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PubMed2004

Diagnostic utility of a low-dose gonadotropin-releasing hormone test in the context of puberty disorders.

OBJECTIVES: The 10-microg gonadotropin-releasing hormone (GnRH) test assesses pituitary gonadotroph responsiveness, whereas the 100-microg dose assesses maximal secretory capacity. Our aims were to establish normative data for the low-dose test in children and to evaluate the test in diagnosing common pubertal disorders. METHODS: We retrospectively classified 107 children who underwent 10-microg GnRH tests into normal prepubertal (20 boys, 10 girls), normal early pubertal (10 boys, 16 girls), constitutional delay of puberty (CDP, 13 prepubertal boys >12 years), hypogonadotropic hypogonadism (HH, 5 prepubertal boys >12 years), central precocious puberty (CPP, 19 girls) or premature thelarche/variant (13 girls). RESULTS: Peak LH response was higher in prepubertal boys >12 years compared with younger boys (p < 0.01) but showed no further change in early puberty. CDP boys had LH responses similar to prepubertal boys >12 years. HH boys showed an absent LH response which diagnosed HH with 100% sensitivity and 96% specificity. Thelarche girls had LH:FSH peak ratios lower than normal prepubertal (p = 0.001), pubertal (p < 0.05) or CPP (p = 0.001) girls. CONCLUSIONS: We have established normative values for the low-dose GnRH test in children. The test successfully differentiated HH from CDP in boys, and contributed to the differential diagnosis of CPP and premature thelarche in girls.

Adolescent↗
PubMed2005

Gonadotropin-releasing hormone analogue treatment for precocious puberty. Twenty years of experience.

Central precocious puberty (CPP) is the premature onset of puberty due to a precocious activation of gonadotropin-releasing hormone (GnRH) neurons in the hypothalamus. This condition results in accelerated development of secondary sex characteristics, accelerated bone maturation, impaired final height with disproportioned body appearance and can have a disturbing impact on the psychosocial behavior of children suffering from CPP. It is therefore necessary to assess the hormonal status of children who show pubertal signs before the age 8 years in girls and 9 years in boys. The indication for treatment should be made after evaluating pubertal progression, progression of bone age maturation and final height prognosis, development of reproductive function, and psychosocial adjustment and well-being. This paper summarizes the experience of GnRH agonist treatment, which is momentarily the treatment of choice for central precocious puberty in children.

Adolescent↗
PubMed2006

Diencephalic syndrome due to hypothalamic tumor: a model of the relationship between weight and puberty onset.

CONTEXT: Changes in body weight, statural growth rate, and puberty may be the presenting symptoms of hypothalamic-pituitary tumors. OBJECTIVE: The objective of the study was to assess the relationship between the tumor and its treatment and the weight, growth rate, and onset of puberty, using the diencephalic syndrome of emaciation as model. PATIENTS: Eleven patients seen before 1 yr of age, except one aged 9 yr, for diencephalic syndrome of emaciation due to hypothalamic pilocytic astrocytoma, were treated by surgical resection (n = 9), cranial irradiation (n = 7), and/or chemotherapy (n = 10). RESULTS: At diagnosis, growth rate was normal, despite the emaciation, and there was no hypothalamic-pituitary deficiency, except in the oldest patient. After tumor treatment, all had GH and thyroid-stimulating hormone deficiencies, but only three, who underwent major surgical resection, also had ACTH deficiency and diabetes insipidus. Eight became obese, and all but the oldest had transient precocious puberty. Plasma leptin concentrations were very low at diagnosis, increased after tumor treatment, and decreased transiently in one boy when the testosterone increased. The plasma soluble leptin receptor concentrations changed in the opposite direction, leading to an increase in the free leptin index, including in the three patients whose tumor was reduced without surgery. The body mass index was correlated positively with plasma leptin (rho = 0.73, P = 0.0004) and free leptin index (rho = 0.63, P < 0.004) and negatively with ghrelin (rho = -0.49, P < 0.03) concentrations. CONCLUSIONS: The obesity that occurs after treatment of hypothalamic tumors is not due to dysregulation of leptin secretion because it and plasma soluble leptin receptor remain regulated by factors like testosterone. This study also shows the influence of weight, possibly via leptin secretion, on the transient hypothalamic-pituitary-gonadal activation that occurs during the first year of life.

Adrenocorticotropic Hormone↗
PubMed1993

Long-term testolactone therapy for precocious puberty in girls with the McCune-Albright syndrome.

We used the aromatase inhibitor testolactone (40 mg/kg.day) to treat 12 girls with precocious puberty due to the McCune-Albright syndrome for periods of 0.5-5 yr. In the 7 girls who received testolactone for at least 3 yr, the mean +/- SD serum estradiol level was 618 +/- 268 pmol/L at the start of therapy and fell to 156 +/- 84 pmol/L at 1 yr, 116 +/- 48 pmol/L at 2 yr, and 241 +/- 260 pmol/L at 3 yr (P < 0.05 compared to the start of therapy), with recurrent ovarian cysts at 3 yr in 2 patients. These 7 girls averaged 8 menses/yr before therapy. The average frequency of menses decreased to 2 episodes/yr during the first year of treatment, 3/yr during the second year, and 4/yr during the third year. The mean +/- SD testosterone levels were slightly above the normal prepubertal range (0.51 +/- 0.2 nmol/L) before treatment and did not change significantly during treatment. The mean +/- SD androstenedione levels rose from 1.1 +/- 0.6 nmol/L before treatment to 2.1 +/- 0.1 nmol/L at 2 yr and 2.8 +/- 0.1 nmol/L after 3 yr of treatment (P < 0.05 compared to before treatment) and were consistent with normal adrenarche. The mean predicted adult stature was 143.0 +/- 7.8 cm before treatment and 147.3 +/- 11.5 cm at 3 yr (P = NS). In 3 of 12 girls, all with bone age greater than 12 yr, the gonadotropin responses to LHRH indicated early central precocious puberty after 1-4 yr of treatment. The adverse effects of testolactone were transient abdominal pain, headache, and diarrhea in 3 girls and elevated hepatic enzymes in 1 girl who had abnormal liver function before treatment. Six families acknowledged difficulty in adhering to the daily dosing schedule. We conclude that testolactone can be effective in the treatment of LHRH-independent precocious puberty in girls with McCune-Albright syndrome, but that some patients exhibit an escape from the effects of treatment after 1-3 yr.

Age Determination by Skeleton↗
PubMed1998

Bone mineral density and body composition before and during treatment with gonadotropin-releasing hormone agonist in children with central precocious and early puberty.

Major changes in bone mineral density (BMD) and body composition occur during puberty. In the present longitudinal study, we evaluated BMD and calculated volumetric BMD [bone mineral apparent density (BMAD)], bone metabolism, and body composition of children (32 girls and 2 boys) with central precocious and early puberty before and during treatment with GnRH agonist (GnRH). Patients were studied at baseline and during treatment for 6 months (n = 34), 1 yr (n = 33), and 2 yr (n = 16). Lumbar spine and total body BMD and body composition were measured with dual-energy x-ray absorptiometry. The variables were compared with age- and sex-matched reference values of the same population and expressed as SD score (SDS). Bone age was assessed. Serum calcium, phosphate, alkaline phosphatase, osteocalcin, the carboxyterminal propeptide of type I collagen (PICP), cross-linked telopeptide of collagen I (ICTP), 1,25 dihydroxyvitamin D and urinary hydroxyproline/creatinine, and calcium/ creatinine ratios were measured. Mean lumbar spine BMD SDS was significantly higher than zero at baseline (P < 0.02) and did not differ from normal, after 2 yr of treatment. Mean spinal BMAD SDS and total body BMD SDS were not significantly different from zero at baseline and had not changed significantly after 2 yr of treatment. During therapy, fat mass and percentage body fat SDS increased, whereas lean tissue mass SDS decreased. Mean lumbar spine BMD and BMAD and total body BMD SDS, calculated for bone age, were all lower than zero at baseline (BMD P < 0.001 and BMAD P < 0.05) and also after 2 yr treatment (respectively, P < 0.001, P < 0.05, and P < 0.01). Biochemical bone parameters were significantly higher than prepubertal values at baseline, and they decreased during treatment. In conclusion, patients with central precocious and early puberty had normal BMD for chronological age but low BMD for bone age, after 2 yr of treatment with GnRH. Bone turnover decreased during treatment. Changes in body composition resembled those seen in patients with GH deficiency.

Body Composition↗
PubMed2002

Longitudinal follow-up of bone density and body composition in children with precocious or early puberty before, during and after cessation of GnRH agonist therapy.

We studied bone mineral density (BMD), bone metabolism, and body composition in 47 children with central precocious puberty (n = 36) or early puberty (n = 11) before, during, and after cessation of GnRH agonist. Bone density and body composition were measured with dual energy x-ray absorptiometry and expressed as SD scores. Bone age and biochemical parameters of bone turnover were assessed. Measurements were performed at baseline, after 6 months, and on a yearly basis thereafter. Mean lumbar spine BMD SD scores for chronological age were significantly higher than zero at baseline and decreased during treatment. Lumbar spine bone mineral apparent density and total body BMD did not differ from normal at baseline and showed no significant changes during treatment. In contrast, BMD SD scores for bone age were significantly lower than zero at baseline and at cessation of therapy. Two years after therapy, bone mineral apparent density and BMD SD scores for bone age and chronological age did not differ from normal. Markers of bone turnover decreased during treatment, mainly in the first 6 months. Patients had increased percentage of fat and lean body mass at baseline. After an initial increase of percentage body fat during treatment, percentage body fat decreased and normalized within 1 yr after cessation of treatment. Our longitudinal analysis suggests that peak bone mass or body composition will not be impaired in patients with precocious or early puberty after GnRH agonist therapy.

Aging↗
PubMed2001

Unresolved problems concerning optimal therapy of puberty in children with chronic renal diseases.

Many children with chronic renal insufficiency (CRI) show growth retardation and severely delayed pubertal development. Successful renal transplantation (RTx) also rarely results in full growth rehabilitation. Pubertal height gain in CRI patients is only 58% and 48% of that observed in late-maturing boys and girls, respectively. Growth retardation in both CRI and RTx patients is not the result of abnormal GH secretion or decreased levels of IGF-I, but rather of elevated levels of IGFBPs inhibiting the bioavailability of the IGFs. In RTx patients prednisone may also inhibit growth directly via inhibition of bone matrix formation. Several studies have convincingly shown that GH therapy at a dose of 4 IU/m2/day results in a sustained improvement of growth in prepubertal and pubertal children with CRI and in growth-retarded prepubertal and pubertal post-transplant patients. The following consensus was reached concerning optimal therapy of puberty in children with chronic renal disease. GH therapy does not lead to an earlier start of puberty. It is safe to give GH to RTx patients if transplant function is stable. GH therapy will not accelerate bone maturation and can improve the final height of children with CRI and after RTx. Increasing the GH dose above 4 IU/m2/day in pubertal RTx patients does not increase height gain or final height and is not advised as it may increase insulin resistance. GH should best be started before the start of the pubertal growth spurt but will still be effective in RTx patients with advanced bone age. GH testing should not be a prerequisite for starting GH therapy. It is important to optimise other therapies during puberty. During GH therapy of RTx patients use minimum daily, not alternate-day, steroid dosing. Further research is still required on the possible long-term effects of GH therapy in children with chronic diseases. Two studies demonstrated improved long-term growth and final height within the target height range, without significant side effects. Renal graft function did not deteriorate more than in matched controls. A GH dose of 4 IU/m2/day proved adequate.

Adolescent↗
PubMed2000

Signaling between the pituitary gland and the testes: inverse relationship between serum FSH and inhibin B concentrations in boys in early puberty.

OBJECTIVES: To study the relationship between serum inhibin B and sex steroid concentrations and pituitary FSH responsiveness to GnRH in boys in early puberty, and to examine serum inhibin B levels in prepubertal boys with different timing of the onset of gonadotropin deficiency (GD). DESIGN: Twenty-five boys with constitutional delay of puberty (CDP; 20 in Tanner stage G2 and 5 in G3; age range, 13. 5-16.8 years) and eight prepubertal boys (G1P1) with GD (age range, 10.0-13.2 years) were clinically examined, and serum inhibin B, testosterone and estradiol concentrations were measured from sera obtained immediately before the administration of GnRH (Relefact; 3.5 microgram/kg, maximum 100 microgram i.v.). Thereafter, FSH levels were measured at 30min intervals up to 90min. RESULTS: In the boys with CDP, basal inhibin B and FSH levels did not correlate. However, inhibin B and GnRH-stimulated FSH concentrations (r(S)= -0.43 to -0.45, n=25, P<0.05) and the difference between basal and peak serum FSH levels were inversely related (r(S)= -0.63, n=25, P<0.005). This relationship remained significant in boys at stage G2 (r(S)= -0.66, n=20, P<0.005). Basal testosterone concentrations and GnRH-induced FSH levels did not correlate. Estradiol levels were too low (64% of the boys had estradiol levels below the assay sensitivity) to allow correlation analysis. The boys with GD had low inhibin B concentrations (range, <15.6-53pg/ml); the lowest levels were observed in boys with presumably congenital onset of the disease. Serum inhibin B levels and testis volumes correlated positively (r(S)=0.70, n=8, P=0.07). CONCLUSIONS: These results suggest that, in boys, the reciprocal regulation between inhibin B and FSH is in operation before mid-puberty. Moreover, autonomous inhibin B secretion by the prepubertal human testis is likely to reflect the number of Sertoli cells.

Adolescent↗
PubMed2004

Benefit of postponing normal puberty for improving final height.

Experiments of nature and clinical observations have provided indications that postponing puberty may increase final height in short children. In children with central precocious puberty, a GnRH analog (GnRHa) alone is efficacious in increasing final height, but in other conditions a combination of growth hormone (GH) and GnRHa is needed. In GH-deficient children with early onset of puberty and poor height prediction, the combination of GH and GnRHa increases final height by 1.0-1.3 s.d. In children with idiopathic short stature and persistent short stature after intrauterine growth retardation, the combination also appears to be beneficial. Potential side effects include weight gain, a negative effect on bone mineralization, and psychosocial consequences. More data on long-term safety have to be collected before the combination of GH and GnRHa in children with idiopathic short stature should be considered for clinical use outside clinical trials.

Adaptation, Psychological↗
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↗
PubMed2005

[Puberty development of the healthy adolescent girls of Daqing city, Heilongjiang province].

OBJECTIVE: To investigate the process of puberty development of healthy adolescent girls in Northern China. METHODS: 288 adolescent girls of Daqing city, Heilongjiang province, aged 5 to 16, were studied and followed up yearly for four years. The height, weight, fat percentage, second sex characteristics, and the blood levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), and estradiol (E(2)) were examined. RESULTS: The mean age of puberty onset of these healthy adolescent girls was 8.5 years +/- 1.1 years. The blood levels of FSH, LH and E(2) were 0.2 mIU/L, 1.1 mIU/L and 0.06 nmol/L respectively (the 95 percentiles were 2.5 mIU/L, 2.3 mIU/L and 0.12 nmol/L respectively). Their mean age of menarche was 12.4 years +/- 1.2 years. The mean age of breast development was 8.8 years +/- 1.1 years. CONCLUSION: The girls in Northern China begin their puberty development at younger ages than reported before.

Adolescent↗
PubMedDate not supplied

Decrease in plasma high-density lipoprotein cholesterol levels at puberty in boys with delayed adolescence. Correlation with plasma testosterone levels.

A three-phase study tested the hypothesis that the decrease in the high-density lipoprotein cholesterol (HDL-C) level observed in boys at puberty is related to an increase in the plasma testosterone concentration. In phase I, 57 boys aged 10 to 17 years were categorized into four pubertal stages based on clinical parameters and plasma testosterone levels. These four groups showed increasing plasma testosterone values and decreasing HDL-C levels. In phase II, 14 boys with delayed adolescence were treated with testosterone enanthate (100, 200, and 200 mg/mo, respectively, for three months). Plasma testosterone levels during therapy were in the adult male range. Levels of HDL-C decreased by a mean of 7.4 mg/dL (0.20 mmol/L) and 13.7 mg/dL (0.35 mmol/L), respectively, after the first two doses. In phase III, 13 boys with delayed adolescence demonstrated increasing plasma testosterone levels and decreasing HDL-C levels (-12.0 mg/dL [-0.30 mmol/L]) during spontaneous puberty. Levels of HDL-C and apolipoprotein A-1 were correlated during induced and spontaneous puberty. Testosterone should be considered a significant determinant (not necessarily directly causal) of plasma HDL-C levels during pubertal development.

Adolescent↗
PubMed1981

Delayed puberty.

Delayed puberty is the cause of much distress to adolescents and with modern techniques it is possible to arrive at a therapy-orientated diagnosis in the majority of instances. A relatively wide choice of therapeutic interventions is now available and may be employed, even in endocrinologically normal patients, if the situation warrants. In such patients, ther duration of therapy is very short. In patients with pathological causes of delayed puberty, the aim must be to reproduce the normal pubertal changes over the normal span of time and large doses of sex steroids should not be used early in the induction of puberty.

Adolescent↗
PubMed1985

Precocious puberty associated with neurofibromatosis and optic gliomas. Treatment with luteinizing hormone releasing hormone analogue.

Seven children with central precocious puberty and either neurofibromatosis and/or optic gliomas were referred to the National Institutes of Health, Bethesda, Md, for evaluation and treatment with the long-acting luteinizing hormone releasing hormone analogue (LHRHa) D-Trp6-Pro9-NEt-LHRH. Only six of the seven children chose to receive treatment. Four children presented with neurofibromatosis, three of whom also had optic gliomas; the remaining three children had isolated optic gliomas, without other neurocutaneous stigmas. All had central precocious puberty mediated by activation of the hypothalamic-pituitary-gonadal axis. Six months of LHRHa therapy caused suppression of gonadotropin and sex steroid levels, stabilization or regression of secondary sexual characteristics, and decreases in growth velocity and the rate of bone age maturation. We conclude that LHRHa therapy is effective in the treatment of central precocious puberty secondary to neurofibromatosis and/or optic gliomas.

17-alpha-Hydroxyprogesterone↗
PubMedDate not supplied

Longitudinal estimates of puberty timing in Senegalese adolescent girls.

This study aimed to assess the timing of sexual maturation (breast development and menarche occurrence) among sub-Saharan African adolescent girls from rural areas. In the framework of a longitudinal study of growth at puberty, the stages of pubertal development (Tanner classification) and menarche occurrence were recorded at intervals between 1995 and 2000 in a sample of 406 Senegalese adolescent girls from a rural area. Nutritional status was estimated during infancy, childhood, and adolescence within this sample, and body composition was estimated only during adolescence. At the beginning of the study (1995), the adolescent girls were 11.4 years old (SD = 0.6). At the end of the study, they were 16.5 years old (SD = 0.6). Median and quartile ages at entry into each maturity stage and its confidence limits were estimated by a lognormal parametric survival model. These adolescent girls were shorter and thinner than girls of the same age from developed countries. Median age at the onset of breast development was 12.6 years (95% CI = 12.5-12.8). Median age at the end of sexual maturation and median age at menarche were estimated respectively at 15.8 years (95% CI = 15.7-15.9) and 15.9 years (95% CI = 15.7-15.9). These adolescent girls were less mature than other adolescent girls of the same age from other developing countries. Their puberty was extremely delayed compared to that of adolescent girls of the same age from industrialized countries. Puberty in these Senegalese adolescent girls is delayed by about 3 years. This may be due to malnutrition, significant energy expenditure, and poor diet and living conditions, and possibly to genetic control.

Adolescent↗
PubMed1988

Do some patients with fragile X syndrome have precocious puberty?

We report on an 8 1/2-year-old white girl with fra (X) syndrome; she had mental deficiency, hyperactivity, speech disturbances, slightly prominent ears, mild joint laxity and 20% fra (X) expression. Additional findings include idiopathic precocious puberty and a right ovarian cyst. Ovarian cysts have been reported previously in heterozygous females, but to our knowledge idiopathic precocious puberty is a new finding in this syndrome. Whether precocious puberty is a coincidental finding in this patient or a previously unreported manifestation of the fra (X) syndrome is not clear.

Female↗
PubMed1995

Short-term effect of testosterone treatment on reduced bone density in boys with constitutional delay of puberty.

We studied bone mineral content (BMC), bone mineral density (BMD), cortical thickness/total width (CT/TW) ratio and cortical area/total area (CA/TA) ratio in boys with constitutional delay of puberty and the effect of short-term testosterone treatment on bone mass. Seventeen boys (age 13.1-15.8 years) who met the family history and the clinical criteria of constitutional delay of puberty were selected and enrolled in the study. All subjects were eating a diet assuring an adequate intake of calories and calcium. A subset of 8 boys (group A) was treated with testosterone depot (100 mg/month x 6 months) while 9 boys (group B) were not. At inclusion, BMC and BMD were reduced in the patients according to their chronological age (BMC -4.04 +/- 1.34 standard deviation scores [SDS]; BMD -2.95 +/- 0.56 SDS), statural age (BMC -1.75 +/- 0.79 SDS; BMD -1.69 +/- 0.78 SDS), and bone age (BMC -1.80 +/- 0.65 SDS; BMD -1.86 +/- 0.68 SDS). No significant differences between the groups were found (group A: BMC 0.480 +/- 0.57 g/cm, BMD 0.488 +/- 0.037 g/cm2, CT/TW ratio 0.43 +/- 0.4, CA/TA ratio 0.68 +/- 0.04; group B: BMC 0.476 +/- 0.060, p = NS vs. group A; BMD 0.491 +/- 0.036 g/cm2, p = NS vs. group A). At 12 months of follow-up, BMC, BMD, CT/TW ratio, and CA/TA ratio significantly increased in group A (BMC 0.70 +/- 0.13 g/cm, delta +41.1 +/- 28.8%, p < 0.003 vs. 0 month; BMD 0.617 +/- 0.082 g/cm2, delta +26.2 +/- 13.6%, p < 0.005 vs. 0 month; CT/TW ratio 0.52 +/- 0.05, delta +20.59 +/- 10.65%, p < 0.001 vs. 0 month; CA/TA ratio 0.77 +/- 0.05 vs. 0 month; CT/TW ratio 13.60 +/- 6.65%, p < 0.004 vs 0 month), but not in group B (BMC: 0.48 +/- 0.05 g/cm; delta +5.1 7.8%, p = NS vs. 00 month; BMD: 0.492 +/- 0.037 g/cm2; delta +0.54 +/- 8.7%, p = NS vs. 0 month; CT/TW ratio 0.44 +/- 0.04, delta +4.04 +/- 6.75%, p = NS vs. 0 month; CA/TA ratio 0.68 +/- 0.05, delta +2.39 +/- 5.90%, p = NS vs. 0 month). We conclude that boys with constitutional delay of puberty have reduced BMC and BMD. The delay in statural and bone ages did not totally account for the decreased bone mass. Testosterone treatment for 6 months significantly increased BMC, BMD, CT/TW ratio, and CA/TA ratio in these patients, but definitive conclusions on the efficacy of the treatment in improving adult bone mass can be drawn only when our patients reach early childhood.

Adolescent↗
PubMed1986

Sonographic monitoring of LHRH analogue therapy in idiopathic precocious puberty in young girls.

Precocious puberty in young girls is defined as the development of secondary sexual characteristics and gonadal growth before 8 years of age. Approximately 60% of isosexual precocious development in girls has no organic cause and is termed idiopathic precocious puberty. Thirteen young girls with idiopathic precocious puberty were treated with LHRH analogue under a well-established protocol. Pelvic ultrasound was added to the protocol to examine ultrasound's role in supplying a morphologic parameter of suppression of the pubertal process. Initially, 11 patients had ovarian volumes greater than normal, and ovarian cysts measuring 0.5 cm to 4 cm in diameter were identified in seven patients. All 13 patients had enlarged pretreatment uteri greater than 3 cm in length. Eleven of these patients had a pubertal or adult uterine configuration. After 1 year of therapy, 11 patients had normal prepubertal ovarian volumes, and 12 of 13 patients had a decrease in ovarian volume. No demonstrable cysts were present at 1 year. Eleven had a reduction in uterine length. Nine of the 11 patients with a pubertal uterine configuration reverted to a more prepubertal-like morphology. The sonographic morphologic changes correlated well with laboratory and clinical data indicating suppression of the hypothalamic-pituitary-gonadal axis.

Child↗