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PubMed1990

Precocious puberty in a boy with a PRL-, LH- and FSH-secreting pituitary tumour: hormonal and immunocytochemical studies.

The case of a 7-year-old boy affected with precocious puberty and a large intra- and suprasellar pituitary tumour is described. He had hyperprolactinemia and elevated serum LH, FSH and testosterone concentrations. Pre-operative dynamic hormonal studies showed a rise of PRL, LH and FSH levels after TRH (200 micrograms iv) and a rise of LH and FSH after GnRH (100 micrograms iv). Dopamine infusion (4 micrograms.kg-1.min-1 for 180 min) did not affect gonadotropins and greatly reduced serum PRL. GnRH analogue (buserelin, 0.5 mg sc t.i.d. for 10 days) administration inhibited both LH and FSH, but did not affect PRL concentration. Serum LH and FSH increased after ethinyl-estradiol (0.5 mg orally) administration, and were not affected by bromocriptine (5-7.5 mg/day for 10 days), which decreased serum PRL levels. The patient underwent transfrontal neurosurgery and a large tumour mass was completely removed. Morphological study of the excised tumour, by electron microscope double label immunotechnique, revealed that a large number of tumour cells (70-85%) were positive for PRL, LH and FSH, co-localized in the same secretory granule. After neurosurgery, serum PRL, LH, FSH and testosterone levels fell to within the normal limits. Two months later the patient was well and signs of precocious puberty had partially regressed; hormone levels were in the normal range and MR imaging control did not demonstrate any residual lesion in the sellar region.

Adenoma↗

PubMed1990

Luteinizing hormone-releasing hormone analogue (Buserelin) treatment for central precocious puberty: a multi-centre trial.

A multi-centre open trial of Buserelin, a luteinizing hormone-releasing hormone (LHRH) analogue, was conducted in 13 children with central precocious puberty. Eleven children (eight girls and three boys), aged 3.4-10.2 years at commencement, completed the required 12 month period of treatment. Initially all patients received the drug by intranasal spray in a dose of 1200 micrograms/day, but by the end of the 12 month period two were having daily subcutaneous injections and three were receiving an increased dose intranasally. The first month of treatment was associated in one boy with increased aggression and masturbation, and in the girls with an increase in the prevalence of vaginal bleeding. Thereafter, however, both behavioural abnormalities and menstruation were suppressed. Median bone age increased significantly during the study, but without any significant change in the ratio of height age to bone age. The median predicted adult height for the group therefore did not alter significantly over the twelve months of the study. Buserelin treatment caused a reduction in the peak luteinizing hormone and follicle-stimulating hormone (FSH) responses to LHRH, mostly to prepubertal levels, and also suppressed basal FSH. In the first weeks of treatment, the girls' serum oestradiol levels rose significantly and then fell to prepubertal or early pubertal levels. A similar pattern was seen for serum testosterone levels. Serum somatomedin-C levels, however, showed little fluctuation over the course of the study. Buserelin treatment was safe and well accepted, and offers the promise of improved linear growth potential in precocious puberty.

Administration, Inhalation↗

PubMedDate not supplied

Central precocious puberty and chronic renal failure: a reversible condition post renal transplantation.

A 3 year-old boy with chronic renal failure associated with prune belly syndrome who developed central precocious puberty is described. He had been maintained on cyclic peritoneal dialysis from age 13 months with creatinine levels of 400-600 mumol/l. Increased linear growth rate probably began at 18 months, and by 38 months of age he had testicular enlargement and pubic hair consistent with Tanner stage 2. Elevated levels of serum testosterone (3.6 nmol/l; normal < 0.7 nmol/l) and luteinizing hormone (LH) (2.8 IU/l; normal < 1.0 IU/l) were demonstrated with a pubertal response to luteinizing hormone-releasing hormone (LHRH) stimulation (peak LH 43.5 IU/l). Other endocrine tests demonstrated hyperprolactinemia (170 micrograms/l; normal 3.4-22 micrograms/l), but normal pituitary-thyroid and pituitary-adrenal functions and normal cranial MR imaging. Despite LHRH-agonist therapy with leuprolide over the next 8 months, he showed an incomplete response with only partial inhibition of basal LH and testosterone levels, and continued significant increments in height standard deviation scores (Ht-SDS) and bone age estimates. However, the sexual precocity appeared fully reversible following a successful living-related renal transplant at age 50 months. Despite discontinuation of leuprolide treatment post-operatively, there was a full reversal of his serum LH and testosterone to a prepubertal profile as well as normalization of the serum prolactin levels. Whereas most boys with chronic renal failure show delayed pubertal development and suppressed linear growth, our patient presents a unique phenomenon of reversible central precocious puberty. The effects of leuprolide therapy in the presence of a uremic milieu and the outcome of successful renal transplantation on sexual precocity are described.

Child, Preschool↗

PubMed2003

Quantitative calcaneal ultrasound parameters and bone mineral density at final height in girls treated with depot gonadotrophin-releasing hormone agonist for central precocious puberty or idiopathic short stature.

UNLABELLED: To evaluate the effect of gonadotrophin-releasing hormone (GnRH) agonist treatment on bone quality at final height, we studied girls with central precocious puberty (CPP) and with idiopathic short stature (ISS). A total of 25 Caucasian girls were included: group A (n=14) with idiopathic CPP (mean age at start 7.4 years) and group B (n=11) with ISS (mean age at start 11.7 years). Treatment duration was 3.8 and 1.7 years respectively. The quantitative ultrasound parameters (QUS) broadband ultrasound attenuation (BUA) and speed of sound (SOS) were measured at the calcaneus (UBIS 3000 device). Lumbar spine bone mineral density (BMD; L2-L4) was measured by dual energy X-ray absorptiometry (DXA) (Hologic QDR1000). Measurements were performed at final height and expressed as Z-scores corrected for bone age. Mean Z-scores of QUS parameters, areal BMD and volumetric BMD (BMDvol) were above -1 in both groups (group A: BUA Z-score -0.21, SOS Z-score -0.29, BMD Z-score 0.02, BMDvol Z-score 0.05, group B: BUA Z-score -0.93, SOS Z-score -0.40, BMD Z-score -0.86, BMDvol Z-score -0.68), although mean Z-scores of BUA and areal BMD in group B were significantly different from zero (P=0.03 and P=0.02 respectively). Mean Z-score BMDvol was not significantly different from zero (P=0.05), we found no significant difference between the groups for BMDvol (P=0.13). CONCLUSION: Although quantitative ultrasound parameters parameters and bone mineral density were normal in girls with central precocious puberty at final height after gonadotrophin-releasing hormone agonist treatment, mean Z-score for broadband ultrasound attenuation and areal bone mineral density were significantly different from zero and mean Z-score for volumetric bone mineral density was (just) not significantly different from zero in idiopathic short stature girls with normal puberty treated with gonadotrophin-releasing hormone agonists. Therefore we cannot say that this treatment is safe in these girls with regard to bone health.

Absorptiometry, Photon↗

PubMed1993

Reduction of bone density: an effect of gonadotropin releasing hormone analogue treatment in central precocious puberty.

Gonadal steroids drive the significant bone mineral increase that occurs at puberty. Oestrogen deprivation in women results in bone loss. We investigated bone mineralization by single photon absorptiometry in girls with central precocious puberty (n = 13, age 3.8-8.5 years) before and during 1 year of treatment with gonadotropin releasing hormone analogue (GnRH-a = long-acting D-Trp6-GnRH, 60 micrograms i.m. every 28 days). Before GnRH-a therapy, bone mineral density (BMD) was significantly higher in patients than in ten control girls matched for chronological age (patients 0.575 +/- 0.097 g/cm2, controls 0.433 +/- 0.049 g/cm2, P < 0.001). Patient BMD was not significantly different from that of ten control girls matched according to patient bone, age (0.550 +/- 0.046 g/cm2, P = NS). During GnRH-a treatment, pituitary-gonadal axis was suppressed and patient BMD significantly decreased (6 months: -6.0%, P < 0.002 vs baseline; 12 months: -8.0%, P < 0.001 vs baseline). We conclude that in girls with precocious puberty the activation of gonadal steroid secretion induces an increase in bone mineralization and that oestrogen deprivation by GnRH-a treatment caused a significant decrease in BMD.

Absorptiometry, Photon↗

PubMed1986

[Pseudo- and central precocious puberty due to adrenogenital syndrome].

We describe three patients in whom at the age of 4-7 yrs the diagnosis adrenogenital syndrome (21-hydroxylase deficiency) was made. There was no salt-loss. Two boys presented with precocious pubic hair development and increased growth velocity and bone maturation. The third patient was a severely virilized girl raised as a boy until she was 4 yrs old. Following an extensive psychiatric evaluation, it was decided to raise her as a girl and feminoplasty was performed. Clinical and biochemical evidence of central precocious puberty was present in one boy at the time of diagnosis at age 7 and developed under hydrocortisone substitution therapy in the two other patients. The precocious puberty was treated in two patients with the anti-androgen cyproterone acetate. In one boy suppression of pituitary gonadotropin secretion was obtained by LH-RH analogue (Buserelin) treatment.

Adrenal Hyperplasia, Congenital↗

PubMed1985

Steroid receptors in a granulosa cell tumor (GCT) in an infant with precocious puberty.

A granulosa theca cell tumor was found in a 10-month-old girl with precocious puberty. Steroid hormone receptors were measured in fractionated tumor cells. Estrogen and progesterone receptors were measured in the cytosol, and estrogen receptors were measured in the nuclear fraction of the tumor. Although high affinity (Kd 0.4 nM) progesterone receptors were present in the cytosol of this tumor-54 fmole/mg protein-no cytosolic estradiol receptors could be detected; however, these receptors were found to be tightly bound to the nuclear fraction of the tumor. The nuclear protein had lower apparent Kd for the hormones-5.4 nM. This tumor produced and released various steroid hormones. The plasma steroid levels before removal of the tumor were 1,200 pg/ml for estradiol, 350 pg/ml for testosterone, and 5 ng/ml for progesterone. All these steroid hormones declined postoperatively to undetectable levels, with total remission of pubertal signs. Plasma-dehydroepiandrosterone, prolactin, and gonadotropin levels were in the normal range before and after surgery. These results suggest that cytosolic progesterone receptor as an estrogenic marker and/or nuclear estrogen receptors may predict the hormonal dependency of these estrogen-producing tumors.

Cell Nucleus↗

PubMed1986

True precocious puberty of a girl with hamartoma of the CNS successfully treated by operation.

A girl with precocious puberty due to a hypothalamic hamartoma is presented. At the age of 0.41 years vaginal bleeding was documented and signs of puberty were noted: PHIII, BII according to Tanner. The bone age was 1.3 years, and height velocity rose from the 50th to 90th percentile. Plasma concentrations of LH (5.85 mU/ml), FSH (3.29 mU/ml), growth hormone (30 ng/ml), and oestradiol (90 pg/ml) were elevated. The results of a neurological examination including an EEC recording as well as a skull roentgenogram, were unremarkable. The visual evoked potentials were grossly abnormal. A native and contrast CT scan visualized a tumour close to the suprasellar cisterna reaching the chiasma opticum. At the age of 1.2 years the tumours was removed. Histologically the tissue was identified as a hamartoma. Immediately after the operation vaginal bleeding ceased, pubertal development regressed, bone age did not advance any further, the visual evoked potentials normalized and the contrast CT did not show any tumour mass. The levels of LH, FSH, growth hormone and oestradiol 4 months post operation were decreased as follow: LH: 1.14 mU/ml, FSH: 0.70 mU/ml, GH: 15.1 ng/ml, oestradiol: 10 pg/ml. However, there was an increase of FSH (3 mU/ml) 1 year after the operation. No secondary sexual characters reappeared.

Estradiol↗

PubMed1989

Stereotactic decompression of a prepontine arachnoid cyst with resolution of precocious puberty.

A case of a prepontine (clival) arachnoid cyst is reported. The patient presented with isosexual precocious puberty. Treatment was initially with fenestration by suboccipital craniectomy, however, definitive treatment was via stereotactic transfrontal placement of a cystoperitoneal shunt. Normalization of endocrine function has occurred and has persisted for 1 year. This case is presented as a contrast to the two approaches for the treatment of arachnoid cysts. The case will be described and the literature reviewed.

Arachnoid↗

PubMed1992

Assessment of depot leuprolide acetate dose-adequacy for central precocious puberty.

The development of GnRH analogs (GnRHa) has made it possible to treat children with central precocious puberty (CPP). This treatment may prevent adult short stature due to premature epiphyseal fusion. Achievement of this goal, however, is dependent upon adequate suppression of gonadal steroid production as a result of GnRHa-induced pituitary desensitization and decreased gonadotropin release. A depot formulation of a GnRHa [leuprolide acetate (dLA)] is being used by many clinicians for the treatment of CPP, but studies to establish the optimal dose of dLA have not been performed. In this study we evaluated the effectiveness of dLA (7.5 mg, im, every 4 weeks). Six children (7-10 yr old) with CPP treated with dLA were assessed clinically and divided into two groups: A (incompletely suppressed) and B (well suppressed). Each group had overnight blood sampling and a GnRH stimulation test the following morning. LH pulses were analyzed and compared to 11 normal prepubertal children. Mean LH concentration, LH curve area, LH pulse frequency, and mean LH pulse amplitude were significantly greater (P less than 0.03) in group A than in group B or the normal prepubertal children. There was no significant difference among the three groups in GnRH-stimulated peak LH release. These results indicate that dLA (7.5 mg, im, every 4 weeks) does not produce complete desensitization in all children with CPP and suggest that overnight monitoring of LH release is more sensitive than GnRH stimulation testing for the assessment of dLA dose adequacy.

Child↗

PubMed1995

Long-term GnRH-agonist treatment does not postpone central development of the GnRH pule generator in girls with idiopathic precocious puberty.

Gonadotropin and estradiol secretion were studied in two groups of female patients with idiopathic central precocious puberty, at diagnosis (group 1, age 4.8-8.7 yr) and during recovery after long-term treatment with a GnRH agonist (group 2, age 6.5-9.4 yr). The protocol included 24-h sampling of blood at 10-min intervals just before GnRH-agonist treatment (group 1, n = 7), and at 4 and 10 months after discontinuation of treatment (group 2, n = 8). LH was estimated at 10-min intervals, and FSH and estradiol were estimated at 1-h intervals for 6-h periods during the day (wake) and during the night (sleep). In group 2, height was measured in the follow-up at 4 and at 10 months. In group 1, all the girls showed a pulsatile LH secretion with a clear wake-sleep difference in mean LH and LH pulse amplitude: mean LH daytime levels were 1.33 IU/L (range 0.57-7.34 IU/L) vs. nighttime levels of 3.12 IU/L (range 2.35-5.19 IU/L) (P < 0.05). Mean LH pulse amplitudes were 1.39 IU/L (range 0.35-1.76 IU/L) at daytime and 3.85 IU/L (range 1.10-12.37 IU/L) at night (P < 0.05). In group 2, all girls showed pulsatile LH patterns after 4 months as well as after 10 months. At both sampling periods, no wake sleep differences in LH pulse frequency, mean LH levels, or LH pulse amplitude were observed. Mean daytime LH levels increased from 1.66 IU/L (range 0.67-3.29 IU/L) at 4 months to 3.04 IU/L (range 0.73-5.59 IU/L) at 10 months, after therapy (P < 0.05). The number of LH pulses were not different at 4 and at 10 months. The mean LH pulse amplitude increased from 1.68 IU/L (range 0.54-2.04 IU/L) to 2.79 IU/L (range 1.01-3.41 IU/L), comparing 4 months with 10 months (P < 0.05) at daytime. The mean FSH level increased from 1.0 IU/L (range 0.5-2.1 IU/L) at discontinuation of treatment to 4.29 IU/L (range 3.15-5.12 IU/L) at 4 months (P < 0.01) and to 4.49 IU/L (range 2.72-6.50 IU/L) at 10 months (daytime = NS). The estradiol levels increased from less than 37-51 pmol/L at the end of treatment to 77.5 pmol/L (range < 37.0-102.4 pmol/L) and 96.8 pmol/L (range 61.8-169.8 pmol/L) (daytime) at 4 and 10 months, respectively (P < 0.05). Menarche occurred in five of the eight girls within 13 months after treatment. No pubertal growth spurt was observed after treatment.(ABSTRACT TRUNCATED AT 400 WORDS)

Body Height↗

PubMed2006

Ultrasonographic and clinical parameters for early differentiation between precocious puberty and premature thelarche.

OBJECTIVE: To determine if uterine and ovarian measurements can significantly distinguish between precocious puberty (PP) and premature thelarche (PT) and whether ultrasound has any advantage over the gonadotropin-releasing hormone (GnRH) stimulation test. DESIGN: Prospective. METHODS: One hundred and three girls referred consecutively for evaluation of breast budding before age 8 years underwent physical examination, GnRH stimulation test, bone age assessment, and transabdominal pelvic ultrasound. The diagnosis of PP or PT was based on clinical judgment. The clinical, laboratory, and ultrasound data of the PP and PT groups were compared. RESULTS: Eighty-one girls were diagnosed with PP and 22 with PT. Significant differences in most of the uterine and ovarian measurements were found between the groups. On logistic regression analysis, bone age standard deviation score, uterine transverse diameter, and uterine volume were the most significant variables predicting PP. Comparison of 30 girls with PP and 21 with PT in whom peak luteinizing hormone was <5 mIU/ml on the GnRH stimulation test, using analysis of variance, yielded significant differences in uterine width (P<0.001), fundus diameter (P <0.04), uterine volume (P= 0.006), and ovarian circumference (P <0.02). CONCLUSIONS: Increased uterine and ovarian measurements may be an early and sensitive sign of PP. Pelvic ultrasound, a noninvasive, inexpensive, and reliable tool, may give the clinician a complementary indication to the GnRH test in distinguishing isolated PT from early-stage PP in girls with early breast budding.

Age Determination by Skeleton↗

PubMed2003

Serum leptin levels in girls with precocious puberty.

Few data are available regarding leptin levels in children with different pubertal stages or with precocious puberty (PP). The aim of this study was to assess the changes in serum leptin levels in patients with PP. We studied 20 girls with PP, with Tanner stage II-III; the age at the beginning of pubertal signs ranged from 4.2 to 7.1 yr; all the girls had an advantaged bone age. Controls were subdivided in two groups: group 1: 20 pre-pubertal girls with the same chronological age of the patients, without any signs of pubertal development (Tanner stage I); group 2: 20 additional girls with the same bone age, pubertal stage and body mass index (BMI) of the girls with PP. Serum leptin levels in females with PP are similar to those found in subjects with normal puberty (9.0 +/- 0.8 vs 9.1 +/- 0.9 ng/ml; ns) and different from subjects with the same chronological age without activation of puberty (5.6 +/- 0.9 ng/ml, p < 0.001). In all groups leptin levels correlated significantly with BMI (girls with PP: r = 0.5 1, p < 0.02; control group 1 girls: r = 0.71; p < 0.0001; control group 2 girls: r = 0.49; p < 0.02), there was no significant relationship between leptin and activation of hypothalamic-pituitary-gonadal axis. Our results indicate that the serum leptin levels in the girls with PP are not significantly different from levels in healthy girls at a similar stage of pubertal development, suggesting that the relationship between serum leptin levels and BMI is also present in this pathological situation.

Age Determination by Skeleton↗

PubMed1989

[Assessment of the effectiveness of Androcur in the treatment of precocious puberty].

The data are provided on the continuous use of Androcur in the treatment of genuine precocious puberty in children. The drug produced a beneficial effect in 100% of cases in respect to suppression of the secondary sexual characters, menstrual function in girls, and behavior normalization in boys. During treatment, the improvement of the growth prognosis was negligible. Stabilization of the processes of osseous maturation requires administration of the maximal drug doses, which may suppress glucocorticoid function of the adrenals. This fact should be taken into account during treatment, particularly on its discontinuation. The treatment should be discontinued according to the schedule similar to that applied in glucocorticoid discontinuation.

Androgen Antagonists↗

PubMedDate not supplied

[Precocious puberty due to HCG secreting pinealoma (author's transl)].

The present report concerns a six years nine months old boy in whom a HCG secreting pineal tumor (pinealocytoma type I) was responsible for precocious puberty. Features : polydipsia, deepened voice, pubic hair, penile enlargement without corresponding testicular growth. Serum basal concentrations of LH (150 mU/ml), testosterone (85.80 nanomole/l), HCG (115 ng/ml) and its beta subunit (15 ng/ml) were markedly elevated, FSH was low (3.9 mU/ml) ] dissociated hypopituitarism was also present. A surgical removal of the tumor was performed (RIA of the neoplastic tissue revealed high HCG and beta HCG activity) and after the operation the child had radiation therapy. Recovery for the foregoing procedure was rapid, but after some months, in spite chemotherapy his condition deteriorated progressively. The apparent limitation of pinealoma and precocious puberty to the male sex is discussed and supposed to be partly the result of the ectopic gonadotropin secretion. These tumors are compared to other HCG secreting carcinomas located elsewhere in the body and causing sexual precocity in boys only.

Brain Neoplasms↗

PubMed1984

Precocious puberty in myelomeningocele patients.

Of a group of 79 patients (45 males, 34 females) with myelomeningocele (MMC), 52 had associated hydrocephalus. Three of the hydrocephalic patients (two arrested and one shunted) were found to have precocious sexual development. Endocrine investigations confirmed true isosexual precocity. Hydrocephalus is known to be associated with precocious puberty, but the occurrence of sexual precocity in patients with hydrocephalus in conjunction with MMC has not been described to date. As the clinical diagnosis of hydrocephalus in a young child is often unreliable, routine computerized tomographic scans of all MMC patients is advised, and even patients with arrested hydrocephalus should be followed carefully for signs of precocious puberty. In addition, a high incidence (15%) of cryptorchidism was found in the group of MMC patients reviewed.

Child↗

PubMed2006

Efficacy of subcutaneous administration of gonadotropin-releasing hormone agonist on idiopathic central precocious puberty.

In order to assess the feasibility of subcutaneous administration of Triptorelin with 6-week intervals for the suppression of pituitary-gonadal axis and changes of clinical signs in girls with idiopathic central precocious puberty (ICPP), 46 girls with ICPP were treated with GnRHa. Triptorelin (Decapeptyl, 3.75 mg) was administered subcutaneously (SC) at 6-weeks intervals or intramuscularly (IM) at 4-weeks intervals randomly for more than 12 months consecutively. During GnRHa therapy, clinical parameters and laboratory data, including height, weight, pubertal stage, bone age, uterine volume and ovarian size, serum levels of luteinizing hormone (LH), follicle stimulating hormone (FSH) and estradiol (E2), were monitored and analyzed. It was found that both treatment regimes led to regression of precocious puberty and reversal of secondary sexual characteristics. Breast developments regressed. Uterine volume was decreased after treatment, but there was no statistically significant difference. Mean ovarian volume did not change significantly during treatment. The height velocity was decreased significantly from 6.3+/-1.4 cm/year to 5.8+/-1.2 cm/year in group SC and 6.7+/-1.3 cm/year to 5.4+/-1.0 cm/year in group IM, respectively. The rate of bone maturation was reduced significantly during treatment. The ratio of deltaBA/deltaCA 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 was increased significantly and progressively during therapy. The levels of serum LH, FSH and E2 returned to the prepubertal condition. No significant side effects of therapy were noted. The most common side effect during SC treatment was that a non-irritating, 1 cm in diameter mass was palpated at the site of subcutaneous injection in the abdominal wall of patients, which disappeared after 6-12 weeks. Two girls had minimal withdrawal vaginal bleeding episodes after the first injection. It was concluded that both IM and SC triptorelin administrations were clinically effective. They 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 be a safe and acceptable regimen for ICPP

Bone Development↗

PubMed1993

Growth velocity and serum aminoterminal propeptide of type III procollagen in precocious puberty during gonadotropin-releasing hormone analogue treatment.

Growth velocity and serum aminoterminal propeptide of type III procollagen (P-III-NP) were evaluated in 11 girls (age 3.8-8.5 years) with central precocious puberty during luteinizing hormone releasing hormone (LH-RH) analogue treatment (D-Trp6-LH-RH, 60 micrograms/kg im for 28 days, n = 7; D-ser(TBU)6-LH-RH, 1600 micrograms/day intranasally, n = 4). Before treatment, growth velocity (10.2 +/- 1.9 cm/year) and P-III-NP concentrations (12.8 +/- 4.3 micrograms/l) were in the pubertal range. During therapy, growth velocity significantly decreased to the prepubertal levels. P-III-NP concentrations decreased significantly after six months of therapy (7.9 +/- 3.7 micrograms/l, p < 0.001). Three girls with low growth velocity ( < 4 cm/year), stimulated growth hormone peak < 10 micrograms/l, and altered 12-h nocturnal growth hormone secretion at 12 and/or 18 months of treatment, had a more marked decrease in P-III-NP concentrations (patient 3: -65.9%; patient 5: -58.7%; patient 10: -61.0%) after 6 months of therapy. Our results suggest that LH-RH analogue treatment in central precocious puberty may impair growth. In these cases, measurement of serum P-III-NP levels may be an additional marker to monitor growth.

Child↗