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PubMed2004

[Personal observations of puberty in girls after unilateral ovariectomy].

The authors present the course of puberty in three girls after surgery because of hormonally active ovarian tumours diagnosed and operated at the age of 3, 6 and 9 years, respectively. In the youngest patient with folliculoma ovari chemotherapy was also given, and girl No. 3 with luteinic capsule was treated for one year with decapeptyl because idiopathic precocious puberty was diagnosed. At present all three girls are in good physical condition with age-adequate development and puberty.

Antineoplastic Agents↗
PubMed2004

Induction of puberty in hypogonadal children.

Puberty is the transitional period between childhood and adulthood when physical, sexual, and psychosocial maturation occurs. The onset of puberty is controlled by the gonadotropin-releasing hormone (GnRH) neuron and is triggered when inhibition of the neuron is lifted. Subsequently, GnRH induces secretion of other hormones, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which in turn stimulate the gonads. Concurrently, increases in estrogen levels in both boys and girls stimulate growth hormone (GH) and insulin-like growth factor-I (IGF-I) secretion, which are responsible for the pubertal growth spurt. In hypogonadal children, however, hypothalamic/pituitary defects or gonadal diseases preclude the production of these hormones, preventing the onset of puberty. Hormone replacement therapy with either estrogen or testosterone is a viable treatment option for hypogonadal children. These should be administered with consideration of sexual maturation rates, statural and bone growth rates, and occurrence of adverse effects. The merits and disadvantages of various hormone replacement therapies for girls and for boys are discussed.

Adolescent↗
PubMed2004

[Clinical study of subcutaneous administration of gonadotropin-releasing hormone agonist every six weeks in girls with idiopathic central precocious puberty].

OBJECTIVE: Gonadotropin-releasing hormone agonist (GnRHa) is widely used for the treatment of precocious puberty, but there was no identical regime for the dosage and the interval of administration. The aim of this study was to assess the feasibility of subcutaneous administration of Triptorelin with a prolonged interval (six weeks) for the suppression of pituitary-gonadal axis and clinical signs in girls with idiopathic central precocious puberty (ICPP). METHODS: Forty-six girls with ICPP were enrolled in this trial and were divided into two groups at random, with 26 patients in group A and 20 in group B. There were no significantly differences in chronological age, height, weight, age at clinical onset of puberty and bone age between the two groups before treatment. Triptorelin (Decapeptyl, 3.75 mg) was administered subcutaneously (SC) at 6 weeks intervals in group A or intramuscularly (IM) at 4 weeks intervals in group B. Both forms were given for more than 12 months consecutively. During the period of treatment, the clinical parameters including height, weight, pubertal stage, bone age, uterine volume and ovarian size were documented. The serum levels of luteinizing hormone (LH), follicle stimulating hormone (FSH) and estradiol (E(2)) were monitored using immunoenzymometric assay. RESULTS: Both treatment regimes can completely suppressed the pituitary-gonadal axis. The clinical signs of pubertal development regressed or stabilized in all patients. Breast developments, as reflected by Tanner staging, were regressed. Uterine volume decreased after treatment, however, this decrease did not reach statistical significance. Mean ovarian volume did not change significantly during treatment. The height velocity was significantly decreased from a pretreatment value of 6.3 +/- 1.4 cm/year to 5.8 +/- 1.2 cm/year in group A and 6.7 +/- 1.3 cm/year to 5.4 +/- 1.0 cm/year in group B, respectively. The rate of skeletal maturation was reduced significantly during treatment. The ratio of bone age/chronological age was 1.2 +/- 0.2 or 1.3 +/- 0.3 at the onset of therapy and decreased significantly after the treatment to 0.7 +/- 0.2 or 0.9 +/- 0.1, respectively. The predicted adult height increased significantly and progressively during therapy. The levels of serum LH, FSH and E(2) were returned to the prepubertal condition after 6 - 8 weeks treatment and remained suppressed for the duration of treatment. No significantly side effects of therapy were noted. The most common adverse event during SC treatment was that a non-irritating, 1 cm in diameter mass can be palpated at the site of subcutaneous injection in the abdominal wall of group A patients. It gradually decreased in size, and disappeared after 8 - 12 weeks. Two girls had minimal withdrawal virginal bleeding episodes after the first injection. CONCLUSION: Both IM and SC triptorelin administration were clinically effective. They can induce profound suppression of hypothalamic-pituitary-gonadal axis while stabilizing height velocity, slowing bone maturation and increasing predicted adult height. These results suggest that subcutaneous injection of triptorelin in 6 weeks intervals at a dosage of 3.75 mg was a safe and acceptable regime for ICPP with good efficacy.

Body Height↗
PubMed2005

[Treatment of central precocious puberty with Gonadotropin-Releasing Hormone agonist (triptorelin) in girls: breast development, skeletal maturation, height and weight evolution during and after treatment].

Central precocious puberty (CPP) is treated with GnRH analogues to stabilize secondary sexual characteristics and to prevent loss of final height (FH) due to accelerated bone maturation. However, some studies suggest that FH is not always improved and that treatment may induce excessive weight gain. We analysed data from 19 girls treated for CPP with monthly injections of 3.75 mg triptorelin. Pubertal development, bone age, height, weight and body mass index (BMI) were evaluated at start (chronological age: 7.8 +/- 1.8 yrs, mean +/- SD), at the end of treatment (10.6 +/- 1.1 yrs) and at FH (14.9 +/- 2.5 yrs). At start of treatment, breast (B) development was B3 (from 2 to 4), bone age 10.6 +/- 1.7 yrs, height 2.1 +/- 1.1 SDS and BMI 1.3 +/- 0.8 SDS. Treatment stabilized or reduced breast development and decreased bone maturation. Final height was 162.3 +/- 6.6 cm (0.0 +/- 1.1 SDS) and was comparable to predicted adult height at the start of treatment and to corrected mid-parental height. BMI SDS at the start, the end of treatment and at final evaluation were 1.3 +/- 0.8, 1.6 +/- 0.8 and 1.4 +/- 0.9 SDS. In conclusion, in our girls with central precocious puberty, treatment with GnRH agonist stabilized or decreased breast development and stabilized bone maturation, but did not increase neither final height nor weight. Aspects other than height should also be taken into account when considering treatment of children with precocious puberty.

Body Height↗
PubMed2005

Precocious puberty with congenital hypothyroidism.

Precocious puberty associated with profound hypothyroidism is a rare condition. It is usually characterized by breast development, vaginal bleeding, lack of pubic hair and delayed bone age. Multicystic ovaries in profound hypothyroid patients with precocious puberty have been rarely described. Vaginal bleeding in adolescent girls should be considered as a clinical significance particularly when it is prolonged or heavy, whereas vaginal bleeding in younger girls, regardless of its duration and quantity is always of clinical importance. Bleeding in such patients could be caused by local causes such as vulvar or vaginal lesions, or it could be from the endometrium, which is usually a sign of systemic hormonal disturbance [1]. In this report a rare case of vaginal bleeding, large, multicystic ovaries, precocious puberty and delayed bone age in a 7 years old girl with profound hypothyroidism is described.

Breast↗
PubMed2005

Hypogonadism in adolescent females: new insights and rationale supporting the use of physiologic regimens to induce puberty.

Puberty in girls begins with nocturnal pulsatile gonadotropin releasing hormone (GnRH) secretion which increases gradually over a 4 year period and occurs throughout the day. Pulsatile GnRH secretion stimulates pituitary luteinizing hormone (LH) and follicle stimulating hormone (FSH) which induces gonadal steroid secretion, ovulation and oogenesis. Over the past decade, naturally occurring genetic mutations have been identified in a number of genes that impact the onset and progression of puberty and continued progress in this area will lead to earlier diagnosis of hypogonadotropic hypogonadism (HypoH) and potentially improved therapeutic options. Data are accumulating to support the use of more physiological hormone regimens to induce puberty. In addition, our better understanding of how estrogen interacts with the growth hormone - insulin-like growth factor-1 (GH-IGF-1) axis and of differential effects of oral versus non-oral estrogen on various biological parameters have important therapeutic implications for the management of hypogonadal adolescent girls. These implications will be addressed.

Adolescent↗
PubMed2005

Growth hormone / insulin-like growth factor-1 axis during puberty.

Puberty is a dynamic, transitional period of life which is characterized by the acquisition of secondary sexual characteristics leading to the development of fertility. Puberty is accompanied by sexually dimorphic changes in linear growth, body proportions and body composition. The pubertal growth spurt is influenced by a number of factors such as hormones, nutrition, physical activity and general health, acting mostly in concert in order to modify a genetic potential for growth. Growth hormone (GH) is traditionally considered to be the main regulator of growth. During puberty, elevated sex steroid concentrations (especially oestrogens) stimulate GH production, leading to an activation of the whole GH/Insulinlike growth factor-1 (IGF-1) axis. This activation is mostly characterized by an increase in the amplitude of GH pulses rather than an increase in frequency or in duration. Interactions between GH and sex steroids (especially androgens) express an anabolic effect on muscle mass, bone mineralization and body proportion which constitutes the male and the female adult body composition.

Carrier Proteins↗
PubMed1991

The contributions of growth and puberty to peak bone mass.

Lumbar spine bone mass was measured by dual photon absorptiometry (DPA) in 236 subjects aged between 3 and 30 years. Expected values of bone mineral density (BMD) and bone mass (BMC) for the lumbar vertebrae L2 to L4 were derived as a function of age, by non-linear regression analysis. The selected regression equation was the sum of two logistic expressions, one of which was assigned to growth at the time of puberty and the other to the slower long term component of growth. Growth during puberty contributed about 50% of peak bone mass in females, while in males this contribution was closer to 15%. No increase was found in lumbar spine bone mass in females after puberty.

Absorptiometry, Photon↗
PubMed1991

[Undulating course of precocious puberty].

The normal course of precocious puberty is progredient resulting eventually in full sexual maturation. In few cases a transient form of the disease has been recorded, characterized by a temporary appearance of signs of sexual maturation. We report on a female patient with an undulating course of the disorder: after precocious initiation of puberty, a temporary interruption and subsequent resumption of sexual maturation occurred. Presently, the patient is successfully treated with an LHRH-analogon. Within the framework of this case problems in diagnosis and treatment of precocious puberty are being discussed.

Age Determination by Skeleton↗
PubMed1990

[The role of pulsatile LHRH therapy in women: the treatment of delayed puberty and of hypothalamic amenorrhea].

The importance of gonadotropin pulsatility for normal hypothalamic-pituitary-gonadal axis function is well known. The most important aim of exogenous LHRH administration, given in females with delayed puberty or hypothalamic amenorrhea is to physiologically restore LH pulsatility to a more physiologic way as possible. In fact, a variable degree of LHRH endogenous defect is present in these conditions. Moreover, exogenous LHRH pulsatile administration is able to restore normal pubertal development until menarche appears and normal ovulatory cycles occur and pregnancy is induced. We reported our experience and review the literature regarding the importance and use of LHRH pulsatile therapy in delayed puberty and hypothalamic amenorrhea. We have also evaluated the data for various administration routes, the choice of patients, response to therapy and the possible diagnostic use of pulsatile LHRH with regard to the differential diagnosis of delayed puberty.

Adolescent↗
PubMed1990

[Growth and puberty in 7-to-16-year-old female gymnasts: a prospective study].

The female members of two different gym squads who where subject to hard training (12 to 15 hours a week), were investigated in regard to their growth parameters shortly after the beginning of intensive training and at yearly intervals thereafter. 12 of the initial 25 girls gave up training before reaching their 14th year. Only data compiled during the training period were included in the study. At the beginning of training, the gymnasts were comparable to the standard population (Zurich Longitudinal Study of Growth and Development) in regard to height and bone age: their weight was slightly subaverage. Height, growth rate, bone age, weight development and skinfold thickness remained clearly below standard values during the years of training. Due to a prolonged growth spurt during puberty, the final height and body weight were again comparable to standard values. Thelarche, pubarche and menarche were also significantly delayed; thelarche and menarche did occur, though, when the same body measurements (height, weight) as compared to the standard population were reached. FH, FSH and estradiol showed the puberty rise only after the 14th year, i.e. with considerable delay. When separately analyzing the data of the girls who gave up training before completing their 14th year, preexisting greater body measurements (including bone age) as well as more rapid development during the first years of training were found. Thus, the observed physical growth retardation is partly due to predisposition in the form of a constitutional late puberty, and is partly caused by the intensive training. A permanent physical developmental loss was not observed.

Adolescent↗
PubMedDate not supplied

[Growth of girls and boys at puberty].

Growth at puberty varies according to age and individual maturity. Changes in height and weight of girls (aged 10 to 16 years) and boys (aged 11 to 17 years) which participate in a follow-up study at northern metropolitan Santiago, Chile, are described. Sexual maturity seems more determinant than chronological age on weight and height at puberty. For instance height of the whole sample of boys from 12 to 15.5 years of age ranged from 141 to 164 cm in contrast to 147 to 160 for those of the same age range but in the third stage of public hair development (Tanner). Sexual maturity should be taken into account for appropriate growth evaluation at puberty.

Adolescent↗
PubMed1989

Physiology of puberty.

Adolescence represents the period of important somatic changes which lead to sexual maturation, pubertal growth and active functions of reproduction. Mean ages of onset of puberty are 10.9 and 11.2 in girls and boys respectively. Menarche occurs at a mean age of 13.4 yr and may be related to a critical weight. In boys, testicular growth above 4 cm2 or 4 ml is the first clinical sign of gonadal pubertal maturation. In girls, the first sign is the budding of the breast. At onset of puberty, the hypothalamus after a "quiescent" period resumes a marked pulsatile secretion of gonadotrophin-releasing hormone, leading to an increased secretion of pituitary gonadotropins which in turn stimulate the gonadal functions, i.e. the secretion of testosterone or estradiol and maturation of the spermatogenesis or the ovarian follicle. Neuroendocrine factors which probably control the onset of puberty are numerous: cerebral adrenergic and/or dopamine neurotransmitters, endogenous opioids, melatonin from the pineal gland. Gonadal maturation (gonadarche) is preceded in the infant by a post-natal surge of luteinizing hormone and at age 7 to 8 yr by an adrenal maturation (adrenarche).

Adolescent↗
PubMed1989

Polymalformative syndromes and puberty.

Polymalformative syndromes may involve an alteration of the two pubertal components: sexual maturation and pubertal growth spurt. An absence of pubertal development, generally without changing of final height, or an advance of puberty, with reduction of adult height are possible in some syndromes. Moreover, a normal pubertal evolution, with lack of pubertal growth spurt, is the result in bone growth anomalies. Puberty increases bone strength, in some conditions in which it is reduced, and finally this period of rapid growth may cause an alteration of structure and bone segments. A series of examples on correlations between polymalformative syndromes and puberty is presented.

Abnormalities, Multiple↗
PubMed1985

[Puberty and growth development in patients with a 21-hydroxylase defect].

Twenty six females suffering from congenital adrenal hyperplasia due to 21-hydroxylase-deficiency with and without salt wasting were evaluated to determine their growth patterns with special regard to their pubertal growth spurt. 17 patients have been substituted with hydrocortisone 20-25 mg/m2 and if necessary with 9 alpha-fluoro-cortisol 0.025-0.15 mg (group 1), 9 patients have got an additional cyproterone-acetate-therapy during their pubertal development (group 2). Group 1: A pubertal growth spurt was found in 14 females (82.4%) with a peak height velocity of 6.2 +/- 1.6 (SD) cm/yr. At the beginning of puberty the early treated girls showed a progressing retardation of bone age. Therefore the peak height velocity based on advancing bone age was elevated up to 8.7 +/- 1.4 (SD) cm/yr bone age (p = 0.01). Salt wasting (n = 10) did not seem to influence the pubertal growth velocity and the pubertal growth spurt (p = 0.1, p greater than 0.1), but the growth until cessation which was found to be markedly decreased (p less than 0.1). Group 2: Cyproterone-acetate suppressed symptoms of puberty but did not extinguish growth spurt. During 6.3 +/- 1.3 (SD) yrs of treatment bone age advanced only 4.2 +/- 0.7 (SD) yrs. However, in this period height increased by 20.8 +/- 6.4 (SD) cm which corresponds to a mean height velocity of 3.3 +/- 0.8 (SD) cm/yr, and 4.9 +/- 0.8 (SD) cm/yr bone age. Furthermore at puberty peak height velocity results in 4.5 +/- 0.7 (SD) cm/yr and in 10.4 +/- 4.6 (SD) cm/yr bone age.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

[Precocious puberty and ovarian follicular cysts].

Ovarian follicular cysts have been detected by ultrasound in 2 to 8 years old girls with precocious puberty, central puberty (2 cases), transient precocity (1 case) or premature menarche (1 case). Complete regression of the cysts was either spontaneous (1 case) or due to suppressive therapy. The mechanisms of precocious puberty with follicular cysts, dependent or independent of gonadotropins, and their spontaneous evolution guide both the management and the therapy with LH-RH analogues and/or aromatase inhibitors.

Child↗
PubMed1986

[Role of pelvic ultrasonography in the diagnosis, therapeutic indications and surveillance of central precocious puberty].

The use of pelvic ultrasonography was evaluated as a diagnostic and follow-up tool in girls with precocious puberty. Before treatment 23 of 33 patients with central precocious puberty presented an increased size of the uterus. In 10 cases with prepubertal size of the uterus, the precocious puberty was only beginning or of mild severity. During treatment with a LHRH analogue, changes in uterine size were slow in spite of a satisfactory and rapid control of estrogen secretion. At onset of treatment, transient ovarian cysts were seen in 2 patients. In our experience, pelvic ultrasonography did not provide significant information on the control of the disease by LHRH analogue therapy. Of 16 girls with presumed premature thelarche, 3 presented signs of estrogenic stimulation of the uterus. It remains a useful technique to rule out the presence of ovarian cysts or tumors at time of diagnosis.

Buserelin↗
PubMed1977

Plasma LH and FSH response to LRH and plasma testosterone levels in boys with irregular puberty.

Nineteen boys with irregular puberty (IP), defined as a discrepancy of two or more pubertal stages between the criteria for genitalia and that for pubic hair, were subjected to a standard LRH test (50 microng/m2, iv) and the response of gonadotrophins as well as the basal levels of plasma testosterone, LH and FSH were compared to those of boys with normal, regular puberty. When the results were plotted against the pubertal stage for genitalia (Pg), it was found that in the boys with IP the basal plasma testosterone levels were lower and the response of plasma LH to LRH stimulation lesser than in the controls. However, when these parameters were plotted against the pubertal stage for pubic hair (Ph) it was found, that in the boys with IP the plasma testosterone levels were significantly higher and the response of both LH and FSH stimulation greater than in the control group. It was concluded that irregular puberty in boys may be regarded as a normal variation. The delayed development of sexual hair and penile length, and retarded pubertal growth spurt and bone age maturation seen in these boys, with normal testicular development, may be explained by a temporary reduced peripheral sensitivity to androgens and a compensatory effort by the pituitary, manifested in increased secretion of LH and testosterone, relatively to their pubertal stage for pubic hair.

Adolescent↗