PRECOCIOUS GROWTH OF SEXUAL HAIR WITHOUT OTHER SECONDARY SEXUAL DEVELOPMENT; "PREMATURE PUBARCHE," A CONSTITUTIONAL VARIATION OF ADOLESCENCE

PEDIATRICS ◽  
1952 ◽  
Vol 10 (4) ◽  
pp. 426-432
Author(s):  
SAMUEL H. SILVERMAN ◽  
CLAUDE MIGEON ◽  
EUGENIA ROSEMBERG ◽  
LAWSON WILKINS

GROWTH of sexual hair in a young child suggests the possibility that adrenal tumor or hyperplasia may be causing virilization or that true sexual precocity may be beginning. However, neither of these relatively serious conditions may exist. Approximately 10 years ago workers in the Endocrine Clinic of the Harriet Lane Home became aware of the fact that sexual hair may appear in early life long before there is any other secondary sexual development dependent upon either androgen or estrogen. Although this syndrome has been referred to briefly in textbooks as "precocious adrenarche" and "premature pubarche," no detailed studies of a series of cases have been recorded. The present report is based on a study of 29 children who developed sexual hair before the age of 8 years. It was possible to follow a number of these patients long enough to demonstrate that the condition is a benign variation in the pattern of sexual development and is followed later by normal adolescence. It seems important to bring the findings to the attention of pediatricians who may not be familiar with the syndrome and to discuss its differential diagnosis and probable etiology. Methods Urinary 17-ketosteroids (17-KS) were determined by a modification of the method of Callow, Callow and Emmons previously described, urinary estrogens were measured as the "fluorogenic phenols" by the method of Jailer. Vaginal smears stained by the method of Shorr were interpreted as described elsewhere. The "bone age" was based on the average epiphysial development at all the joints. Clinical and Laboratory Findings

2016 ◽  
Vol 50 (1) ◽  
pp. 49
Author(s):  
Ida Ayu Sri Kusuma Dewi ◽  
Soetjiningsih Soetjiningsih ◽  
Yudha Patria

Background Obesity is a pathological condition due to consumption of excessive amount of food and is associated with early sexual maturation and irregular cycle of menstruation. Early sexual maturation is estimated from the age of menarche.Objective To determine relationship of obesity and age of secondary sexual development in girls.Methods This cross-sectional study was performed on all elementary school students in 4 sub-districts at Denpasar. Nutritional status was determined by BMI. Radiologic examination was performed to determine the bone age. Data were analyzed with appropriate statstical methods.Results Mean chronological age of breasts development for B2 and B3 stage on obese group was younger than non-obese groups (9.0 vs 9.9, P = 0.001; 9.7 vs 10.9, P = 0.006). Early menarche more frequent in obese group than non-obese groups {PR 5 (CI 95% 1.33 to 19.71)}. Mean age of children who experienced menarche on obese group was younger than non-obese group {10.9(SD 0.61) vs 11.1 (SD 0.28). Univariate analysis showed that maturation age of secondary sexual development on obese groups was differed with non-obese group {8.9 (SD 0.21) vs 9.4 (SD 0.13). Linear regression analysis showed relationship between age of breasts and pubic hair growth on both groups.Conclusions This study established that mean age of secondary sexual development was younger in obese girl than non-obese group. Bone age range on obese girls was wider than non-obese girls. [Paediatr Indones. 2010;50:49-5].


2008 ◽  
Vol 237 (10) ◽  
pp. 2963-2972 ◽  
Author(s):  
Xi Wang ◽  
Nishita Desai ◽  
Ya-Ping Hu ◽  
Sandy M. Price ◽  
Cory Abate-Shen ◽  
...  

1966 ◽  
Vol 3 (2) ◽  
pp. 129-133 ◽  
Author(s):  
A M Bishop ◽  
C E Blank ◽  
K Simpson ◽  
C J Dewhurst

PEDIATRICS ◽  
1962 ◽  
Vol 29 (6) ◽  
pp. 977-977
Author(s):  
Nathan B. Talbot

This volume reports the author's clinical observations on 100 children with sex precocity seen in Denmark and compares these with the data of the literature. Those who are particularly interested in this subject will find some valuable information concerning the physical development of precocious children in the neatly designed tables and graphs. They will not find much in the line of physiologic explorations, new concepts or original opinions however. It is unfortunate, too, that chance failed to make available to the author examples of all the various types of sexual precocity known at this time such as the sodium-losing variety of congenital adrenocortical virilism, the incomplete type of central sex precocity in boys with development of the interstitial cells but not the tubules of the testes and others.


2007 ◽  
Vol 84 (3) ◽  
pp. 321-327 ◽  
Author(s):  
Zhan-Fen Qin ◽  
Xiao-Fei Qin ◽  
Lei Yang ◽  
Han-Ting Li ◽  
Xing-Ru Zhao ◽  
...  

2012 ◽  
Vol 158A (11) ◽  
pp. 2733-2742 ◽  
Author(s):  
Sonja A. de Munnik ◽  
Barto J. Otten ◽  
Jeroen Schoots ◽  
Louise S. Bicknell ◽  
Salim Aftimos ◽  
...  

2014 ◽  
Vol 99 (8) ◽  
pp. 2878-2886 ◽  
Author(s):  
Ahmet Uçar ◽  
Michal Yackobovitch-Gavan ◽  
Oğuz Bülent Erol ◽  
Ensar Yekeler ◽  
Nurçin Saka ◽  
...  

Context: The causes of polycystic ovarian syndrome (PCOS) in girls with precocious adrenarche (PA) remain unclear. Objective: Our goal was to compare the clinical, biochemical, and ultrasound characteristics of girls with PA whose size at birth was appropriate for gestational age (AGA) vs those born small for gestational age (SGA). PCOS-associated metabolic and morphological correlates were examined. Design: Glucose tolerance, ACTH stimulation, and transabdominal ultrasounds were examined in 56 AGA and 31 SGA girls with PA. Bone age and hormonal profiles were determined. SGA girls were divided into 2 groups by catch-up growth (CUG) status. Subgroups were compared. Results: Chronological age, Tanner stage for pubarche, ovarian volume, and uterine volume were similar between the groups. SGA girls had lower body mass index and higher bone age-adjusted post-corticotropin cortisol. We found increased body mass index-adjusted mean serum insulin, reduced insulin sensitivity, and reduced IGF-binding protein-1 in SGA girls. Multicystic ovaries were more common in SGA girls (odds ratio [OR] = 9.69, 95% confidence interval [CI] = 3.34–28.15; P < .001). SGA girls without CUG had a higher incidence of multicystic ovaries than CUG counterparts (OR = 8.4, 95% CI = 1.4–19.3; P = .027). Being born SGA (OR = 43.4, 95% CI = 6.9–84.7; P = .001] and exaggerated 17-hydroxyprogesterone response (OR = 15.8, 95% CI = 1.7–49.8; P = .015) were associated with multicystic ovaries. Conclusions: Significant differences in hormone levels, insulin sensitivity, and ovarian maturity were found in prepubertal girls with PA who were SGA. Longitudinal follow-up will help determine whether these factors contribute to a specific PCOS phenotype in SGA girls with PA.


2005 ◽  
Vol 90 (4) ◽  
pp. 2076-2080 ◽  
Author(s):  
Trine H. Johannsen ◽  
Delphine Mallet ◽  
Harriet Dige-Petersen ◽  
Jørn Müller ◽  
Katharina M. Main ◽  
...  

Abstract Classical 3β-hydroxysteroid dehydrogenase (3β-HSD) deficiency is a rare cause of congenital adrenal hyperplasia. We report two sisters presenting with delayed diagnoses of classical 3β-HSD, despite salt wasting (SW) episodes in infancy. Sibling 1 was referred for premature pubarche, slight growth acceleration, and advanced bone age, whereas sibling 2 had no signs of virilization. At referral, increased 17α-hydroxyprogesterone associated with premature pubarche at first suggested a nonclassical 21-hydroxylase deficiency. Sequencing of the CYP21 gene showed both girls only heterozygotes (V281L mutation). This result, combined with SW in infancy, suggested a 3β-HSD deficiency because of increased dehydroepiandrosterone sulfate levels. Further hormonal studies showed markedly elevated Δ5-steroids, in particular 17α-hydroxypregnenolone greater than 100 nmol/liter (the clue to the diagnosis) and elevated Δ5-/Δ4-steroid ratios. Sequencing of the type II 3β-HSD gene documented that both girls were compound heterozygotes for T181I and 1105delA mutations. Retrospectively, elevated levels of 17α-hydroxyprogesterone were found on blood spots from Guthrie’s test. There is no previous report of the combination of SW and premature pubarche due to mutations in the type II 3β-HSD gene. Because neonatal diagnosis could have prevented life-threatening crises in these girls, this report further supports the benefits for neonatal screening for congenital adrenal hyperplasia whatever the etiology.


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