ESPE Abstracts (2015) 84 P-1-117

ESPE2015 Poster Presentations Poster Category 1 Puberty (11 abstracts)

Transient Breast Budding in Healthy Girls is a Frequent Phenomenon: Description of Pubertal Progression and Associations to Gonadotropins, Estradiol and FSHB/FSHR Genetic Polymorphisms

Marie Lindhardt Johansen , Casper P Hagen , Mikkel G Mieritz , Jørgen Holm Petersen & Anders Juul


Department of Growth and Reproduction, Copenhagen University Hospital, Copenhagen, Denmark

Background: Intermittent breast budding (girls entering stage B2 and then subsequently regressing to B1) in healthy girls is a frequent phenomenon observed by most clinicians. However, little is known of normal progression of female puberty, and the phenomenon of transient breast development has, to our knowledge, never been studied in details.

Objective and hypotheses: We present and validate the female Puberty Nomogram indicating age specific SD scores for Tanner breast stages (based on Van Buuren et al.’s stage-line diagram). Moreover, we evaluate pubertal progression, longitudinal reproductive hormone profiles, and genetic polymorphisms affecting FSH signalling in girls with transient breast budding.

Method: The Puberty Nomogram was based on 1375 healthy, Caucasian girls from cross-sectional studies in Copenhagen and Randers, and was validated using data from 98 girls from the longitudinal part of the COPENHAGEN Puberty Study. DNA was isolated from blood and FSHB c.-211G>T, FSHR c.-29 G>A and FSHR c.2039 A>G were assessed by KASP genotyping assays.

Results: Thirteen (out of 98) girls (13%) from the longitudinal cohort presented with transient breast budding. On the Puberty Nomogram it is apparent that after a variable period of time, pubertal development progresses normally in girls with intermittent breasts (median +1.7 years, range 1.14–4.29). Transient breast budding was associated with lower concentrations of hormones, significantly for LH (P=0.016) and inhibin B (p=0.019), at the time of the initial B2 compared to girls who initiated and progress normally. The distributions of FSHB and FSHR SNPs were not associated with transient breast budding.

Conclusion: Transient breast development is a clinical phenomenon observed in 13% of healthy girls and is not associated with a pubertal rise in gonadotropins and reproductive hormone concentrations at the initial breast development. Genetic polymorphisms affecting FSH signalling did not appear to be associated with the phenomenon in this pilot study.

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