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PubMed2006

Early and late weight gain and the timing of puberty.

Nutrition is an important regulator of the tempo of growth and obesity is usually associated with tall childhood stature and earlier pubertal development. Several longitudinal studies have demonstrated that timing of puberty is most closely linked to infancy weight gain: suggesting an early window for programming of growth and development. Earlier puberty in the UK MRC 1946 birth cohort was related to smaller size at birth and rapid growth between 0 and 2 years. Rapid early weight gain leads to taller childhood stature and higher insulin-like growth factor I (IGF-I) levels, possibly through early induction of growth hormone (GH) receptor numbers, and such children are also at risk of childhood obesity. In the Avon Longitudinal Study of Parents and Children, rapid infancy weight gain was associated with increased risk of obesity at 5 and 8 years, with evidence of insulin resistance, exaggerated adrenarche and reduced levels of sex hormone binding globulin (SHBG). Potentially the elevated IGF-I and adrenal androgen levels, increased aromatase activity and increased 'free' sex steroid levels consequent to lower SHBG levels could all promote activity of the GnRH pulse generator. In addition obese children have higher leptin levels, a proven permissive factor in initiating LH pulsatility. Obesity could also affect the rate of progression through puberty as nutrition and SHBG may act respectively as an accelerator and brake on peripheral sex steroid action. Early weight gain and early pubertal development might also be associated with loss of the pubertal growth spurt perhaps through obesity-related suppression of GH secretion. Trans-generational recurrence of low birth weight, early catch-up weight gain, earlier menarche, and shorter adult stature have been observed in women, and could contribute to the strong heritability in age at menarche.

Age Factors↗
PubMed2006

Bone age and onset of puberty in normal boys.

Many conditions that delay skeletal maturation also delay the onset of puberty, whereas conditions that accelerate skeletal maturation often hasten the onset puberty, raising the possibility that skeletal maturation influences pubertal onset. To determine whether this concordance is also present in normal children, we analyzed data from 30 normal boys participating in a longitudinal study. Height, weight, and serum testosterone concentrations were assessed every 6 months and bone age (Fels method) every year. Pubertal onset was defined by serum testosterone > or =30 ng/dL. The variability in bone age at onset of puberty was not less than the variability in chronological age. In addition, there was no significant correlation between skeletal advancement and pubertal advancement (r=0.01, P=0.9). Similarly, there was not a significant correlation between pubertal advancement and height age advancement, weight age advancement, or BMI age advancement. Our findings do not support the hypothesis that skeletal maturation directly influences the age of pubertal onset in normal boys.

Adolescent↗
PubMed2005

Human chorionic gonadotropin therapy in adolescent boys with constitutional delayed puberty vs those with beta-thalassemia major.

We studied 12 adolescent boys with beta-thalassemia major and delayed puberty (age, 15.8 +/- 1 years) with Tanner I sexual development treated with a long-term low-transfusion regimen. Ten nonthalassemic adolescents (> 14 years) with constitutional delay of growth and puberty (CDGP) served as controls. Auxologic parameters and testicular size were measured, and bone age was determined. Measurement of basal gonadotropin (luteinizing hormone [LH] and follicle-stimulating hormone [FSH]) and testosterone (T) levels taken at 8 am revealed prepubertal levels in both groups of patients. Human chorionic gonadotropin (hCG, 2500 U/m(2)) was injected intramuscularly twice weekly for 6 months, and anthropometric data, testicular diameter, and serum T concentrations were remeasured after 1 and 6 months. The testicular diameter after 6 month of hCG therapy was significantly correlated with the testicular diameter and T level after 1 month of therapy (r = 0.93 and 0.39, respectively, P < .01). After 6 months of hCG therapy, the mean growth velocity (GV) increased from 4.1 to 8.6 cm/y in thalassemic patients and from 4.6 to 10.3 cm/y in those with CDGP during hCG therapy. In thalassemic boys, the mean T concentration increased from 0.93 to 2.7 nmol/L (mean increase = 1.8 nmol/L) vs an increase from 0.47 to 4.81 nmol/L (mean increase = 4.32 nmol/L) in those with CDGP. All adolescents with CDGP, but only 7 the 12 thalassemic adolescents, had T secretion above 2 nmol/L after 6 months of hCG therapy and maintained their growth and pubertal development for a year after stopping hCG. The 5 thalassemic patients with defective T secretion after hCG therapy had significantly higher ferritin level (1985 +/- 658 ng/mL) vs the other 7 patients (1100 +/- 425 ng/mL). These findings denoted significant testicular dysfunction in those patients with higher iron overload (testicular siderosis). Statural GV was significantly correlated with insulin-like growth factor 1 (IGF-1) concentrations and testicular diameter after hCG therapy (r = 0.5 and 0.43 respectively, P < .001). In summary, hCG therapy was effective in treating 7 of 12 (58%) of thalassemic adolescents with delayed puberty. In the rest of patients (5/12, 46%) with significantly higher iron overload, hCG therapy failed to stimulate testicular growth and adequate T. Proper iron chelation appears to protect against testicular dysfunction. In the first group of patients, hCG therapy can be used for the treatment of their hypogonadism, whereas T replacement remains the therapy of choice for the second group.

Adolescent↗
PubMed2004

Decreased hypothalamic aromatization in female rats of true precocious puberty.

The true precocious puberty animal model induced by the single dose of danazol was used for investigating the expressions of hypothalamic aromatase in the advanced onset of puberty in rats. The day of vaginal opening and first estrus showed significant advancement in the model rats compared with the normal and vehicle rats (P < 0.01, respectively). The hypothalamic gonadotropin-releasing hormone (GnRH) mRNA expression increased significantly in the model rats compared with that in the normal and vehicle ones (P < 0.01). The levels of aromatase mRNA and protein expressions detected by RT-PCR and Western blot both decreased in the model rats compared with those in the normal and vehicle groups (P < 0.05). The results suggested that the hypothalamic aromatization might diminish in the onset of true precocious puberty of female rats.

Animals↗
PubMed2004

GPR54 and puberty.

At puberty, pulsatile secretion of hormones initiates sexual maturation of the gonads. The G-protein-coupled receptor GPR54 is crucially involved in the initiation of puberty, along with its ligand metastin. Mice lacking GPR54 fail to undergo puberty and have immature reproductive organs and low levels of sex steroids and gonadotrophic hormones, but have normal levels of gonadotrophin-releasing hormone in the hypothalamus. In humans, several cases of hypogonadism have been ascribed to mutations in GPR54. Production of metastin and, to a lesser extent, GPR54 are negatively regulated by testosterone and oestrogen, and injecting GPR54 ligands can increase hormone secretion in rodents. Thus, GPR54 is required for normal functioning of the hypothalamic-pituitary-gonadal axis, probably at the level of gonadotrophin-releasing-hormone secretion.

Animals↗
PubMed1985

Pulsatile gonadotropin-releasing hormone therapy in male patients with Kallmann's syndrome or constitutional delay of puberty.

The response to low-dose pulsatile gonadotropin-releasing hormone (GnRH) therapy was tested in three hypogonadotropic hypogonadal male patients and a boy with delayed puberty showing different luteinizing hormone responses (delta LH) to test doses of 25 micrograms GnRH intravenously before treatment. Four male patients, 16 to 20 years of age, three with Kallmann's syndrome and one with idiopathic delay of puberty, received 2 micrograms GnRH subcutaneously every 2 1/2 hours for 3 months by the use of the Zyklomat pump (Ferring GmbH, Kiel, FRG). In two patients with Kallmann's syndrome and decreased delta LH, serum testosterone did not increase during treatment, even after increasing the dosage and changing the route of administration (4 micrograms subcutaneously or 8 micrograms intravenously every 2 1/2 hours for 4 weeks with every dosage). The third patient with Kallmann's syndrome and the boy with delayed puberty, both with normal delta LH, presented normal serum testosterone after 3 months of subcutaneous low-dose treatment. The different responses to a GnRH test dose corresponding to the response to pulsatile GnRH therapy probably reflect different degrees of maturation of the pituitary gonadotrophs.

Eunuchism↗
PubMed1992

Height prognosis of children with true precocious puberty and growth hormone deficiency: effect of combination therapy with gonadotropin releasing hormone agonist and growth hormone.

We evaluated height prognosis and therapeutic efficacy of long-term, combination therapy with gonadotropin releasing-hormone agonist and growth hormone (GH) in five children (three girls) with coexistent precocious puberty and GH deficiency. Their clinical characteristics and growth response were compared with those of 12 girls with idiopathic true precocious puberty and eight prepubertal GH-deficient children (one girl). Precocious GH-deficient subjects were older than the precocious GH-sufficient children (9.5 +/- 1.8 years vs 6.5 +/- 1.3 years; mean +/- SD), but bone ages were comparable (12 +/- 3.7 years vs 10 +/- 0.9 years); their chronologic age was similar to that of the prepubertal GH-deficient children (9.6 +/- 2.1 years), but bone age was significantly more advanced (6.9 +/- 2.3 years). The mean height velocity of the prepubertal GH-deficient children (3.8 +/- 1.5 cm/yr) was lower than that of the precocious GH-deficient subjects (6.7 +/- 1.6 cm/yr) and the precocious GH-sufficient children (9.5 +/- 2.9 cm/yr). Baseline adult height prediction z scores were significantly lower in the precocious GH-deficient children (-3.7 +/- 1.0) than in either the precocious GH-sufficient children (-2.2 +/- 1.0) or the prepubertal GH-deficient subjects (-1.5 +/- 0.8). During therapy with gonadotropin releasing-hormone agonist, growth rates slowed to an average of 3.7 cm/yr in the precocious GH-deficient children but increased after the addition of GH to 7.4 cm during the first year of combination therapy. After 2 to 3 years of combination therapy, height predictions increased an average of 10 cm, compared with an increase of 2.8 cm in the precocious GH-sufficient group treated with gonadotropin releasing-hormone agonist alone. We conclude that combination treatment with gonadotropin releasing-hormone agonist and GH improves the height prognosis of children with coexistent true precocious puberty and GH deficiency, but falls short of achieving normal adult height potential.

Age Determination by Skeleton↗
PubMed1983

How many cases of true precocious puberty in girls are idiopathic?

Fifteen girls with true precocious puberty were examined by computerized tomography. In seven hypothalamic hamartomas were suspected. A pneumoencephalogram was performed in six cases (one patient refused), with the following results. In five, the radiological features were highly suggestive of tuber cinereum hamartoma. All of our patients with pubertal signs appearing before the age of 2 years and 80% of the girls with early menstruation were in the group with suspected hamartoma. The luteinizing hormone and follicle-stimulating hormone levels of these five girls were significantly higher than those observed in the other girls with idiopathic precocious puberty. We conclude that there is a high frequency of small hypothalamic masses (suspected hamartoma) in girls with true precocious puberty (33% of the patients in our group), that it is important to confirm the presence of the mass with pneumoencephalography, and that surgery for diagnostic and therapeutic purposes should be carefully considered, given the absence of any neurologic symptoms for a long time after the appearance of the first pubertal signs.

Child↗
PubMed1986

Intranasal nafarelin: an LH-RH analogue treatment of gonadotropin-dependent precocious puberty.

The agonistic analogues of luteinizing hormone releasing hormone decrease biochemical findings and clinical signs of gonadotropin-dependent precocious puberty. We tested a new analogue, nafarelin acetate, in 15 girls with gonadotropin-dependent precocious puberty. The hydrophobic nature and potency of this compound allow it to be administered by intranasal inhalation. Laboratory assessment of vaginal cytology, estradiol and urinary gonadotropin levels, and growth velocity revealed that nafarelin acetate 800 to 1200 micrograms/day diminished these values during a 6-month treatment period. These results suggest gonadotropin-dependent precocious puberty in girls can be treated with intranasal administration of nafarelin acetate.

Administration, Intranasal↗
PubMed1987

Puberty decreases insulin sensitivity.

Puberty is commonly associated with an increase in insulin requirement in patients with insulin-dependent diabetes. To investigate whether this pubertal increase in insulin requirement is confined to diabetic subjects, we examined insulin responses during oral glucose tolerance testing with glucose loads per unit weight (1.75 g/kg) or unit surface area (55 g/m2), and insulin sensitivity via euglycemic-hyperinsulinemic clamp in prepubertal and pubertal children without diabetes. Irrespective of glucose dose, glucose tolerance testing elicited a threefold greater insulin response, but equivalent euglycemia, in pubertal versus prepubertal children (P less than 0.05). As assessed by the clamp procedure, prepubertal children were approximately 30% more sensitive than their pubertal counterparts (P less than 0.01). Insulin sensitivity correlated inversely with body mass index (r = -0.49, P less than 0.02), serum dehydroepiandrosterone sulphate concentration (r = -0.57, P less than 0.01), and log somatomedin C/insulinlike growth factor I (r = -0.45, P less than 0.05). We conclude that puberty is associated with decreased sensitivity to insulin that normally is compensated for by increased insulin secretion. Thus, in patients with insulin-dependent diabetes, an approximately 30% increase in insulin dosage should be anticipated with the onset of puberty.

Adolescent↗
PubMed1988

Pelvic ultrasonography in girls with precocious puberty, congenital adrenal hyperplasia, obesity, or hirsutism.

Real-time ultrasonography of the pelvic organs was performed on 151 girls with various complete and incomplete forms of precocious puberty, 20 girls with congenital adrenal hyperplasia, 20 with hirsutism, 18 with obesity, and 133 age-matched normal girls. Uterine and ovarian volumes were calculated and the ovarian morphologic picture was classified as homogeneous, nonhomogeneous (less than three small cystic areas), microcystic (four or more small cystic areas less than 9 mm in diameter), follicular (at least one cystic area greater than 9 mm), and macrocystic (large cystic area greater than 20 mm). Ultrasound imaging allowed an easy distinction between true precocious puberty and premature thelarche or idiopathic premature adrenarche. It was also helpful in the diagnosis of transient sexual precocity, although in these cases the differential diagnosis of precocious puberty can be difficult. In postmenarcheal patients with congenital adrenal hyperplasia, ultrasound study showed a low uterine volume and, frequently, a macrocyst in the ovary. In hirsute girls and in a few obese patients, ovaries had an increased volume and a microcystic structure, similar to those in polycystic ovary syndrome. Pelvic ultrasonography can be useful not only in diagnosing disorders in sexual development but also for greater understanding of the pathogenesis of these and other disorders.

Adrenal Hyperplasia, Congenital↗
PubMed1989

Increased insulin secretion in puberty: a compensatory response to reductions in insulin sensitivity.

Recent studies have suggested that insulin action is reduced during puberty in normal children. To determine whether such resistance leads to excessive insulin secretion, we used the hyperglycemic clamp technique to produce a standard hyperglycemic stimulus (125 mg/dl above fasting levels for 120 minutes) in 9 preadolescent and 14 adolescent healthy children and in 14 normal adults. Fasting plasma insulin and C-peptide concentrations were higher in adolescents than in preadolescents and adults (p less than or equal to 0.02). Despite identical glucose increments during the glucose clamp procedure, both first- and second-phase plasma insulin and C-peptide responses were also markedly greater in adolescents than in preadolescents or adults (p less than 0.01 vs. other groups). Despite sharply increased insulin responses in adolescents, the amount of exogenous glucose required to maintain hyperglycemia was similar in all three groups. Insulin responses in the children were directly correlated with fasting plasma levels of insulin-like growth factor I (r = 0.60 to 0.70, p less than 0.01). We conclude that glucose-stimulated insulin secretion is normally increased during puberty, a response that may compensate for puberty-induced defects in insulin sensitivity.

Adolescent↗
PubMed1995

Precocious puberty in children with neurofibromatosis type 1.

We undertook a comprehensive study of children with neurofibromatosis type 1 (NF-1) cared for in a large multidisciplinary clinic to determine the prevalence of precocious puberty and its relationship to optic pathway tumors (OPTs). Precocious puberty was diagnosed in 7 of 219 children with NF-1 (5 boys and 2 girls) examined between Jan. 1, 1985, and April 20, 1993. All seven children had OPTs involving the optic chiasm; they represented 39% of children with NF-1 and chiasmal tumors (95% confidence interval, 17% to 64%). Eleven prepubertal children (aged 2 to 10 years) with NF-1 and OPTs, and age- and sex-matched NF-1 control subjects without OPTs, underwent luteinizing hormone-releasing hormone (LH-RH) stimulation tests. Two boys with OPTs had pubertal luteinizing hormone (LH) responses, and testosterone levels > 10 ng/dl. Basal LH levels were also elevated in these two boys when tested with a very sensitive immunochemiluminometric assay. None of the children without an OPT had either a pubertal response to LH-RH or an elevated basal LH level. We conclude that precocious puberty in children with NF-1 is found exclusively in those who have OPTs involving the optic chiasm; it is a common complication in those children. With the use of a highly sensitive LH assay, biochemical evidence of hypothalamic-pituitary-gonadal axis activation may be demonstrated, even without provocative testing.

Child↗
PubMed2001

A specific aromatase inhibitor and potential increase in adult height in boys with delayed puberty: a randomised controlled trial.

BACKGROUND: The role of oestrogens in the closure of growth plates in both sexes is unequivocal. We postulated that inhibition of oestrogen synthesis in boys with delayed puberty would delay maturation of the growth plates and ultimately result in increased adult height. METHODS: We did a randomised, double-blind, placebo-controlled study in which we treated boys with constitutional delay of puberty with testosterone and placebo, or testosterone and letrozole. Boys who decided to wait for the spontaneous progression of puberty without medical intervention composed the untreated group. FINDINGS: Letrozole effectively inhibited oestrogen synthesis and delayed bone maturation. Progression of bone maturation was slower in the letrozole group than in the placebo group. In 18 months, bone age had advanced 1.1 (SD 0.8) years in the untreated group and 1.7 (0.9) years in the group treated with testosterone and placebo, but only 0.9 (0.6) years in the letrozole group (p=0.03 between the treatment groups). Predicted adult height did not change significantly in the untreated group and in the placebo group, whereas in the group treated with letrozole the increase was 5.1 (3.7) cm (p=0.004). INTERPRETATIONS: Our findings suggest that if oestrogen action is inhibited in growing adolescents, adult height will increase. This finding provides a rationale for studies that aim to delay bone maturation in several growth disorders.

Adolescent↗
PubMed1981

Clinical value of adrenal androgen measurement in the diagnosis of delayed puberty.

Serum levels of the adrenal androgens dehydroepiandrosterone (DHA), dehydroepiandrosterone sulphate (DHAS), and androstenedione (A) were measured in 90 males (age range 14 1/2--26 years) presenting with delayed puberty to an adult endocrine clinic over a period of 3 years. The results show that adrenal androgen levels are significantly lower (p less than 0.0005) in subjects with growth-hormone (GH) deficiency than in patients with simple and constitutional delayed puberty and other, less common, conditions. By contrast, subjects with hypogonadotropic hypogonadism had significantly raised values (p less than 0.0005). On initial presentation DHA and DHAS measurements correctly identified all GH-deficient subjects and in addition DHAS measurements identified 89% of subjects with hypogonadotropic hypogonadism. It is suggested that measurement of serum levels of DHA and DHAS may assist greatly in the early diagnosis of conditions causing delayed puberty, and thus may prevent unnecessary delay in treatment.

Adolescent↗
PubMed1996

Epidermal nevus syndrome: association with central precocious puberty and woolly hair nevus.

The epidermal nevus syndrome is characterized by the association of epidermal nevi with abnormalities of the skin, skeletal system, central nervous system, eyes, and cardiovascular system, as well as with malignant conditions. We describe a 2-year-old girl with an extensive epidermal nevus involving the left side of the body (nevus unius lateris) and associated with a woolly hair nevus on the left parietal area of the scalp and multiple acquired melanocytic nevi. Idiopathic central precocious puberty characterized by premature breast and public hair development and advanced bone age developed at the age of 20 months. A sharp increase in serum gonadotropins after a luteinizing hormone releasing hormone (LHRH) stimulation test confirmed the presence of central precocious puberty. This is the third reported case of precocious puberty associated with the epidermal nevus syndrome.

Child, Preschool↗
PubMed1998

Androgen replacement in children with constitutional delay of puberty: the case for aggressive therapy.

Puberty describes the complex physiological transition between childhood and adulthood. Dramatic physical changes occur, most notably the development of secondary sexual characteristics and the pubertal growth spurt. During the adolescent growth spurt, growth velocity increases from pre-pubertal rates of 4-6 cm per year to as much as 10-15 cm per year. Accompanying the increase in gonadal steroids is an increase in amplitude of growth hormone secretory bursts. Evidence suggests that adequate growth hormone and gonadal steroids are both necessary for the attainment of a normal pubertal growth velocity, and the complex interplay between these two hormonal axes is under intense investigation. Delayed onset of puberty, or constitutional delay of growth and adolescence, is a common phenomenon presenting particularly in boys. Physiologically, it represents an extension of the normal pre-pubertal hypogonadotropic hypogonadal state. Without intervention, these children will spontaneously undergo puberty and often reach their genetic height potential, but their delay compared with that of their peers is often of concern to the children and their families. Recent evidence suggest long-term physiological benefits of early androgen replacement therapy in these boys, including maximizing attained bone mineral density. Androgen replacement therapy in male adolescents with constitutional delay of growth and adolescence is beneficial psychologically as well as physiologically and should be initiated promptly.

Adolescent↗
PubMed1999

Puberty in chronic renal failure.

Puberty is a period of transition characterized by a sequence of profound physical and psychological changes leading to full sexual maturity. This process is driven and orchestrated by the awakening of the gonadotropic hormone axis. Chronic renal failure and its treatment may interfere with the onset and progress of puberty by numerous mechanisms including endocrine, metabolic and neuropsychological abnormalities, and drug effects. On average, the onset of puberty is delayed by 2 years in children with chronic renal failure, even after successful transplantation. Moreover, pubertal height gain is only 50% of that observed in healthy children. In this report, we discuss the endocrine mechanisms underlying these alterations and highlight new therapeutical options for pubertal growth failure.

Female↗