Serum AMH levels are lower in healthy boys who develop pubertal gynaecomastia

Publikation: Bidrag til tidsskriftKonferenceabstrakt i tidsskriftForskningfagfællebedømt

Standard

Serum AMH levels are lower in healthy boys who develop pubertal gynaecomastia. / Mieritz, Mikkel G.; Hagen, Casper P.; Almstrup, Kristian; Petersen, Jørgen Holm; Raket, Lars Lau; Sommer, Stefan Horst; Juul, Anders.

I: Hormone Research in Paediatrics, Bind 84, Nr. Supplement 1, P2-526, 2015, s. 290-291.

Publikation: Bidrag til tidsskriftKonferenceabstrakt i tidsskriftForskningfagfællebedømt

Harvard

Mieritz, MG, Hagen, CP, Almstrup, K, Petersen, JH, Raket, LL, Sommer, SH & Juul, A 2015, 'Serum AMH levels are lower in healthy boys who develop pubertal gynaecomastia', Hormone Research in Paediatrics, bind 84, nr. Supplement 1, P2-526, s. 290-291. https://doi.org/10.1159/000437032

APA

Mieritz, M. G., Hagen, C. P., Almstrup, K., Petersen, J. H., Raket, L. L., Sommer, S. H., & Juul, A. (2015). Serum AMH levels are lower in healthy boys who develop pubertal gynaecomastia. Hormone Research in Paediatrics, 84(Supplement 1), 290-291. [P2-526]. https://doi.org/10.1159/000437032

Vancouver

Mieritz MG, Hagen CP, Almstrup K, Petersen JH, Raket LL, Sommer SH o.a. Serum AMH levels are lower in healthy boys who develop pubertal gynaecomastia. Hormone Research in Paediatrics. 2015;84(Supplement 1):290-291. P2-526. https://doi.org/10.1159/000437032

Author

Mieritz, Mikkel G. ; Hagen, Casper P. ; Almstrup, Kristian ; Petersen, Jørgen Holm ; Raket, Lars Lau ; Sommer, Stefan Horst ; Juul, Anders. / Serum AMH levels are lower in healthy boys who develop pubertal gynaecomastia. I: Hormone Research in Paediatrics. 2015 ; Bind 84, Nr. Supplement 1. s. 290-291.

Bibtex

@article{83d61affbe2f4223949ec6bc3abd9c57,
title = "Serum AMH levels are lower in healthy boys who develop pubertal gynaecomastia",
abstract = "Background: Pubertal gynaecomastia is thought to be a clinical sign of an oestrogen-androgen imbalance, affecting up to 60{\%} of boys. In most cases no underlying endocrinopathy can be identified. In boys, Anti-mullerian hormone (AMH) is produced by immature Sertoli cells and circulating level decreases as testosterone increases during pubertal maturation. In a previous cross sectional study we found significant lower levels of AMH in boys with pubertal gynaecomastia (Mieritz et al., Clin Endocrinol, 2013). Objective and hypotheses: To investigate serum AMH levels and genetic polymorphisms in boys with or without gynaecomastia. Method: 99 healthy Danish boys (aged 5.8-16.4 years) were followed in a prospective cohort over 8 years with semi-annual examinations (total examinations, n=951), including breast palpations and blood samples. Serum AMH concentrations were analysed by immunoassay (Beckman Coulter). Furthermore, we analysed two single nucleotide polymorphisms (SNPs) located in exon 1 of the gene encoding AMH (AMH rs10407022 (Table Presented)>G) and in a putative enhancer of the AMH-receptor (AMHR2 rs11170547 C>T) respectively. Results: Pubertal gynaecomastia was observed in 47/95 (49{\%}) of the boys during follow-up. Circulating levels of AMH were significantly lower in boys with pubertal gynaecomastia compared to boys without - even after controlling for pubertal stage (P2) or AMH-receptor SNPs (CC vs CT, P=0.963). Conclusion: This is to our knowledge the first longitudinal study to find an association between low serum levels of AMH and the development of pubertal gynaecomastia. We speculate that this might be due to impaired testicular function in these boys.",
keywords = "European, Sertoli cell, allele, androgen, blood level, blood sampling, boy, breast, cross sectional study, endocrine disease, endocrinology, enhancer region, estrogen, examination, exon, follow up, gene, genetic polymorphism, gynecomastia, hormone, human, hypothesis, immunoassay, longitudinal study, male, maturation, palpation, puberty, receptor, salicylate sodium, serum, single nucleotide polymorphism, society, testis function, testosterone",
author = "Mieritz, {Mikkel G.} and Hagen, {Casper P.} and Kristian Almstrup and Petersen, {J{\o}rgen Holm} and Raket, {Lars Lau} and Sommer, {Stefan Horst} and Anders Juul",
year = "2015",
doi = "10.1159/000437032",
language = "English",
volume = "84",
pages = "290--291",
journal = "Hormone Research in Paediatrics",
issn = "1663-2818",
publisher = "S Karger AG",
number = "Supplement 1",

}

RIS

TY - ABST

T1 - Serum AMH levels are lower in healthy boys who develop pubertal gynaecomastia

AU - Mieritz, Mikkel G.

AU - Hagen, Casper P.

AU - Almstrup, Kristian

AU - Petersen, Jørgen Holm

AU - Raket, Lars Lau

AU - Sommer, Stefan Horst

AU - Juul, Anders

PY - 2015

Y1 - 2015

N2 - Background: Pubertal gynaecomastia is thought to be a clinical sign of an oestrogen-androgen imbalance, affecting up to 60% of boys. In most cases no underlying endocrinopathy can be identified. In boys, Anti-mullerian hormone (AMH) is produced by immature Sertoli cells and circulating level decreases as testosterone increases during pubertal maturation. In a previous cross sectional study we found significant lower levels of AMH in boys with pubertal gynaecomastia (Mieritz et al., Clin Endocrinol, 2013). Objective and hypotheses: To investigate serum AMH levels and genetic polymorphisms in boys with or without gynaecomastia. Method: 99 healthy Danish boys (aged 5.8-16.4 years) were followed in a prospective cohort over 8 years with semi-annual examinations (total examinations, n=951), including breast palpations and blood samples. Serum AMH concentrations were analysed by immunoassay (Beckman Coulter). Furthermore, we analysed two single nucleotide polymorphisms (SNPs) located in exon 1 of the gene encoding AMH (AMH rs10407022 (Table Presented)>G) and in a putative enhancer of the AMH-receptor (AMHR2 rs11170547 C>T) respectively. Results: Pubertal gynaecomastia was observed in 47/95 (49%) of the boys during follow-up. Circulating levels of AMH were significantly lower in boys with pubertal gynaecomastia compared to boys without - even after controlling for pubertal stage (P2) or AMH-receptor SNPs (CC vs CT, P=0.963). Conclusion: This is to our knowledge the first longitudinal study to find an association between low serum levels of AMH and the development of pubertal gynaecomastia. We speculate that this might be due to impaired testicular function in these boys.

AB - Background: Pubertal gynaecomastia is thought to be a clinical sign of an oestrogen-androgen imbalance, affecting up to 60% of boys. In most cases no underlying endocrinopathy can be identified. In boys, Anti-mullerian hormone (AMH) is produced by immature Sertoli cells and circulating level decreases as testosterone increases during pubertal maturation. In a previous cross sectional study we found significant lower levels of AMH in boys with pubertal gynaecomastia (Mieritz et al., Clin Endocrinol, 2013). Objective and hypotheses: To investigate serum AMH levels and genetic polymorphisms in boys with or without gynaecomastia. Method: 99 healthy Danish boys (aged 5.8-16.4 years) were followed in a prospective cohort over 8 years with semi-annual examinations (total examinations, n=951), including breast palpations and blood samples. Serum AMH concentrations were analysed by immunoassay (Beckman Coulter). Furthermore, we analysed two single nucleotide polymorphisms (SNPs) located in exon 1 of the gene encoding AMH (AMH rs10407022 (Table Presented)>G) and in a putative enhancer of the AMH-receptor (AMHR2 rs11170547 C>T) respectively. Results: Pubertal gynaecomastia was observed in 47/95 (49%) of the boys during follow-up. Circulating levels of AMH were significantly lower in boys with pubertal gynaecomastia compared to boys without - even after controlling for pubertal stage (P2) or AMH-receptor SNPs (CC vs CT, P=0.963). Conclusion: This is to our knowledge the first longitudinal study to find an association between low serum levels of AMH and the development of pubertal gynaecomastia. We speculate that this might be due to impaired testicular function in these boys.

KW - European

KW - Sertoli cell

KW - allele

KW - androgen

KW - blood level

KW - blood sampling

KW - boy

KW - breast

KW - cross sectional study

KW - endocrine disease

KW - endocrinology

KW - enhancer region

KW - estrogen

KW - examination

KW - exon

KW - follow up

KW - gene

KW - genetic polymorphism

KW - gynecomastia

KW - hormone

KW - human

KW - hypothesis

KW - immunoassay

KW - longitudinal study

KW - male

KW - maturation

KW - palpation

KW - puberty

KW - receptor

KW - salicylate sodium

KW - serum

KW - single nucleotide polymorphism

KW - society

KW - testis function

KW - testosterone

U2 - 10.1159/000437032

DO - 10.1159/000437032

M3 - Conference abstract in journal

C2 - 72085906

VL - 84

SP - 290

EP - 291

JO - Hormone Research in Paediatrics

JF - Hormone Research in Paediatrics

SN - 1663-2818

IS - Supplement 1

M1 - P2-526

ER -

ID: 167505646