Pubertal gynecomastia coincides with peak height velocity (original) (raw)
Related papers
The Journal of Clinical Endocrinology & Metabolism, 2015
Context: Physiological gynecomastia is common and affects a large proportion of otherwise healthy adolescent boys. It is thought to be caused by an imbalance between estrogen and testosterone, although this is rarely evident in analyses of serum. Objective: This study aimed to describe the frequency of physiological gynecomastia and to determine possible etiological factors (eg, auxology and serum hormone levels) in a longitudinal setup. Design, Settings, and Participants: A prospective cohort study of 106 healthy Danish boys (5.8–16.4 years) participated in the longitudinal part of the COPENHAGEN Puberty Study. The boys were examined every 6 months during an 8-year follow-up. Median number of examinations was 10 (2–15). Main outcome measurements: Blood samples were analyzed for FSH, LH, testosterone, estradiol, SHBG, inhibin B, anti-Müllerian hormone, IGF-1, and IGF binding protein-3 by immunoassays. Auxological parameters, pubertal development, and the presence of gynecomastia wer...
Clinical and Biochemical Phenotype of Adolescent Males with Gynecomastia
Journal of Clinical Research in Pediatric Endocrinology, 2019
Objective: Gynecomastia is defined as benign proliferation of male breast glandular tissue. Its prevalence during puberty stands at 50-60% and this condition is common also in neonatal and elderly males. It develops mainly due to the disequilibrium between estrogen and androgen activity in breast tissue, where estradiol binds to estrogen receptor and stimulates ductal and glandular cells. The aim of this work was to find a relationship between the sex hormones alterations and the natural history (evolution) of gynecomastia. Furthermore, the work tries to indicate the importance of checking the E2/TTE ratio. Materials and Methods: Participants in this study were 93 male patients aged 9 to 18 (mean age 13.8 ± 2.6) referred to an outpatient clinic between January 2011 and February 2016 with breast enlargement. Results: In 63 of 93 boys the gynecomastia was confirmed and 28 of them were follow-up (median of 3 months). None of all observed boys have reduced the size of breast during the observation and there was no correlation between BMI Z-Score and size of breast (p>0.05). Breast enlargement progressed in 9 boys (32.1%). We have observed a positive correlation between E2/TTE Ratio and Tanner B stage (r=0.47; p=0.034). Conclusions: The E2/TTE ratio may be a helpful tool in diagnosing gynecomastia. Altered E2/TTE ratio might be responsible for part of cases described previously as idiopathic. Additionally, weight loss does not imply reduction of breast size in boys, nonetheless it should be the first step before further treatment of prolonged gynecomastia.
Advances in pubertal growth and factors influencing it: Can we increase pubertal growth?
Indian Journal of Endocrinology and Metabolism, 2014
Puberty is a period of development characterized by partially concurrent changes which includes growth acceleration, alteration in body composition and appearance of secondary sex characteristics. Puberty is characterized by an acceleration and then deceleration in skeletal growth. The initiation, duration and amount of growth vary considerably during the growth spurt. Pubertal growth and biological maturation are dynamic processes regulated by a variety of genetic and environmental factors. Changes in skeletal maturation and bone mineral accretion concomitant with the stage of pubertal development constitute essential components in the evaluation of growth during this pubertal period. Genetic, endocrine and nutritional factors and ethnicity contribute variably to the amount of growth gained during this important period of rapid changes. Many studies investigated the possibility of increasing pubertal growth to gain taller fi nal adult height in adolescents with idiopathic short stature (ISS). The pattern of pubertal growth, its relation to sex maturity rating and factors affecting them has been addressed in this review. The results of different trials to increase fi nal adult height of adolescents using different hormones have been summarized. These data enables Endocrinologists to give in-depth explanations to patients and families about the effi cacy and clinical signifi cance as well as the safety of using these therapies in the treatment of adolescents with ISS.
Analysis of puberty and pubertal growth in healthy boys
European Journal of Pediatrics, 2007
The aim of this study was to provide normative data for the onset and tempo of puberty in healthy boys. The analyses are based on data that were collected and evaluated biannually on 1112 Turkish school children aged from 8 to 18 years and a subsample of 30 boys who had reached final height (FH). The data were analyzed crosssectionally in the total group and longitudinally in the subsample. Mean age and height (Ht) at onset of puberty were 11.6±1.2 years and 146.1±7.7 cm, respectively. Peak height velocity (HtV) was 10.1±1.6 cm. Total pubertal height gain was 26.4±4.3 cm. The duration of puberty was 4.9±0.6 years. Height at onset of puberty was positively correlated with FH (p < 0.0001) and with duration of puberty (p=0.03). Body mass index at onset of puberty correlated negatively with age at onset of puberty (p<0.009) and with the duration of puberty (p=0.05) but not with FH. In conclusion, these results provide normative data for Ht and HtV for each testicular volume stage for boys in puberty. Height at onset of puberty is the most important determinant of FH. There is no secular trend for the onset of puberty. Weight does seem to affect the onset and tempo of puberty but not FH.
Hormonal, anthropometric and lipid factors associated with idiopathic pubertal gynecomastia
Annals of Saudi medicine
To determine factors associated with pubertal gynecomastia. A cross-sectional study among healthy male school children and adolescents in Riyadh, Saudi Arabia. Subjects were selected from diverse socioeconomic backgrounds. Tanner stage, height, weight, blood hormonal levels (leutilizing hormone [LH], follicle-stimulating hormone [FSH], total testosterone, and estradiol), and anthropometric and lipid parameters (body mass index [BMI], triglycerides, high-density lipoprotein [HDL], and low-density lipoprotein [LDL]), were collected and compared in children with and without gynecomastia. The study included 542 children and adolescents. Median (interquartile range) age in the whole group was 11(8-13) years. The prevalence of gynecomastia was 185/542 (34%), with a peak at age 14. The 2 groups compared had nonsignificant difference in cholesterol (P=.331), LH (P=.215) and FSH (P=.571) levels. Those with gynecomastia were significantly older, had lower gonad stage, had higher anthropometri...
Andrology, 2016
Pubertal gynecomastia is a common condition observed in up to 65% of adolescent males. It is usually idiopathic and tends to regress within 1-2 years. In this descriptive cross-sectional study, we investigated 25 adolescent males with prominent (>B3) and/or persistent (>2 years) pubertal gynecomastia (P/PPG) to determine whether a hormonal/genetic defect might underline this condition. Endocrine investigation revealed the absence of hormonal disturbance for 18 boys (72%). Three patients presented Klinefelter syndrome and three a partial androgen insensitivity syndrome (PAIS) as a result of p.Ala646Asp and p.Ala45Gly mutations of the androgen receptor gene. The last patient showed a 17a-hydroxylase/17,20-lyase deficiency as a result of a compound heterozygous mutation of the CYP17A1 gene leading to p.Pro35Thr(P35T) and p.Arg239Stop(R239X) in the P450c17 protein. Enzymatic activity was analyzed: the mutant protein bearing the premature stop codon R239X showed a complete loss of 17a-hydroxylase and 17,20-lyase activity. The mutant P35T seemed to retain 15-20% of 17a-hydroxylase and about 8-10% of 17,20-lyase activity. This work demonstrates that P/PPG had an endocrine/genetic cause in 28% of our cases. PAIS may be expressed only by isolated gynecomastia as well as by 17a-hydroxylase/17,20-lyase deficiency. Isolated P/PPG is not always a 'physiological' condition and should thus be investigated through adequate endocrine and genetic investigations, even though larger studies are needed to better determine the real prevalence of genetic defects in such patients.
American Journal of Human Biology, 2001
This paper analyzed the intensity and duration of height growth during puberty in boys and girls in relation to rhythm of maturation. A longitudinal clinical follow-up between ages of 10 and 20 years, was carried out in a sample of 251 children grouped according to age at pubertal onset: boys (genital stage 2) at the ages of 11 (n ס 28), 12 (n ס 38), 13 (n ס 42), and 14 (n ס 27); and girls (breast stage 2) at the ages of 10 (n ס 37), 11 (n ס 47), 12 (n ס 19), and 13 (n ס 13). Height was measured annually. Testicular volume and genital development were assessed in boys, and breast development was assessed in girls. There were significant differences (P < 0.001) in height at the age of pubertal onset among maturity groups. Late maturers were taller than early maturers (r ס 0.49, P < 0.001 for girls; r ס 0.38, P < 0.001 for boys). However, final heights did not differ according to age of onset in either sex. In boys, later onset of puberty was associated with a smaller pubertal height gain (r ס −0.60, P < 0.001) and a shorter period of pubertal growth (r ס −0.61, P < 0.001). Equally in girls, earlier onset of puberty was associated with a greater pubertal height gain (r ס −0.68, P < 0.001) and a longer period of pubertal growth (r ס −0.59, P < 0.001). In conclusion, age of pubertal onset does not affect final height attained in both sexes, since there is an inverse compensatory phenomenon in both sexes between height at pubertal onset and the intensity and duration of pubertal growth. Am.
Role of Testosterone and Dihydrotestosterone in Spontaneous Gynecomastia of Adolescents
Systems Biology in Reproductive Medicine, 1992
To test a possible hormonal mechanism of gynecomastia at puberty, a group of pubertal spontaneous gynecomastia (PSG) and healthy young volunteers (HYV), Tanner's stage 11-V, were studied. Peripheral blood samples were obtained for measuring follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), testosterone (T), dihydrotestosterone (DHT), estradiol (E-2) and estrone (E-I). No difference was established in steroids in pituitary hormonal concentration when both groups were compared on a sexual stage-matched control basis, except for T 2 SD in 519 subjects of PSG and DHT 2 SD in all of PSG. The T:DHT ratio varied from 5.0 to 15.4 in PSG and from 0.42 to 2.224 in HYV. Whether spontaneous gynecomastia might exist in an enzimatic blockade of Sa-reductase and whether a decrease in the T:DHT ratio might favor the estrogen action for the progression of breast enlargement deserve further analysis.
Management of Adolescent Gynecomastia: An Update
PubMed, 2017
Gynecomastia refers to an enlargement of the male breast caused by benign proliferation of the glands ducts and stromal components including fat. It is the most common form of breast swelling seen in adolescent males. During pubertal development, gynecomastia can develop as a result of transient relative imbalances between androgens and estrogens. Pubertal gynecomastia is self-limited in 75 to 90% of adolescents and regresses over 1 to 3 years. However it may cause significant psychological stress and depression in adolescents. For boys with persistent gynecomastia that is causing substantial tenderness or embarrassment a tailored approach of close follow-up and use of anti-estrogen drugs may be recommended. These drugs block the effects of estrogens in the body and can reduce the size of the breasts somewhat. It appears that pharmacological therapy of persistent adolescent gynecomastia is reasonable effective if given early in the course of the disease and more successful in cases with small or moderate breast enlargement. However, neither of these drugs is universally approved for the treatment of gynecomastia because the risks and benefits have not been studied completely. Surgical approach may be needed under special conditions for cosmetic reasons. In this update, we review the different published trials for managing adolescent gynecomastia.
European journal of …, 2008
By retrospectively collecting data from nine Italian centres of pediatric endocrinology, we assessed the different management and final outcome of children with short stature and idiopathic delayed puberty. Data were obtained in 77 patients (54 males, 23 females) diagnosed and followed-up in the various centres during the last 15 years. Inclusion criteria were short stature at initial observation and idiopathic delayed puberty diagnosed during follow-up. At first observation, age was 13.8± 1.0 years and height standard deviation score (SDS) was-2.6±0.6 in males. In females age was 13.1±0.9 years and height SDS-2.6±0.4. Local diagnostic and therapeutic protocols included testing for growth-hormone deficiency (six centres) and treatment in case of deficiency or, in the remaining centres, testosterone or no treatment in males, and no treatment in females. At diagnosis, both in males and in females, the auxological features (height SDS, target height SDS and bone age delay) were similar in the patients treated with growth hormone, testosterone or not treated. Overall 32 patients received growth hormone (25 males, 7 females), 33 no treatment (17 males, 16 females) and 12 testosterone. There was no difference in the adult height of males and females in the different treatment groups. In males there were no differences between adult and target