Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PUBERTY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 631 records · Page 35Linked to original sources
PubMed1998

Exercise before puberty may confer residual benefits in bone density in adulthood: studies in active prepubertal and retired female gymnasts.

Exercise during growth may contribute to the prevention of osteoporosis by increasing peak bone mineral density (BMD). However, exercise during puberty may be associated with primary amenorrhea and low peak BMD, while exercise after puberty may be associated with secondary amenorrhea and bone loss. As growth before puberty is relatively sex hormone independent, are the prepubertal years the time during which exercise results in higher BMD? Are any benefits retained in adulthood? We measured areal BMD (g/cm2) by dual-energy X-ray absorptiometry in 45 active prepubertal female gymnasts aged 10.4 +/- 0.3 years (mean +/- SEM), 36 retired female gymnasts aged 25.0 +/- 0.9 years, and 50 controls. The results were expressed as a standardized deviation (SD) or Z score adjusted for bone age in prepubertal gymnasts and chronological age in retired gymnasts. In the cross-sectional analyses, areal BMD in the active prepubertal gymnasts was 0.7-1.9 SD higher at the weight-bearing sites than the predicted mean in controls (p < 0.01). The Z scores increased as the duration of training increased (r = 0.32-0.48, p ranging between <0.04 and <0.002). During 12 months, the increase in areal BMD (g/cm2/year) of the total body, spine, and legs in the active prepubertal gymnasts was 30-85% greater than in prepubertal controls (all p < 0.05). In the retired gymnasts, the areal BMD was 0.5-1.5 SD higher than the predicted mean in controls at all sites, except the skull (p ranging between <0.06 and <0.0001). There was no diminution across the 20 years since retirement (mean 8 +/- 1 years), despite the lower frequency and intensity of exercise. The prepubertal years are likely to be an opportune time for exercise to increase bone density. As residual benefits are maintained into adulthood, exercise before puberty may reduce fracture risk after menopause.

Adolescent↗
PubMedDate not supplied

Basal and gonadotropin-releasing hormone-releasable serum follicle-stimulating hormone charge isoform distribution and in vitro biological-to-immunological ratio in male puberty.

Follicle-stimulating hormone is synthesized and secreted as a mixture of heterogeneous isoforms that differ from each other in carbohydrate structure, biological potency, and plasma half-life. The relative abundance of the FSH isoforms will depend on the endocrine status of the donor at the time of sample collection. In the present study, we attempted to define the impact of the changing endocrine milieu characteristic of male puberty on the charge heterogeneity and plasma half-life of the serum FSH isoforms released under endogenous and exogenous GnRH drives, and examined whether such a varying hormone milieu modifies the capability of the circulating hormone to trigger intracellular signal transduction at the human FSH receptor level. Forty healthy male subjects at Tanner stages (Ts) 1 to 5 were sampled at 10 min intervals for 10 h. Serum from successive samples collected across 2-4 h intervals containing FSH released under basal, low-dose (10 microg), and high-dose (90 microg) exogenous GnRH-stimulated conditions was subjected to preparative chromatofocusing and tested for bioactivity employing a homologous cell in vitro bioassay system. Deconvolution analysis was applied to estimate the apparent endogenous FSH plasma half-life in samples obtained after administration of low-dose exogenous GnRH. Under all conditions studied, serum FSH charge isoforms were distributed along a pH range of 7.0 to less than 3.0. Comparisons across the different Tanner stages revealed a significant and selective increase in the ratio of FSH isoforms with elution pH values <4.50 relative to those with values >/=4.50 at Ts-2. At Ts-3, this ratio returned to that present at Ts-1, to decline thereafter during the ensuing pubertal stages. Serum bioactive FSH concentrations progressively increased (from 3.72 +/- 1.3 to 16.2 +/- 5.3 IU/L) throughout puberty, and in all conditions bioactive FSH concentrations exceeded those detected by a specific radioimmunoassay. The biological to immunological (B:I) FSH ratio at baseline was significantly (p < 0.05) lower at Ts-1 and Ts-2 (1.33 +/- 0.30 and 1.62 +/- 0.34, respectively) than at more advanced stages of pubertal development (2.28 +/- 0.20, 2.96 +/- 0.38, and 2.77 +/- 0.63 at Ts-3-, 4-, and -5, respectively) Similar differences were detected in samples containing FSH molecules released after low- and high-dose GnRH administration. The apparent endogenous FSH half-life of the deconvolved GnRH-induced FSH pulses was similar in the five study groups. These results demonstrate that the transition from infancy to sexual maturity in men is accompanied by qualitative changes in the circulating FSH isoform mixture. Although the changes in FSH glycosylation occurring throughout puberty are not of sufficient magnitude to alter the survival of the gonadotropin in circulation, they allow preferential secretion of bioactive FSH. The enrichment of the circulating mix of FSH isoforms with highly bioactive variants throughout spontaneous puberty may potentially favor the development of spermatogenesis and acquisition of reproductive competence.

Adolescent↗
PubMed2000

Genetic and endocrinological evaluations of three 46,XX patients with congenital lipoid adrenal hyperplasia previously reported as having presented spontaneous puberty.

Congenital lipoid adrenal hyperplasia (CLAH) is an autosomal recessive disorder characterized by impaired synthesis of adrenal and gonadal steroids. It was demonstrated that loss-of-function mutations in the steroidogenic acute regulatory protein (StAR) gene cause CLAH and that 46,XX patients with CLAH develop spontaneous puberty. We had reported that three 46,XX patients with CLAH had presented spontaneous puberty and one of the patients had developed life-threatening ovarian cysts, before the etiology of CLAH had been clarified. In the present study, we analyzed their StAR gene and demonstrated mutations. Endocrinological examinations of the patients revealed that serum LH and FSH levels and their responses to the LHRH stimulation were not exaggerated before the onset of puberty. Serum LH levels and its response to LHRH were increased during puberty, whereas serum FSH levels remained within the normal range. Serum estradiol increased after the administration of human menopausal gonadotropins in the pubertal patient, suggesting that the ovary might have another system than StAR to facilitate cholesterol transport into the mitochondria. Although the patients had menstrual cycles, they remained anovulatory, and the resultant increased secretion of LH was speculated to be responsible for the development of ovarian cysts.

Adrenal Hyperplasia, Congenital↗
PubMed1984

Puberty due to ectopic HCG production in a girl with suprasellar ectopic pinealoma associated with panhypopituitarism.

A 13.5-year-old girl who developed puberty due to HCG production by suprasellar ectopic pinealoma was reported. This girl appeared to be in a state of precocious puberty at the age of 5 when ectopic pinealoma was first diagnosed. Her breasts started to develop at 13 years of age in spite of hypopituitarism. Plasma LH was found to increase for several months and gave rise to suspicion of the recurrence of the tumor, which was confirmed by the detection of HCG in plasma and CSF. Precocious puberty or puberty can be a characteristic endocrinological manifestation of an HCG producing tumor not only in boys but also in girls. The measurement of plasma HCG (or LH) can be a useful tumor marker in following the clinical course of an HCG producing tumor.

Adolescent↗
PubMedDate not supplied

Sonographic appearance of ovaries and gonadotropin secretions as prognostic tools of spontaneous puberty in girls with Turner's syndrome.

We evaluated the possibility of anticipating spontaneous puberty in peripubertal Turner girls, in order to plan substitutive estrogen treatment. In the 24 patients studied, spontaneous puberty was seen in 4/11 girls with 45 XO karyotype, 5/5 with mosaicisms, 1 out of 2 with structural aberrations of the X chromosome and 0 out of 6 with Xq isochromosomes. When considering sonographic findings, the 6 girls with normal ovaries and 4/9 of those with intermediate ovarian appearance showed spontaneous puberty; the remaining 5 with intermediate ovaries and 9 with streak gonads did not undergo spontaneous puberty. Gonadotropin secretion was normal in girls with normal ovaries, moderately elevated in patients with intermediate ovarian appearance, and very high in those with streak gonads. The prognostic value of sonography and gonadotropins is particularly important in girls with intermediate ovaries. Therefore these evaluations should be performed at peripubertal age in patients with Turner's syndrome to elucidate the degree of ovarian insufficiency.

Child↗
PubMedDate not supplied

Precocious puberty in three boys with Sanfilippo A (mucopolysaccharidosis III A).

Three boys with mucopolysaccharidosis type III A (Sanfilippo) entered puberty at the ages of 5.9, 6.6 and 9.6 years. The diagnosis of central precocious puberty (GnRH-dependent) was established on the basis of pubertal levels of basal and GnRH-stimulated gonadotropins, LH and FSH. All the patients were tall from early infancy, but there was no acceleration of growth velocity or bone maturation despite advanced pubertal stage and high testosterone levels. Computerized tomography of the brain showed changes which are characteristic for Sanfilippo. This is the first time that precocious puberty has been described in Sanfilippo patients. The question of whether the precocious puberty in our Sanfilippo patients is a coincidence or is related in some way remains open.

Brain↗
PubMedDate not supplied

Growth, puberty and endocrine function in beta-thalassaemia major.

Although delay in onset of puberty is a common cause of growth failure in adolescent thalassaemic patients, growth retardation could also be due to iron overload, the toxic effects of desferrioxamine, or the development of other endocrinopathies such as GH insufficiency or primary hypothyroidism. Abnormal body proportions with truncal shortening are commonly seen and could be due to the disease itself, iron toxicity, delay in puberty or the toxic effects of desferrioxamine. The absence of a pubertal growth spurt during spontaneous or induced puberty is detrimental to the achievement of a normal final adult height. Low serum IGF-I and normal GH reserve in short thalassaemic children imply that a state of relative GH resistance exists. The rise in IGF-I and improvement in growth with GH therapy suggest that this GH resistance is only partial. Although the results of short-term GH therapy are encouraging, the impact of treatment on final height of non-GH deficient short thalassaemic children remains uncertain. Multiple endocrinopathies, including hypogonadism, hypothyroidism and diabetes mellitus, occur mainly in older patients who tend to have high serum ferritin levels. Prognosis for survival is greatly improved if the serum ferritin is kept below 2000 micrograms/l by regular chelation. Chelation therapy initiated early before the accumulation of a significant iron burden or dosages of desferrioxamine in excess of 50 mg/kg/day should be avoided. Serum ferritin should be checked regularly and the "toxicity index" should be used to monitor chelation therapy. In cases of delayed puberty, sexual development should be induced at an appropriate age.

Adolescent↗
PubMedDate not supplied

Bone age progression during five years of substitutive therapy for the induction of puberty in thalassemic girls--effects on height and sitting height.

UNLABELLED: It is known that in thalassemic patients there is a disproportion between lower and upper segments whose causes have not yet been identified. We evaluated whether the administration of estrogens to induce puberty in hypogonadic thalassemic girls caused an inappropriate acceleration of bone maturation and whether this had a negative influence on final and sitting height. MATERIALS AND METHODS: Twelve thalassemic patients with spontaneous puberty (Group A) and seven patients with hypogonadism (Group B) were studied. The mutations of the beta gene were identified by DNA analysis. We took into account four observations, ranging from the onset of spontaneous puberty in group A or the start of substitutive therapy in group B, to 5 years later. At each observation we considered: chronological age (CA), bone age (BA), height (Ht) expressed in cm and as standard deviation score (HtSDS) calculated with respect to CA (HtSDSCA) and BA (HtSDSBA), growth spurt, sitting height, expressed as SDS (SH-SDS), and height gain (HG). The delta BA and delta CA were calculated between the first and the final observation values to evaluate the bone age acceleration (delta BA/delta CA). RESULTS: No acceleration of BA was noted. delta BA/delta CA was 0.98 +/- 0.1 in group A and 0.89 +/- 0.1 in group B (p > 0.05). All patients in group B had the most severe form (beta degree/beta degree) of thalassemia. During the final observation, SH-SDS was -1.43 +/- 1.2 and -2.9 +/- 0.6 in group A and B respectively (p < 0.002), while no difference between the two groups for HtSDSCA and HtSDSBA was observed. HG was greater in group A than in group B (17.7 +/- 5.4 cm vs 10.8 +/- 5.2 cm) (p < 0.002), such as the spurt 8.6 +/- 1.4 cm (group A) and 6.1 +/- 2.6 cm (group B) (p < 0.05). CONCLUSIONS: Girls with hypogonadism did not show an inappropriate acceleration of BA, as they reached near final height similar to girls with spontaneous puberty. The auxological parameters showed a more severe body disproportion with the prevalence of the lower segment in the hypogonadic girls. This could be explained by a higher degree of bone marrow hyperplasia related to the most severe form of thalassemia and a higher blood consumption. As a consequence, damage at the vertebral level might determine an inability of the bone tissue to respond to estrogens. We suggest beginning estrogen therapy earlier in order to obtain better truncal growth.

Adolescent↗
PubMed2000

Hypothalamic hamartoma as a cause of precocious puberty in neurofibromatosis type 1: patient report.

Precocious puberty resulting from hypothalamic hamartoma is well known. Neurofibromatosis type 1 can also present with precocious puberty. However, hypothalamic hamartoma as the cause of precocious puberty in patients with neurofibromatosis type 1 has never been described in the literature. This rare occurrence of these two together in a patient with precocious puberty is reported.

Adult↗
PubMed2000

Etiology and age incidence of precocious puberty in girls: a multicentric study.

We review the etiology and age incidence of precocious puberty in 438 girls examined between 1988-1998; 428 (97.7%) had central precocious puberty (CPP), the remaining 10 (2.3%) gonadotropin-independent precocious puberty (GIPP) of ovarian origin. The majority of CPP girls (59.6%) were aged between 7-7.9 yr, 22.4% were 6 year olds, and only 18% were under 6 years old. Cranial CT and/or MRI performed in 304/428 girls, showed neurogenic abnormalities in 56/304 (18.4%) CPP girls; 30 (9.9%) were due to previously diagnosed intracranial abnormalities and the remaining 26 (8.5%) were detected at the diagnosis of CPP. The frequency of neurogenic CPP tended to be higher in girls under 4 years of age while the frequency of idiopathic CPP tended to be higher in girls aged between 7-7.9 years, but no statistically significant differences were found. Interestingly, some CNS anomalies either of tumoral or congenital origin were detected at presentation in 7% of the girls aged over 7 years. Other related or coincidental clinical anomalies, mainly due to genetic diseases, were observed in 22/304 (7.2%) patients. History of precocious maternal menarche was found in 12/304 (4%) girls. In conclusion, idiopathic CPP was observed in 74% of the girls in this study. Neurogenic anomalies or other coincidental or related clinical findings were observed in the remaining 26%. The increased frequency of idiopathic CPP in girls aged over 7 years may suggest an early, but otherwise normal onset of puberty in many of these girls as a consequence of the trend towards earlier maturation. Nonetheless, the finding of CNS anomalies also in the older patients, raises the question of whether these patients should undergo a complete diagnostic work-up.

Abnormalities, Multiple↗
PubMed2000

Experience with cyproterone acetate in the treatment of precocious puberty.

The authors review their experience (1967-present) in the use of cyproterone acetate (CPA) in precocious puberty. CPA was found effective in persistently suppressing pituitary gonadotropic secretion when administered orally at a dose of 50 mg b.i.d. (70-100 mg/d). After the introduction of gonadotropic analogues (GnRHa) for treatment of central precocious puberty, short term use of CPA was found useful to counteract the initial stimulatory effect of the GnRHa as well as an adjunct drug in case of very active adrenarche causing advanced bone age during GnRHa treatment. The final heights of girls treated with CPA and girls treated with D-Trp6-LHRH were found comparable: 157.8+/-5.1 cm vs 159.6+/-6.3 cm, respectively. The main adverse effects were occasional fatigue due to partial adrenal insufficiency with CPA and gynecomastia in a few boys. Liver function tests were normal in all patients with the exception of one boy with severe hypothalamic disease, including precocious puberty, who developed liver cirrhosis 3 years after stopping CPA following 5 years treatment. Other indications for CPA treatment during childhood and adolescence, such as fast puberty, congenital adrenal hyperplasia and acne, are also mentioned.

Body Height↗
PubMed2000

Precocious puberty in immigrant children: indications for treatment.

Immigration from developing countries to Europe has greatly increased during the last few years. Very little information is available on children who immigrated with their biological family, thus this paper deals only with children immigrating by adoption. In recent years some studies have shown an increased incidence of precocious puberty among adopted children, but information on this issue is scanty. Several hypotheses have been put forward to explain precocious puberty in adopted children, including nutritional, ethnic and/or emotional factors. Untreated precocious puberty is associated with short stature and has social and psychological consequences in addition to those related to adoption. Therefore, indications for therapy need to be carefully planned. In adopted children age estimation is a possible source of error in timing of puberty as date of birth is often missing or inaccurate. Thus each child must be carefully evaluated.

Adoption↗
PubMed2000

Neurofibromatosis type 1 and precocious puberty.

Since neurofibromatosis type 1 (NF1) is a well known cause of precocious puberty (PP), we reviewed 412 NF1 pediatric patients to evaluate the prevalence of PP, the association with optic pathway tumors (OPT), and other clinical, auxological and hormonal data. Thirty-one of 412 patients had OPT (7.5%), 10/412 PP (2.4%), and in seven of these PP was associated with OPT (7/31, 22.6%). OPT in patients with PP involved the chiasm in four patients, and the optic nerves alone in three patients. The age at the onset of puberty (or better at diagnosis) ranged from 5.2 to 7.5 yr in girls (n=6) and from 7.9 to 8.9 yr in boys (n=4). LHRH agonist therapy was used in only three children because in the others the predicted height at diagnosis was good, treatment was refused or the patients were referred to us too late. The three treated patients attained a final height within the familial range. In the untreated patients the progression of puberty was not too rapid and final height was slightly below the genetic target in four patients; however, three patients had a final height markedly below the familial range. In conclusion, the prevalence of PP is increased in children with NF1, and frequently but not exclusively is associated with OPT. Moreover, sexual precocity does not seem to be necessarily bound to chiasmatic OPT. Treatment seems to be useful in the children with younger age at the onset of puberty or with a progressive decline in predicted final height.

Adolescent↗
PubMed2004

Precocious, early and fast puberty in males with Chiari I malformation.

Type I Chiari malformation is a disorder characterized by a displacement of the cerebellar tonsils through the foramen magnum into the upper cervical spinal canal and, contrary to type II Arnold-Chiari malformation, without the presence of myelomeningocele. As described in the literature, patients suffering from Arnold-Chiari malformation with myelomeningocele can frequently present with precocious puberty, whereas only one report shows an association between Chiari I malformation and early puberty. We describe three young males--8.8, 9.4 and 10.4 years old--who were diagnosed with precocious, early and fast puberty associated with type I Chiari malformation. In patients 2 and 3, the reason for diagnostic management recommendation was a rapid progression of pubertal development over one year. None of the patients manifested hypophyseal-hypothalamic axis dysfunction other than sexual precocity. Neurological and ophthalmological examinations were normal in all patients. Our data show that type I Chiari malformation can be considered one of the possible causes for precocious, early and accelerated puberty in male patients, suggesting the need to carry out brain nuclear magnetic resonance imaging in order to investigate the presence of this malformation.

Arnold-Chiari Malformation↗
PubMed2002

Spermaturia and serum hormone concentrations at the age of puberty in boys prenatally exposed to polychlorinated biphenyls.

OBJECTIVE: To determine whether prenatal exposure to polychlorinated biphenyls (PCBs) with possible hormone-disrupting effects is capable of affecting sexual differentiation in boys at the age of puberty. DESIGN: Following analysis for PCB in their umbilical cords, 196 boys from a Faroese birth cohort were examined for the development of puberty at 14 years of age. METHODS: Physical examination included determination of Tanner stages and testicular size. A morning urine sample was centrifuged and examined for the presence of sperm. Serum was analyzed for sex hormones. RESULTS: twenty boys (10.2%) had abnormalities in testicular development, mainly cryptorchidism. only three of them had a positive spermaturia test, but the level of exposure to pcbs in this group had not been increased. occurrence of spermaturia in 58 of the remaining 176 boys was also not associated with pcb exposure but showed highly significant associations with tanner stages and testicular size. serum concentrations of testosterone, fsh and lh were higher in boys with spermaturia, while sex hormone-binding globulin was lower and no difference occurred in inhibin b. serum hormone parameters showed only weak associations with the level of prenatal pcb exposure. CONCLUSIONS: These findings support the validity of spermaturia as a useful indicator of puberty, although a substantial rate of false negatives must be taken into account. Despite the wide range of exposure to PCB, the findings did not reveal any definite associations with the development of puberty. However, because of the limited size of the cohort, small effects cannot be excluded.

Adolescent↗
PubMed2004

Increase of serum leptin after short-term pulsatile GnRH administration in children with delayed puberty.

OBJECTIVE: Leptin is known to play an important role in pubertal development in humans, probably acting as one permissive factor for the onset of puberty. Leptin serum concentrations change during pubertal development and an initial increase before the onset of puberty has been reported. The underlying mechanism for this increase in leptin levels is unknown. We hypothesized that the pulsatile release of GnRH stimulates leptin metabolism. In this study, the effect of short-term pulsatile GnRH administration on leptin levels in children with delayed onset of puberty was investigated. METHODS: Nineteen children (15 males and four females, mean age 15.5 years, range 13.1-20.5 years), who underwent evaluation for delayed sexual maturation, were included in the study. Sixteen subjects received 36 h of pulsatile intravenous GnRH, using an infusion pump that released 5 microg GnRH every 90 min. Serum concentrations of LH, FSH, testosterone, estradiol and leptin were analysed before and up to 36 h after GnRH administration. Eight patients received a single dose GnRH-agonist stimulation test (buserelin acetate test, 10 microg/kg body weight) with a 24-h follow-up (five patients underwent both tests). RESULTS: Mean (+/-s.e.m.) serum leptin increased significantly (P<0.01) after 36 h of pulsatile GnRH administration (7.26+/-1.35 vs 9.75+/-1.76 ng/ml). In contrast, no increase in leptin concentrations was observed after administration of a single dose of buserelin. CONCLUSIONS: These findings suggested that the increase in serum leptin at the onset of puberty is triggered by the pulsatile release of GnRH.

Adolescent↗
PubMed2005

Changes in serum inhibin B during normal male puberty.

OBJECTIVE: In adult men, inhibin B (InhB) regulates FSH secretion by a negative feedback. The aims of this study were to evaluate the changes of InhB during puberty in the male and the relationship between InhB and FSH, LH, testosterone and testicular volume. DESIGN: Cross-sectional study. METHODS: InhB was measured using a two-site ELISA in 100 healthy boys subdivided by their pubertal development according to Tanner into five groups of 20. RESULTS: During puberty we observed an increase of InhB level (G1 = 84.3 pg/ml, G3 = 132.2 pg/ml, G5 = 206.1 pg/ml). In G1, InhB correlated positively with FSH (P = 0.0001), LH (P = 0.005), testosterone (P = 0.001) and testicular volume (P = 0.007); in G5, InhB correlated inversely with FSH (P = 0.001) and LH (P = 0.045) and directly with testicular volume (P = 0.013). The multivariate analysis demonstrated that: in G1, FSH is the most important, and testosterone the second most significant, stimulus for InhB increase; in G2 only FSH has a positive effect on InhB variation; in G3 only mean testicular volume fits the model (G1-G3: InhB dependent variable); considering the FSH dependent variable, in G4, InhB is the most important stimulus for FSH decrease and mean testicular volume is a secondary directly proportional variable; in G5, only InhB shows a significant inverse relationship with FSH. CONCLUSIONS: During puberty there is a regular increase of InhB. In the first phases of gonadal maturation, InhB and FSH correlate positively, while in mid-late stages the relationship is inverse. We found that in mid-puberty (G3-G4), the serum concentration of InhB increases, as its inverse relationship with FSH is being established and hence spermatogenesis.

Adolescent↗
PubMed2007

Circulating ghrelin levels in girls with central precocious puberty are reduced during treatment with LHRH analog.

UNLABELLED: Decreased levels of ghrelin have been measured in growing children during puberty. No data are available for girls with central precocious puberty (CPP). AIMS: To explore ghrelin changes before, during, and after GnRH analog treatment in girls with CPP. SUBJECTS AND METHODS: A sample of 20 Caucasian girls (8.08 +/- 0.65 years of age) with CPP was recruited. Height and weight, bone age, LH, FSH, 17beta estradiol (E(2)), and ghrelin were measured before starting treatment with GnRH analog, 18 months after therapy began and again 6 months after therapy discontinuation. RESULTS: LH and E(2) serum levels decreased significantly during treatment (2.45 +/- 2.03 vs 0.67 +/- 0.49 UI/l, P < 0.01 and 28.17 +/- 9.7 vs 15 pmol/l, P < 0.01 respectively), returning to baseline levels after the discontinuation of therapy (4.75 +/- 1.66 UI/l and 29.23 +/- 6.99 pmol/l respectively). LH peaked following LHRH stimulation significantly (P < 0.01) decreased during treatment (24.45 +/- 14.17 vs 1.3 +/- 0.18 UI/l) and then increased after therapy discontinuation (12.58 +/- 6.09, P < 0.01). Ghrelin decreased significantly (P < 0.05) during treatment (1849 +/- 322 vs 1207 +/- 637 pg/ml), and increased, though not significantly (P = 0.09) after therapy withdrawal (1567 +/- 629 pg/ml). CONCLUSIONS: Contrary to what is expected in physiologic puberty, where ghrelin is progressively reduced, the prepubertal hormone milieau induced by GnRHa treatment in patients suffering from central precocious puberty (CPP) did not promote an increase in ghrelin circulating levels. Therefore, in CPP, ghrelin secretion seems to be independent from pubertal development per se. Concomitant estrogen suppression during treatment may play a potential role in the regulation of ghrelin secretion in these girls.

Body Height↗