 9-13 tahun dengan rata-rata 10,8 tahun, 65% responden belum mendapatkan informasi mengenai kesehatan reproduksi, 67,5% responden belum siap menghadapi menstruasi. Kesiapan remaja meningkat seteleh diberikan paket belajar kesehatan reproduksi. Berdasarkan uji statistik pemberian paket belajar kesehatan reproduksi efektif alam meningkatkan kesiapan remaja putri dalam menghadapi masa pubertas. Kata kunci: kesehatan reproduksi; pubertas; remajaTHE EFFECTIVENESS OF PROVIDING REPRODUCTIVE HEALTH LEARNING PACKAGES ON THE READINESS OF AISYIYAH’S FEMALE ADOLESCENCES IN FACING PUBERTY ABSTRACT Adolescence is marked by physically and mentally change known as puberty. Menarche is a sign that female adolescent have facing the puberty. Adolescents who live in orphanages tend to have different experiences when facing puberty. The female adolescent had not got the comprehensive information about puberty. The changes in puberty would cause anxiety and fear. Providing reproductive health learning is necessary as an effort to increase adolescent readiness to face puberty. Aisyiyah Orphanage is a social institution with the largest number of foster children in the city of Bukittinggi, West Sumatera. Adolescents who live in these orphanege had not informed about reproductive health. The aim of this study was to determine the effectiveness of providing reproductive health learning on the readiness of adolescents to face puberty. This study used a quasy experimental method with pre-test and post-test approaches. The data were collected using a questionnaire designed to obtain data on the readiness of adolescents to face physical and psychological changes during puberty. Paired t-test used to determine how the effectiveness of the reproductive health learning on adolescent readiness to face puberty.This data was collected from 40 adolescent girl who lived in the Aisyiyah Orphanage in Bukittinggi. The results showed that respondents of the study had an age between 9-13 years with an average of 10.8 years, 65% of respondents has not received information about reproductive health, 67.5% of respondents are not ready to face menstruation. The readiness increased after being given reproductive health learning packages. Based on statistical tests, the provision of learning packages for reproductive health was effective in increasing the readiness of female adolescent in facing puberty. Keywords: reproductive health; puberty; adolescent
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Andersson, Anna-Maria, Anders Juul, Jørgen H. Petersen, Jørn Müller, Nigel P. Groome, and Niels E. Skakkebæk. "Serum Inhibin B in Healthy Pubertal and Adolescent Boys: Relation to Age, Stage of Puberty, and Follicle-Stimulating Hormone, Luteinizing Hormone, Testosterone, and Estradiol Levels1." Journal of Clinical Endocrinology & Metabolism 82, no. 12 (December 1, 1997): 3976–81. http://dx.doi.org/10.1210/jcem.82.12.4449.
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Inhibin B levels were measured in serum from 400 healthy Danish prepubertal, pubertal, and adolescent males, aged 6–20 yr, in a cross-sectional study using a recently developed immunoassay that is specific for inhibin B, the physiologically important inhibin form in men. In addition, serum levels of FSH, LH, testosterone, and estradiol levels were measured. Serum levels of inhibin B, FSH, LH, testosterone, and estradiol all increased significantly between stages I and II of puberty. From stage II of puberty the inhibin B level was relatively constant, whereas the FSH level continued to increase between stages II and III. From stage III of puberty the FSH level was also relatively constant, although there was a nonsignificant trend of slightly decreased FSH levels at pubertal stage V compared to stage IV. The levels of serum LH, testosterone, and estradiol increased progressively throughout puberty. In prepubertal boys younger than 9 yr, there were no correlation between inhibin B and the other three hormones. In prepubertal boys older than 9 yr, a significant positive correlation was observed between inhibin B and FSH, LH, and testosterone. However, at this pubertal stage, each hormone correlated strongly with age, and when the effect of age was taken into account, only the partial correlation between inhibin B and LH/testosterone remained statistically significant. At stage II of puberty, the positive partial correlation between inhibin B and LH/testosterone was still present. At stage III of puberty, an negative partial correlation between inhibin B and FSH, LH, and estradiol was present, whereas no correlation between inhibin B and testosterone could be observed from stage III onward. The negative correlation between inhibin B and FSH persisted from stage III of puberty onward, whereas the correlation between inhibin B and LH and between inhibin B and estradiol was nonsignificant at stages IV and V of puberty. In conclusion, in boys, serum inhibin B levels increase early in puberty; by pubertal stage II the adult level of inhibin B has been reached. The correlation of inhibin B to FSH, LH, and testosterone changes during pubertal development. Early puberty is characterized by a positive correlation between inhibin B and LH/testosterone, but no correlation to FSH. Late puberty (from stage III) is characterized by a negative correlation between inhibin B and FSH (which is maintained in adult men), a diminishing negative correlation between inhibin B and LH, and no correlation between inhibin B and testosterone, suggesting that developmental and maturational processes in the hypothalamic-pituitary-gonadal axis take place, leading to the establishment of the closed loop feedback regulation system operating in adult men. The positive correlation between inhibin B and LH/testosterone at the time when serum inhibin B levels rise early in puberty suggests that Leydig cell factors may play an important role in the maturation and stimulation of Sertoli cells in the beginning of pubertal development.
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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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Costanzo, Mariana, José Garcia-Feyling, Nora Saraco, Roxana Marino, Natalia Pérez Garrido, Maria Sol Touzon, Gisela Viterbo, et al. "Accelerated Pubertal Tempo in a 46,XY Aromatase-Deficient Patient." Hormone Research in Paediatrics 90, no. 4 (2018): 275–82. http://dx.doi.org/10.1159/000492128.
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Background: Aromatase deficiency is a rare autosomal recessive disorder. 46,XY-affected patients often remain undiagnosed until late puberty. Only 2 pediatric cases have been reported. Data on pubertal development in affected males are scarce. Aim: To report the clinical phenotype and hormonal studies of an aromatase-deficient boy during the prepubertal and early pubertal period. Results: The patient was the older brother of a 46,XX girl with aromatase deficiency. Molecular analysis revealed a previously reported homozygous mutation (Arg192Cys) in the CYP19A1 gene. Pubertal onset was at 9.8 years. At 11.3 years of age, signs of rapidly progressive puberty were seen. Laboratory tests revealed normal pubertal basal and GnRH-stimulated gonadotropin levels, normal Sertoli cell markers, and increased testosterone. The prepubertal lumbar spine bone mineral density (BMD) was normal but pubertal bone mineral accrual was incomplete, leading to osteopenia. Conclusion: Estrogen restraint on gonadotropin secretion has been demonstrated in animal and human models. Interestingly, our patient presented with accelerated puberty and apparently normal pituitary gonadal function. These findings suggest that aromatase activity may be required to define pubertal progression in boys. Estrogen deficiency due to aromatase deficiency is responsible for insufficient bone mineral accrual during puberty.
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Chu, L., M. C. Riddell, J. E. Schneiderman, B. W. McCrindle, and J. K. Hamilton. "The effect of puberty on fat oxidation rates during exercise in overweight and normal-weight girls." Journal of Applied Physiology 116, no. 1 (January 1, 2014): 76–82. http://dx.doi.org/10.1152/japplphysiol.00888.2013.
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Excess weight is often associated with insulin resistance (IR) and may disrupt fat oxidation during exercise. This effect is further modified by puberty. While studies have shown that maximal fat oxidation rates (FOR) during exercise decrease with puberty in normal-weight (NW) and overweight (OW) boys, the effect of puberty in NW and OW girls is unclear. Thirty-three NW and OW girls ages 8–18 yr old completed a peak aerobic capacity test on a cycle ergometer. FOR were calculated during progressive submaximal exercise. Body composition and Tanner stage were determined. For each participant, a best-fit polynomial curve was constructed using fat oxidation vs. exercise intensity to estimate max FOR. In a subset of the girls, IR derived from an oral glucose tolerance test ( n = 20), and leptin and adiponectin levels ( n = 11) were assessed in relation to FOR. NW pre-early pubertal girls had higher max FOR [6.9 ± 1.4 mg·kg fat free mass (FFM)−1·min−1] than NW mid-late pubertal girls (2.2 ± 0.9 mg·kg FFM−1·min−1) ( P = 0.002), OW pre-early pubertal girls (3.8 ± 2.1 mg·kg FFM−1·min−1), and OW mid-late pubertal girls (3.3 ± 0.9 mg·kg FFM−1·min−1) ( P < 0.05). Bivariable analyses showed positive associations between FOR with homeostatic model assessment of IR ( P = 0.001), leptin ( P < 0.001), and leptin-to-adiponectin ratio ( P = 0.001), independent of percent body fat. Max FOR decreased in NW girls during mid-late puberty; however, this decrease associated with puberty was blunted in OW girls due to lower FOR in pre-early puberty. The presence of IR due to obesity potentially masks the effect of puberty on FOR during exercise in girls.
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Oelkers, Lea, Mandy Vogel, Agnes Kalenda, Hans Christian Surup, Antje Körner, Jürgen Kratzsch, and Wieland Kiess. "Socioeconomic Status Is Related to Pubertal Development in a German Cohort." Hormone Research in Paediatrics 93, no. 9-10 (2020): 548–57. http://dx.doi.org/10.1159/000513787.
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<b><i>Introduction:</i></b> Current health literature suggests that there has been a decline in the age of pubertal onset and that pubertal onset/duration of puberty may, besides weight status, be influenced by socioeconomic context. <b><i>Objective:</i></b> The goal of this study was to determine whether pubertal onset/duration and puberty-triggering hormones luteinizing hormone (LH) and follicle-stimulating hormone (FSH) vary according to socioeconomic status (SES). Moreover, we aimed to propose cutoff values of serum LH and FSH for predicting gonadarche in boys. <b><i>Methods:</i></b> 2,657 apparently healthy children and adolescents between 5.5 and 18 years from the area of Leipzig were recruited from the LIFE Child study. Age at pubertal onset/end of puberty was given in 738/573 children, respectively. Anthropometric parameters of puberty, blood measurements of LH and FSH, and questionnaires assessing SES were evaluated. <b><i>Results:</i></b> Lower SES was associated with earlier thelarche and longer duration of puberty in overweight/obese girls, whereas age of menarche was not affected. In boys with low SES, a trend versus earlier puberty onset can be seen. Lower SES was significantly associated with boys’ age at mutation. No significant differences in boys’ and girls’ serum levels of LH and FSH during puberty according to SES were observed. Serum LH levels of 0.56 IU/L and serum FSH levels of 1.74 IU/L showed the best prediction of gonadarche in boys. <b><i>Conclusion:</i></b> Puberty onset/duration and boys’ age at mutation is affected by SES. The proposed cutoff levels for serum LH and FSH could provide a serological tool to determine gonadarche in boys.
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Marshall-Andon, Tess. "Disorders of puberty." InnovAiT: Education and inspiration for general practice 10, no. 1 (November 10, 2016): 20–28. http://dx.doi.org/10.1177/1755738016676286.
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Disorders of puberty are relatively common problems that affect young people and include precocious puberty and delayed puberty. The disorders of puberty may go unrecognised, as the signs and symptoms may be subtle, and the patient may be embarrassed to bring concerns to the attention of the GP. They are not only a source of significant emotional distress for young people, but also can also lead to long-term adverse consequences, such as failure to achieve target height. Disorders of puberty may also be a sign of a serious underlying condition, which if promptly diagnosed may be treatable. Therefore, early recognition of such disorders by GPs is vital for both the psychological and physical health of the patient. This article aims to give an overview of normal pubertal development, as well as the causes, diagnosis, and treatment of both precocious and delayed puberty.
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Cemeroglu, Ayse Pinar, Damlanur Kaval, and Ozan Ozcan. "Etiology of Increased Referrals for Evaluation of Early Puberty in a Tertiary Care Center in Turkey: True Precocious Puberty, Obesity, or Parental Anxiety and Lack of Knowledge?" Global Pediatric Health 8 (January 2021): 2333794X2110090. http://dx.doi.org/10.1177/2333794x211009096.
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There has been a global increase in pediatric endocrinology referrals for the concerns of early puberty. The objective of this study was to determine the reasons behind this increase. A retrospective cross-sectional study was designed to analyze the clinical characteristics of patients seen for the concerns of early puberty in pediatric endocrinology clinic of a tertiary care center (Study A). Additionally, a prospective questionnaire study was designed to assess the knowledge and concerns of the mothers regarding the timing of puberty in girls (Study B). In study A, of the 305 girls, 42.9% were overweight/obese, 68.5% either had normal pubertal development for age or were prepubertal, 1 had non-classic congenital adrenal hyperplasia, and 2 had central precocious puberty. Of the 36 boys, 56% were overweight/obese, 64% either had normal pubertal development for age or were prepubertal, and 1 had non-classic congenital adrenal hyperplasia. In study B, 95% of the participants thought the girls have been developing earlier, over 10% considered the first sign of puberty to be normal after the age 14 years and 12.4% considered menarche to be normal after age 14 years. The common sources of anxiety for the participants regarding the earlier timing of puberty were psychosocial issues and short final height. In conclusion, many parents had wrong beliefs/information about the normal timing of puberty and were concerned about precocious puberty in girls. Education of parents about the normal timing of puberty may help avoiding unnecessary referrals, parental anxiety, and financial burden to the society.
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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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Al Alwan, Ibrahim, Haifa Alfaraidi, Fahad Al Juraibah, Mohamed Al Dubayee, Amir Babiker, Waleed Tamimi, Dania Musalli, Manal Alsheikh, and Motasim Badri. "Timing of Puberty and Late Pubertal Height in Saudi Schoolboys: Riyadh Puberty Study II." International Journal of Endocrinology 2022 (October 20, 2022): 1–8. http://dx.doi.org/10.1155/2022/4343596.
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Objective. Puberty has a significant contribution to the final height. Therefore, it is crucial to understand the normal variations in the onset and tempo of puberty in a specific population. In this study, we aimed to provide normative data on the timing of puberty and late pubertal height (LPH) in Saudi schoolboys in Riyadh. Methods. This is a cross-sectional field study (2011–2013) including Saudi schoolboys (grades 1–12; aged 6 to 19 years). Schools were chosen to represent the population from urban and rural areas in the Riyadh region. Pubertal maturity staging for gonads was assessed by measuring testicular size using a Prader orchidometer and assessing the Tanner staging of pubic hair. The marginal mean age was calculated using regression analysis. Results. We recruited 1086 schoolboys. The estimated mean age of pubertal onset at G2 was 11.8 (95% CI 11.60–12.0) years, for gonadal development at G3 was 13.2 (95% CI 12.9–13.5), G4 = 15.0 (95% CI 14.7–15.2), and G5 = 16.1 (95% CI 15.9–16.3) years, and for pubic hair stage 2 (PH2) was 12.6 (95% CI 12.4–12.9) years. The estimated time from G2/PH2 to G5/PH5 was 4.3 and 3.9 years, respectively. At the onset of puberty, the mean height was 144.7 cm and it reached 167.8 cm at G5 with a pubertal height gain of 23.1 cm. Conclusion. Our data present the norms of the timing of puberty and LPH in Saudi schoolboys. Saudi adolescent males are shorter than some European and American comparatives mainly due to shortness during childhood. However, they could have shorter LPH than Turkish, Greek, Thai, and Japanese due to a less pubertal height gain.
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Ardayani, Tri, and Neti Sitorus. "Peningkatan Pengetahuan Tentang Puberitas Pada Siswa Kelas 4, 5, 6 SD Negeri Sukawening Kecamatan Ciwidey Kabupaten Bandung." JPKMI (Jurnal Pengabdian Kepada Masyarakat Indonesia) 1, no. 4 (November 3, 2020): 252–61. http://dx.doi.org/10.36596/jpkmi.v1i4.69.
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Abstrak: Setiap anak pasti mengalami pertumbuhan dan perkembangan secara alami, baik secara fisik, mental dan kematangan organ reproduksi mulai berfungsi dan karakteristik seks sekunder mulai muncul pada remaja tersebut. Usia pubertas pada anak remaja sekitar usia 10 tahun sampai 20 tahun. Pada anak perempuan masa ini ditandai dengan menstruasi (menarche), pertumbuhan payudara, tumbuhnya rambut di daerah kemaluan, sedangkan pada anak laki-laki pada masa pubertas ditandai dengan perubahan suara yang disertai dengan tonjolan kerongkongan (Adam’s apple), perubahan panjang penis, dan tumbuhnya rambut kemaluan. Pada awal memasuki masa pubertas, seorang remaja biasanya membutuhkan banyak informasi mengenai perkembangan, pertumbuhan dan perubahan yang dialaminya sehingga anak mencari informasi dengan bertanya kepada orang tua, teman, atau orang-orang yang berada di sekitar lingkunganya, tidak semua orang sekitar lingkungan remaja bisa membantu permasalahan yang dihadapi remaja sehingga mereka mencari dengan cara sendiri, misalnya dengan bertanya pada orang dewasa lainnya, dari majalah, atau bahkan dari internet. Tujuan kegiatan pengabdian masyarakat yang di lakukan oleh Sekolah Tinggi Ilmu Immanuel bekerjasama dengan SD Sukawening adalah untuk meningkatkan pengetahuan anak remaja tentang pubertas, dan mempersiapkan lebih dini datangnya masa pubertas sehingga diharapkan anak lebih siap menghadapi perubahan secara fisik dan psikologis yang akan terjadi nanti sehingga dampak negatif pubertas tidak terjadi pada anak remaja. Metode kegiatan pelaksanaan tersebut meliputi memberikan pendidikan kesehatan tentang pubertas pada anak remaja kelas 4.5.6 dan pemutaran video. Hasil kegiatan pengabdian masyarakat antara lain, pengetahuan anak meningkat tentang pubertas, anak sudah memahami perubahan yang akan terjadi pada masa pubertas baik secara fisiologis maupun secara psikologis, anak mengetahui bagaimana cara menghadapi masa pubertas dan kemana mencari informasi yang benar tentang pubertas jika mengalami masalah atau ada hal yang ingin di tanyakan tentang perubahan yang dialaminya. Peserta yang mengikuti kegiatan sebanyak 60 orang. Abstract: Adolescence experiences growth and development naturally, physically, mentally and the reproductive organs begin to function and secondary sex characteristics appeared. The age of puberty in adolescents is around the age of 10 to 20 years. The female period is being marked by menstruation (menarche), breast and pubic hair growth, while in male, puberty is characterized by voice changes accompanied by Adam's apple protrusion, changes in penis length, and pubic hair. At the beginning of puberty, adolescence usually needs a lot of information about the development, growth, and changes, thus they seek information by asking parents, friends, or people around. Sometimes, people around them will not be able to help; consequently, they search by themselves, such as asking other adults, read magazines, or even from the internet. The purpose of community service activities carried out by Immanuel School of Health Science in collaboration with SD Sukawening were to increase adolescent knowledge about puberty, and prepare for the early arrival of puberty; thus, they are expected to be better prepared facing physical and psychological changes; so that the negative impact puberty does not occur in them. The method of implementation involved providing health education about puberty and video screening to school-aged students in grades 4, 5, 6. The results of community service activities to adolescents such as increasing knowledge about puberty; understanding changes physiologically and psychologically; how to deal with puberty, and where to find correct information if they experience problems or to fulfill curiosity regarding puberty problems. There are sixty respondents participated during the program.
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O’Keeffe, Linda M., Monika Frysz, Joshua A. Bell, Laura D. Howe, and Abigail Fraser. "Puberty timing and adiposity change across childhood and adolescence: disentangling cause and consequence." Human Reproduction 35, no. 12 (November 26, 2020): 2784–92. http://dx.doi.org/10.1093/humrep/deaa213.
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Abstract STUDY QUESTION Is earlier puberty more likely a result of adiposity gain in childhood than a cause of adiposity gain in adulthood? SUMMARY ANSWER Pre-pubertal fat mass is associated with earlier puberty timing but puberty timing is not associated with post-pubertal fat mass change. WHAT IS KNOWN ALREADY Age at puberty onset has decreased substantially in the last several decades. Whether reducing childhood adiposity prevents earlier puberty and if early puberty prevention itself also has additional independent benefits for prevention of adult adiposity is not well understood. STUDY DESIGN, SIZE, DURATION Prospective birth cohort study of 4176 participants born in 1991/1992 with 18 232 repeated measures of fat mass from age 9 to 18 years. PARTICIPANTS/MATERIALS, SETTING, METHODS We used repeated measures of height from 5 to 20 years to identify puberty timing (age at peak height velocity, aPHV) and repeated measures of directly measured fat mass from age 9 to 18 years, from a contemporary UK birth cohort study to model fat mass trajectories by chronological age and by time before and after puberty onset. We then examined associations of these trajectories with puberty timing separately in females and males. MAIN RESULTS AND THE ROLE OF CHANCE In models by chronological age, a 1-year later aPHV was associated with 20.5% (95% confidence interval (CI): 18.6–22.4%) and 23.4% (95% (CI): 21.3–25.5%) lower fat mass in females and males, respectively, at 9 years. These differences were smaller at age 18 years: 7.8% (95% (CI): 5.9–9.6%) and 12.4% (95% (CI): 9.6–15.2%) lower fat mass in females and males per year later aPHV. Trajectories of fat mass by time before and after puberty provided strong evidence for an association of pre-pubertal fat mass with puberty timing, and little evidence of an association of puberty timing with post-pubertal fat mass change. The role of chance is likely to be small in this study given the large sample sizes available. LIMITATIONS, REASONS FOR CAUTION Participants included in our analyses were more socially advantaged than those excluded. The findings of this work may not apply to non-White populations and further work examining associations of puberty timing and fat mass in other ethnicities is required. WIDER IMPLICATIONS OF THE FINDINGS Previous research has relied on self-reported measures of puberty timing such as age of voice breaking in males, has lacked data on pre-and post-pubertal adiposity together and relied predominantly on indirect measures of adiposity such as BMI. This has led to conflicting results on the nature and direction of the association between puberty timing and adiposity in females and males. Our work provides important clarity on this, suggesting that prevention of adiposity in childhood is key for prevention of early puberty, adult adiposity and associated cardiovascular risk. In contrast, our findings suggest that prevention of early puberty without prevention of childhood adiposity would have little impact on prevention of adult adiposity. STUDY FUNDING/COMPETING INTEREST(S) The UK Medical Research Council and Wellcome (Grant ref: 102215/2/13/2) and the University of Bristol provide core support for Avon Longitudinal Study of Parents and Children (ALSPAC). L.M.O.K. is supported by a UK Medical Research Council Population Health Scientist fellowship (MR/M014509/1) and a Health Research Board (HRB) of Ireland Emerging Investigator Award (EIA-FA-2019-007 SCaRLeT). J.A.B. is supported by the Elizabeth Blackwell Institute for Health Research, University of Bristol and the Wellcome Trust Institutional Strategic Support Fund (204813/Z/16/Z). L.D.H. and A.F. are supported by Career Development Awards from the UK Medical Research Council (grants MR/M020894/1 and MR/M009351/1, respectively). All authors work in a unit that receives funds from the UK Medical Research Council (grant MC_UU_00011/3, MC_UU_00011/6). No competing interests to declare. TRIAL REGISTRATION NUMBER N/A.
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Wyatt, Amanda K., Monika Zavodna, Jean L. Viljoen, Jo-Ann L. Stanton, Neil J. Gemmell, and Christine L. Jasoni. "Changes in Methylation Patterns of Kiss1 and Kiss1r Gene Promoters across Puberty." Genetics & Epigenetics 5 (January 2013): GEG.S12897. http://dx.doi.org/10.4137/geg.s12897.
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The initiation of mammalian puberty is underpinned by an increase in Kisspeptin (Kiss1) signaling via its receptor (Kiss1r/GPR54) on gonadotropin-releasing hormone (GnRH) neurons. Animals and humans with loss-of-function mutations in Kiss1 or Kiss1r fail to go through puberty. The timing of puberty is dependent on environmental factors, and malleability in puberty timing suggests a mechanism that can translate environmental signals into patterns of Kiss1/Kiss1r gene expression. Epigenetics is a powerful mechanism that can control gene expression in an environment-dependent manner. We investigated whether epigenetic DNA methylation is associated with gene expression changes at puberty. We used bisulfite-PCR-pyrosequencing to define the methylation in the promoters of Kiss1 and Kiss1r before and after puberty in female rats. Both Kiss1 and Kiss1r showed highly significant puberty-specific differential promoter methylation patterns. By identifying key differentially methylated residues associated with puberty, these findings will be important for further studies investigating the control of gene expression across the pubertal transition.
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Abdulhameed A. Al-Tuhafi, Amenah, and Sajeda Saeed Al-Chalbi. "Changes in bone mineral density during puberty." Tikrit Journal of Pharmaceutical Sciences 8, no. 1 (April 22, 2023): 68–79. http://dx.doi.org/10.25130/tjphs.2012.8.1.9.68.79.
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Puberty is the fundamental period for bone mass acquisition. In this period mineralization is found to increase with levels of high bone formation.. The objective of this cross-sectional study was to determine the changes in bone mineral density (BMD) and growth parameters for healthy pubertal males and females at different pubertal stages in Mosul city/Iraq. In addition, we aimed to detect the relationship between BMD, age, pubertal stage and growth parameters, and to reveal the most important determinant of BMD in the pubertal period. BMD of the lumbar spine was performed by dual-energy X-ray absorptiometry in (177) healthy pubertal children and adolescents (96 males, 81 females), aged (9.9-20.2) years. Growth parameters (Weight and height) were measured, BMI were calculated. Pubertal stages were assessed and the subjects were subdivided into 5 stages (Tanner stages of puberty for males and females). There was a significant effect of age and puberty on BMD. Females had significantly higher BMD across all age groups because females enter puberty earlier than males. When gender comparison was done according to pubertal stages, males had higher values for BMD in all pubertal stages , but without significant differences between them except in stage III, which indicated that boys gain more BMD than girls at this stage. Both sexes showed the main increments in BMD between stage IV and V. The major independent determinant of BMD in both sexes was pubertal stage. BMD of males was also highly correlated with growth parameters, but no such correlations for females. values in the study group were significantly lower than Western normative values, with Z scores for girls was (-1.2±1.2) and for boys was (-1.4±1.1). In conclusion, bone mass increased throughout puberty in both sexes and there was a strong evidence that pubertal development was consistent and independent predictors of BMD in healthy children and adolescents.
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SIMON, A. E., J. WARDLE, M. J. JARVIS, N. STEGGLES, and M. CARTWRIGHT. "Examining the relationship between pubertal stage, adolescent health behaviours and stress." Psychological Medicine 33, no. 8 (October 30, 2003): 1369–79. http://dx.doi.org/10.1017/s0033291703008390.
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Background. This paper examines the associations between puberty and three important health behaviours (smoking, food intake and exercise) and explores whether these associations are mediated by puberty's relationship to stress and psychological difficulties.Method. Data were taken from the first year of the ongoing, 5-year, Health and Behaviours in Teenagers Study (HABITS). This is a school-based study set in 36 schools in London. In the first year of the study, 4320 students (2578 boys, 1742 girls) in their first year of secondary education took part.Results. Among girls, being more pubertally advanced was associated with a greater likelihood of having tried smoking. Among boys, being more pubertally advanced was associated with a greater likelihood of having tried smoking, a higher intake of high-fat food and higher levels of exercise. More pubertally advanced girls experienced more stress but not more psychological difficulties. There were no associations between puberty and either stress or psychological difficulties in boys. Stress and psychological difficulties were associated with health behaviours in girls and boys, but neither of these factors mediated the relationship between pubertal stage and health behaviours found in girls.Conclusions. These results suggest that the onset of puberty has a marked effect on the development of health behaviours. Puberty was related to an acceleration of the development of unhealthy behaviours, except for exercise behaviour in boys, where advanced puberty was associated with more exercise. These changes were unrelated to adolescent issues of stress and a causal explanation for these associations must be sought elsewhere.
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Calcaterra, Valeria, Elvira Verduci, Vittoria Carlotta Magenes, Martina Chiara Pascuzzi, Virginia Rossi, Arianna Sangiorgio, Alessandra Bosetti, Gianvincenzo Zuccotti, and Chiara Mameli. "The Role of Pediatric Nutrition as a Modifiable Risk Factor for Precocious Puberty." Life 11, no. 12 (December 7, 2021): 1353. http://dx.doi.org/10.3390/life11121353.
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Puberty is a critical phase of growth and development characterized by a complex process regulated by the neuroendocrine system. Precocious puberty (PP) is defined as the appearance of physical and hormonal signs of pubertal development at an earlier age than is considered normal. The timing of puberty has important public health, clinical, and social implications. In fact, it is crucial in psychological and physical development and can impact future health. Nutritional status is considered as one of the most important factors modulating pubertal development. This narrative review presents an overview on the role of nutritional factors as determinants of the timing of sexual maturation, focusing on early-life and childhood nutrition. As reported, breast milk seems to have an important protective role against early puberty onset, mainly due to its positive influence on infant growth rate and childhood overweight prevention. The energy imbalance, macro/micronutrient food content, and dietary patterns may modulate the premature activation of the hypothalamic–pituitary–gonadal axis, inducing precocious activation of puberty. An increase in knowledge on the mechanism whereby nutrients may influence puberty will be useful in providing adequate nutritional recommendations to prevent PP and related complications.
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Albertsson-Wikland, Kerstin, Sten Rosberg, Birgitta Lannering, Leo Dunkel, Gunnar Selstam, and Ensio Norjavaara. "Twenty-Four-Hour Profiles of Luteinizing Hormone, Follicle-Stimulating Hormone, Testosterone, and Estradiol Levels: A Semilongitudinal Study throughout Puberty in Healthy Boys*." Journal of Clinical Endocrinology & Metabolism 82, no. 2 (February 1, 1997): 541–49. http://dx.doi.org/10.1210/jcem.82.2.3778.
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Abstract To follow and correlate gonadotropin and sex steroid changes throughout puberty, 24-h profiles of LH, FSH, testosterone, and estradiol were taken on several occasions for between 2–9.5 yr in 12 healthy boys, aged 8.7–18.2 yr. Serum concentrations of LH and FSH were measured every 20 min, whereas testosterone and estradiol were measured every 2–4 h during the 24-h period. The prepubertal boys (Tanner stage 1) were subdivided into two groups: Pre 1, with a testicular volume of 1–2 mL, and Pre 2, with a testicular volume of 3 mL. Pubertal stages were classified, according to testicular volume, as early puberty (pubertal stage 2; 4–9 mL), midpuberty (pubertal stages 3–4; 10–15 mL), and late puberty (pubertal stage 5; ≥16 mL). Mean levels of LH and FSH increased with pubertal development, although the increase in LH was greater than that in FSH. These increases were due to elevated basal levels of LH and FSH as well as to increases in the number of peaks and the peak amplitudes of LH. No diurnal rhythm was found in boys at stage Pre 1. Thereafter, a clear diurnal rhythm appeared for LH, and later in puberty, an ultradian rhythm was superimposed, as shown by time-sequence analyses. A diurnal rhythm also existed for FSH, but was much less marked than that for LH despite a clear covariation between LH and FSH, as shown from cross-correlation studies. Testosterone also showed diurnal variations from the late prepubertal stage, followed by increasing levels during both day and night in puberty. We conclude that during puberty, gonadotropin levels rise differently for LH and FSH, which may be due to the development of differences in feedback mechanisms. Despite covariation between LH and FSH, only LH showed a clear diurnal variation. In parallel, nocturnal variations in testosterone and estradiol were found. Changes in mean levels of LH, testosterone, and estradiol as well as their mean daytime and nighttime levels follow each other from the prepubertal stages to late puberty.
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Sultana, Nusrat, Faria Afsana, Nazma Akhtar, Yasmin Aktar, Mohammad Feroz Amin, Sharmin Chowdhury, Shah Md Emran, et al. "Precocious puberty: diagnosis and management." BIRDEM Medical Journal 12, no. 1 (December 30, 2021): 62–69. http://dx.doi.org/10.3329/birdem.v12i1.57228.
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Precocious puberty is commonly defined as puberty that starts before age 8 years in girls and 9 years in boys. The causes of it may range from a variant of normal development to various pathologic conditions. The etiology of precocious puberty is classified by the underlying pathogenesis into gonadotropin dependent central precocious puberty and peripheral precocious puberty which is independent of gonadotropin but due to different other causes. Variants of precocious puberty include premature thelarche, premature puberche and isolated premature menarche which imply onset of isolated changes without any other signs of sexual development. Precocious puberty might have an impact on final stature owing to premature epiphyseal fusion and also it has got influence on psychosocial wellbeing. Evaluation includes a detailed history, physical examination, biochemical testing and imaging directed towards suspected etiology. Gonadotropin releasing hormone (GnRH) analogues are effective for treatment of central precocious puberty. Treatment of peripheral precocious puberty should be based on the specific cause. Pubertal variants are usually non-progressive and need no treatment but should be monitored carefully. BIRDEM Med J 2022; 12(1): 62-69
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Li, Qingnan, Xiangchun Pan, Nian Li, Wentao Gong, Yaosheng Chen, and Xiaolong Yuan. "Identification of Circular RNAs in Hypothalamus of Gilts during the Onset of Puberty." Genes 12, no. 1 (January 12, 2021): 84. http://dx.doi.org/10.3390/genes12010084.
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The disorders of puberty have shown negative outcomes on health of mammals, and the hypothalamus is thought to be the main regulator of puberty by releasing GnRH. Many studies show that the circular RNAs (circRNAs) might be implicated in the timing of puberty in mammals. However, the circRNAs in the hypothalamus of gilts have not been explored. To profile the changes and biological functions of circRNAs in the hypothalamus during the onset of puberty, RNA-seq was utilized to establish pre-, in-, and post-pubertal hypothalamic circRNAs profiles. In this study, the functions of hypothalamic circRNAs were enriched in the signaling pathway of neurotrophin, progesterone-mediated oocyte maturation, oocyte meiosis, insulin, ErbB, and mTOR, which have been highly suggested to be involved in the timing of puberty. Furthermore, 53 circRNAs were identified to be putative hypothalamus-specific expressed circRNAs, and some of them were exclusively expressed in the one of three pubertal stages. Moreover, 22 differentially expressed circRNAs were identified and chosen to construct the circRNA-miRNA-gene network. Moreover, 10 circRNAs were found to be driven by six puberty-related genes (ESR1, NF1, APP, ENPP2, ARNT, and DICER1). Subsequently, the expression changes of several circRNAs were confirmed by RT-qPCR. Collectively, the preliminary results of hypothalamic circRNAs provided useful information for the investigation of the molecular mechanism for the timing of puberty in gilts.
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Howard, Sasha R. "Genetic regulation in pubertal delay." Journal of Molecular Endocrinology 63, no. 3 (October 2019): R37—R49. http://dx.doi.org/10.1530/jme-19-0130.
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Delayed puberty represents the clinical presentation of a final common pathway for many different pathological mechanisms. In the majority of patients presenting with significantly delayed puberty, there is a clear family history of delayed or disturbed puberty, and pubertal timing is known to be a trait with strong heritability. Thus, genetic factors clearly play a key role in determining the timing of puberty, and mutations in certain genes are recognised as responsible for delayed or absent puberty in a minority of patients. Through the identification of causal genetic defects such as these we have been able to learn a great deal about the pathogenesis of disrupted puberty and its genetic regulation. Firstly, deficiency in key genes that govern the development of the gonadotropin-releasing hormone system during fetal development may result in a spectrum of conditions ranging from isolated delayed puberty to absent puberty with anosmia. Secondly, a balance of inhibitory and excitatory signals, acting upstream of GnRH secretion, are vital for the correct timing of puberty. These act to repress the hypothalamic–pituitary–gonadal axis during mid-childhood and allow it to reactivate at puberty, and alterations in this equilibrium can cause delayed (or precocious) puberty. Thirdly, disturbances of energy metabolism inputs to the kisspeptin–GnRH system may also lead to late onset of puberty associated with changes in body mass.
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Darendeliler, F., P. C. Hindmarsh, M. A. Preece, L. Cox, and C. G. D. Brook. "Growth hormone increases rate of pubertal maturation." Acta Endocrinologica 122, no. 3 (March 1990): 414–16. http://dx.doi.org/10.1530/acta.0.1220414.
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Abstract We have performed a retrospective analysis of the pubertal parameters of 134 children with isolated GH insufficiency on GH treatment and compared them to the standards of Tanner and to a recent longitudinal study of growth and development in the United Kingdom. The age at onset of puberty (13.0 years in boys, 12.1 years in girls) was found to be significantly delayed (Mann-Whitney p<0.001), but duration of puberty (1.5 years in both sexes) was shortened (Kolgomarov-Smirnov p<0.01). Skeletal maturity at the onset of puberty was not advanced excluding this as a contributory factor. There was no association between dose of GH administered and the pubertal parameters. The results suggest that GH accelerates the pubertal process.
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McMurray, Robert G., and Peter A. Hosick. "The Interaction of Obesity and Puberty on Substrate Utilization During Exercise: A Gender Comparison." Pediatric Exercise Science 23, no. 3 (August 2011): 411–31. http://dx.doi.org/10.1123/pes.23.3.411.
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The study evaluated the interactions of puberty and obesity on substrate oxidation of overweight girls (n = 38) and boys (N = 35; BMI > 85th percentile) matched for gender, age, and puberty (pre/pubertal) with normal weight girls and boys. Metabolic rates (VO2) were obtained during rest and at 4, 5.6 and 8 k/h. Carbohydrate oxidation rates (mg/kgFFM/min) adjusted for % predicted VO2max, were higher for prepubertal OW children than pubertal children (p < .03). Fat oxidation rates were higher for NW prepubertal boys compared with other boys. Results indicate that OW children, regardless of gender or pubertal status, increase their carbohydrate oxidation rate to compensate for higher than normal metabolic rates. The effects of obesity on the substrate use is marginally related to puberty.
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Stecchini, Monica F., Zilda Braid, Candy B. More, Davi C. Aragon, Margaret Castro, Ayrton C. Moreira, and Sonir R. Antonini. "Gonadotropin-dependent pubertal disorders are common in patients with virilizing adrenocortical tumors in childhood." Endocrine Connections 8, no. 5 (May 2019): 579–89. http://dx.doi.org/10.1530/ec-19-0141.
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Objective To investigate the impact of early exposure to androgen excess on gonadotropin-dependent puberty (GDP) and final height (FH) of patients with androgen-secreting adrenocortical tumors (ACT) in childhood. Methods Retrospective cohort study. Occurrence of GDP and achievement of FH were evaluated. Central precocious puberty (CPP) and early fast puberty (EFP) were considered pubertal disorders. Patients with normal puberty and pubertal disorders were compared. Results The study included 63 patients (44F), followed in a single institution from 1975 until 2017. At diagnosis of ACT, median age was 25.8 months; duration of signs, 6 months; stature SDS, 0.5 (−3.6 to 3.9) and bone age advancement, 14.7 months (−27.9 to 85.4). To date, 37 patients developed GDP: 26 had normal puberty; one, precocious thelarche; seven, CPP and three, EFP. GnRHa effectively treated CPP/EFP. Tall stature and older age at diagnosis of ACT were associated with risk of CPP alone (RR 4.17 (95% CI 1.17–14.80)) and CPP/EFP (RR 3.0 (95% CI 1.04–8.65)). Recurrence/metastasis during follow-up were associated with risk of CPP alone (RR 4.17 (95% CI 1.17–14.80)) and CPP/EFP (RR 3.0 (95% CI 1.12–8.02)). Among the 19 patients that reached FH, stature SDS dropped from 1.4 to −0.02 since diagnosis of ACT (P = 0.01). Seventeen achieved normal FH. There was no difference in FH SDS between patients with normal puberty and pubertal disorders (P = 0.75). Conclusions Gonadotropin-dependent pubertal disorders are common in patients with androgen-secreting ACT in childhood. FH is usually not impaired. The study reinforces the importance of close follow-up after surgery to identify and treat consequences of early exposure to androgen excess.
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De Leonibus, Chiara, M. Loredana Marcovecchio, and Francesco Chiarelli. "Update on statural growth and pubertal development in obese children." Pediatric Reports 4, no. 4 (December 6, 2012): 35. http://dx.doi.org/10.4081/pr.2012.e35.
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Childhood obesity is a growing and alarming problem, associated with several short-term and long-term metabolic and cardiovascular complications. In addition, it has also been suggested that excess adiposity during childhood influences growth and pubertal development. Several studies have shown that during pre-pubertal years, obese patients present higher growth velocity and that this pre-pubertal advantage tends to gradually decrease during puberty, leading to similar final heights between obese and non-obese children. Excess body weight might also influence pubertal onset, leading to earlier timing of puberty in girls. In addition, obese girls are at increased risk of hyperandrogenism and polycystic ovary syndrome. In boys, a clear evidence does not exist: some studies suggesting an earlier puberty associated with the obesity status, whereas other have found a delayed pubertal onset. Overall, the existing evidence of an association between obesity and modification of growth and pubertal patterns underlines a further reason for fighting the epidemics of childhood obesity.
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Quevedo, Karina M., Stephen D. Benning, Megan R. Gunnar, and Ronald E. Dahl. "The onset of puberty: Effects on the psychophysiology of defensive and appetitive motivation." Development and Psychopathology 21, no. 1 (January 2009): 27–45. http://dx.doi.org/10.1017/s0954579409000030.
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AbstractWe examined puberty-specific effects on affect-related behavior and on the psychophysiology of defensive and appetitive motivation while controlling for age. Adolescents (N = 94, ages = 12 and 13 years) viewed 75 pictures (International Affective Picture System: pleasant, neutral, and aversive) while listening to auditory probes. Startle response and postauricular (PA) reflex were collected as measures of defensive and appetitive motivation, respectively. Pubertal status and measures of anxiety/stress reaction and sensation/thrill seeking were obtained. Mid-/late pubertal adolescents showed enhanced startle amplitude across all picture valences. A Puberty × Valence interaction revealed that mid-/late pubertal adolescents showed appetitive potentiation of the PA, whereas pre-/early pubertal adolescents showed no modulation of the PA reflex. Mid-/late pubertal adolescents also scored significantly higher on measures of sensation/thrill seeking than did their pre-/early pubertal peers and puberty moderated the association between psychophysiology and behavioral measures, suggesting that it plays a role in reorganizing defensive and appetitive motivational systems.
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Souza, Carolina Martins de, Tamara Yamamoto, and Cristiane Kochi. "Evaluation of statural growth and puberty of children and adolescents with overweight and obesity." Revista de Medicina 100, esp (November 8, 2021): 7. http://dx.doi.org/10.11606/issn.1679-9836.v100iespp7-7.
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Introduction: Childhood obesity is one of the main public health problems in Brazil and worldwide and is a risk factor for many other metabolic diseases. Furthermore, studies show that being overweight influences growth and puberty. Objectives: In females, being overweight is associated with the anticipation of puberty. However, in males, few studies have been done and they are controversial. Therefore, this study aimed to evaluate growth and puberty in overweight boys and girls. Methods: In this retrospective study, we analyzed the medical records of patients aged 5 to 19 years, overweight or obese, from the pediatric endocrinology clinic of the Irmandade de Misericórdia, Santa Casa de São Paulo. The data collected were: height (H) and weight, body mass index (BMI), expressed as z-scores (height SDS and BMI SDS, respectively). Pubertal staging was evaluated according to Tanner's criteria. Final height was considered when the growth rate was less than 2 cm/year and/or bone age was over 15 years. Results: Ninety girls were evaluated, with mean (SD) chronological age (CA) at puberty onset of 9.8 (1.2) years. Girls had higher stature compared to the family pattern, but their final height was equal to the genetic target. Eighty-two boys were evaluated, with a mean (SD) CA at puberty at 11.7 (1.2) years. Boys were above family height at the onset of puberty, but reduced height SDS during puberty evolution. There was a reduction in BMI SDS from beginning to end of puberty, different from what was observed in girls. Discussion: In this group evaluation, the onset of puberty occurred within the expected average age for a general population, in both genders, with no pubertal anticipation or delay being observed. Both groups showed taller stature compared to the familiar target at the beginning of puberty, however, they reached the end within the genetic pattern, suggesting that growth is accelerated in the prepubertal phase and then lowered during puberty. Furthermore, in girls, there was no difference between BMI SDS at the beginning and at the end of puberty, indicating that these patients do not show any worsening in weight after menarche. Boys, on the other hand, reduced BMI SDS during puberty, suggesting, therefore, that treatment should be individualized, since body composition is different according to gender.
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Rahma, Jihan Alifa, Adinda Ilsa Maulida, Alma Dyah Perwita, Baiq Ayu Rahmawati, Clara Nadila, Herodya Lajunee Fesmia, Ni Made Utami Wulandari, Zhayyin Palna Rial Novsyaini, and Indana Eva Ajmala. "Precocious Puberty: Etiology and Current Treatment." Jurnal Biologi Tropis 23, no. 1 (November 16, 2023): 148–54. http://dx.doi.org/10.29303/jbt.v23i1.5926.
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Precocious puberty also known as premature puberty is an abnormal pubertal development that can affect a child's growth and development. The clinical manifestations of precocious puberty are generally diverse and based on etiology are classified into central precocious puberty (GnRH dependent) and peripheral precocious puberty (GnRH independent). The main concern with precocious puberty is that precocious puberty can be a clinical symptom of an underlying serious disease such as a brain tumor, adrenal or gonadal tumor and others. Early identification of etiology plays an important role in prevention, diagnosis, and treatment of this disease. This literature review aims to determine the etiology and current management of precocious puberty. This literature review uses the keywords "Precocious Puberty AND etiology AND treatment" through the National Center for Biotechnology Information (NCBI) and Google Scholar databases. This article uses 11 articles that were used as references in its preparation. In conclusion, it is necessary to know the etiology of precocious puberty using imaging examinations for optimal management and excluding malignant abnormalities. The current treatment for central precocious puberty is GnRH agonists (gold-standard) and surgery in cases of intracranial lesions and peripheral precocious puberty using a combination of androgen antagonists (spironolactone) and aromatase inhibitors (anastrozole, testolactone) and surgery is indicated for gonadal and adrenal tumors. The role of parents is very important in early detection of precocious puberty, because the earlier the therapy, the better the prognosis.
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Seifried, Lisa, Elaheh Soleimanpour, Daniela C. Dieterich, and Markus Fendt. "Cognitive Flexibility in Mice: Effects of Puberty and Role of NMDA Receptor Subunits." Cells 12, no. 9 (April 22, 2023): 1212. http://dx.doi.org/10.3390/cells12091212.
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Cognitive flexibility refers to the ability to adapt flexibly to changing circumstances. In laboratory mice, we investigated whether cognitive flexibility is higher in pubertal mice than in adult mice, and whether this difference is related to the expression of distinct NMDA receptor subunits. Using the attentional set shifting task as a measure of cognitive flexibility, we found that cognitive flexibility was increased during puberty. This difference was more pronounced in female pubertal mice. Further, the GluN2A subunit of the NMDA receptor was more expressed during puberty than after puberty. Pharmacological blockade of GluN2A reduced the cognitive flexibility of pubertal mice to adult levels. In adult mice, the expression of GluN2A, GluN2B, and GluN2C in the orbitofrontal cortex correlated positively with performance in the attentional set shifting task, whereas in pubertal mice this was only the case for GluN2C. In conclusion, the present study confirms the observation in humans that cognitive flexibility is higher during puberty than in adulthood. Future studies should investigate whether NMDA receptor subunit-specific agonists are able to rescue deficient cognitive flexibility, and whether they have the potential to be used in human diseases with deficits in cognitive flexibility.
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Lin, Wei-De, Chi-Fung Cheng, Chung-Hsing Wang, Wen-Miin Liang, Chien-Hsiun Chen, Ai-Ru Hsieh, Mu-Lin Chiu, et al. "Genetic factors of idiopathic central precocious puberty and their polygenic risk in early puberty." European Journal of Endocrinology 185, no. 4 (October 1, 2021): 441–51. http://dx.doi.org/10.1530/eje-21-0424.
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Objective, To investigate the genetic characteristics of idiopathic central precocious puberty (ICPP) and validate its polygenic risk for early puberty. Design and methods A bootstrap subsampling and genome-wide association study were performed on Taiwanese Han Chinese girls comprising 321 ICPP patients and 148 controls. Using previous GWAS data on pubertal timing, a replication study was performed. A validation group was also investigated for the weighted polygenic risk score (wPRS) of the risk of early puberty. Results A total of 105 SNPs for the risk of ICPP were identified, of which 22 yielded an area under the receiver operating characteristic curve of 0.713 for the risk of early puberty in the validation group. A replication study showed that 33 SNPs from previous GWAS data of pubertal timing were associated with the risk of ICPP (training group: P-value < 0.05). In the validation group, a cumulative effect was observed between the wPRS and the risk of early puberty in a dose-dependent manner (validation group: Cochran–Armitage trend test: P-value < 1.00E−04; wPRS quartile 2 (Q2) (odds ratio (OR) = 5.00, 95% CI: 1.55–16.16), and wPRS Q3 (OR = 11.67, 95% CI: 2.44–55.83)). Conclusions This study reveals the ICPP genetic characteristics with 22 independent and 33 reported SNPs in the Han Chinese population from Taiwan. This study may contribute to understand the genetic features and underlying biological pathways that control pubertal timing and pathogenesis of ICPP and also to the identification of individuals with a potential genetic risk of early puberty.
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P., Pallavee, and Rupal Samal. "Precocious puberty: a clinical review." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 7, no. 3 (February 27, 2018): 771. http://dx.doi.org/10.18203/2320-1770.ijrcog20180853.
Full textAbstract:
Precocious puberty is defined as pubertal development occurring more than 2.5 standard deviations earlier than the average age. It may comprise of central or gonadotropin-dependent precocious puberty and peripheral or gonadotropin-independent precocious puberty. Variants of precocious puberty include premature thelarche, premature pubarche and isolated premature menarche which principally implies onset of menstruation without any other signs of sexual development. Precocious puberty may have long-term consequences including short stature later on in adulthood owing to premature epiphyseal fusion as also psychosocial problems. Evaluation includes a detailed history, physical examination, biochemical tests and imaging directed towards detecting the cause. Gonadotropin Releasing Hormone (GnRH) analogues are effective for treatment of central precocious puberty. Treatment of peripheral precocious puberty should be based on the cause. Isolated variants are usually normal but should be closely monitored. Multi-speciality consultation with involvement of pediatricians and enocrinologists may improve treatment outcomes in these children, who otherwise pose significant challenges to the gynaecologist.
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Lazar, L., U. Pollak, O. Kalter-Leibovici, A. Pertzelan, and M. Phillip. "Pubertal course of persistently short children born small for gestational age (SGA) compared with idiopathic short children born appropriate for gestational age (AGA)." European Journal of Endocrinology 149, no. 5 (November 1, 2003): 425–32. http://dx.doi.org/10.1530/eje.0.1490425.
Full textAbstract:
OBJECTIVE: Few data are available on the pubertal development of children born small for gestational age (SGA) who fail to show catch-up growth. DESIGN: A longitudinal analysis compared the pubertal course of persistently short children born SGA compared to children with idiopathic short stature who were appropriate for gestational age (AGA). One hundred and twenty-eight short children (height SDS<-1.7), including 76 (31 boys) born SGA and 52 (22 boys) born AGA, were regularly followed from early childhood to completion of puberty. RESULTS: Puberty was attained at normal age (10.5-14 Years in boys, 9.5-13 Years in girls) for most children in both the SGA and AGA groups (boys, 80% and 77%; girls, 76% and 78% respectively). The duration of puberty was similar in the SGA and AGA groups. Menarche occurred at normal age range but was significantly earlier in the SGA girls (P<0.01 by ANOVA). Despite the similar total pubertal growth, the patterns of growth differed significantly: SGA group - accelerated growth and bone maturation rates from onset of puberty with peak height velocity at Tanner stages 2-3, followed by a decelerated growth rate and earlier fusion of the epiphyses; AGA group - steady progression of bone elongation and maturation throughout puberty (pubertal growth, P<0.05 in both sexes; bone maturation, P<0.001 in both sexes). Final height in the SGA group was compromised compared with their target height (P<0.001). CONCLUSION: Children born SGA have a normal pubertal course with a distinct pubertal growth pattern. This pattern may represent an altered regulation of their growth modalities.