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PubMed1996

Increase in first morning voided urinary luteinizing hormone levels precedes the physical onset of puberty.

Determinations of serum gonadotropin concentrations by ultra-sensitive methods have improved the diagnosis of pubertal disorders. The onset of puberty can be estimated by measuring serum gonadotropin pulsation, but as this requires serial nocturnal blood sampling, it is not a routine investigation. Gonadotropin measurements in first morning voided (FMV) urine samples could reflect the integrated nocturnal gonadotropin secretion and predict pubertal development earlier than daytime serum measurements. We studied the value of urinary LH (U-LH) measurements in FMV urine with reference to serum LH (S-LH) levels using an ultrasensitive time-resolved immunofluorometric assay in samples from 297 children and adolescents (145 boys and 152 girls, aged 5-15 yr) with known pubertal stages (Tanner 1-5). Stage 1 subjects (prepubertal) were divided into 5 age groups to assess whether there is an increase in LH before clinical signs of puberty can be detected. The correlation between FMV urine and S-LH values was good (r = 0.64; P < 0.0001). The 2 oldest groups of prepubertal subjects (11 and 12 yr) had significantly higher (P < 0.001) U-LH concentrations than the 3 younger groups. This difference was less marked for S-LH. A significant increase in FMV U-LH concentration occurs before the first clinical signs of puberty in a sex-independent fashion. Our data indicate that FMV U-LH measurement is a clinically relevant, noninvasive method for the evaluation of pubertal development, and it may be helpful in the investigation of pubertal disorders.

Aging↗
PubMed1996

A longitudinal assessment of hormonal and physical alterations during normal puberty in boys. II. Estrogen levels as determined by an ultrasensitive bioassay.

A limited number of reports of estrogen levels in prepubertal and early pubertal boys have been published because previous estrogen assays have lacked adequate sensitivity to quantitate circulating estrogen concentrations. Development of a new ultrasensitive assay has permitted measurement of estrogen levels in 23 normally growing boys progressing through puberty. Concentrations were measured at approximately 4-month intervals over a 5- to 8-yr period. The levels increased with maturation in all and correlated directly with chronological age, bone age, weight, height, pubertal stage, and testosterone and insulin-like growth factor-I levels. Of these factors, the level of testosterone had the greatest influence on the estrogen concentration. The time from peak growth velocity also significantly correlated with estrogen level. The estrogen level correlated positively with growth velocity before the time of peak growth velocity and negatively after peak growth velocity. The estrogen levels first increased significantly an average of 3 yr after pubertal onset and reached a peak by 5 yr after pubertal onset. Peak growth velocity was attained an average of 3 yr after pubertal onset. The greatest increase in the rate of rise of the estrogen level was an 11-fold rise during the year in which puberty began. The next most significant increase was a 4.8-fold rise 3 yr after pubertal onset. With respect to pubertal stage, the greatest absolute change occurred from stage 4 to stage 5 and the greatest fold change occurred from stage 1 to stage 2. The estrogen level did not significantly correlate with the 24-h GH level. In conclusion, circulating estrogen levels are very low in all boys prepubertally and rise steadily during adolescent development. The estrogen level is closely related to testosterone concentration and to the time of peak growth velocity. These findings are consistent with the hypothesis that estrogen at low levels augments skeletal growth and maturation in boys (as well as girls). They are also consistent with the hypothesis that continued exposure to estrogen leads to epiphyseal fusion. Further studies are required to define the separate and combined roles of estrogen, GH, and testosterone, as well as other factors, on growth and sexual development at puberty.

Age Determination by Skeleton↗
PubMed1997

Adult height in 24 patients treated for growth hormone deficiency and early puberty.

This study evaluates the capacity of treatment with the combination of growth hormone (GH) and gonadotropin releasing hormone (GnRH) analog to preserve the height potential of 24 patients (15 girls, 9 boys) with GH deficiency and early puberty (onset at 7.8 +/- 0.5 SE yr in girls and 9.0 +/- 0.7 yr in boys). All but 4 were given cranial irradiation. They (group 1) were compared with 17 patients of normal pubertal age treated with GH for cranial irradiation-induced GH deficiency (group 2) and with 19 girls treated with GnRH analog for idiopathic central precocious puberty (group 3). The adult heights in groups 1, 2 and 3 were -0.5 +/- 0.2, -1.3 +/- 0.2, and -0.2 +/- 0.2 SD, significantly lower (P < 0.01) in group 2. They were lower than the target heights in groups 1 and 2 (P < 0.001), and similar in group 3. They were similar to the predicted heights at the onset of therapy (combined, GH, or GnRH analog therapy), except in group 3 (adult height > predicted height, P < 0.0001) In group 1, as in group 3, the differences between adult and predicted heights (1.1 +/- 1.3 and 6.5 +/- 1.4 cm respectively) correlated positively with the difference between bone and chronological ages (P < 0.05), negatively with the predicted height (P < 0.002), and positively with the difference between the target and predicted heights (P < 0.001) at the onset of therapy. In conclusion, treatment with the combination of GH and GnRH analog in patients with GH deficiency and early puberty leads to a normal adult height. This height is similar to the predicted height at the onset of therapy but lower than the target height.

Adult↗
PubMed1999

A single sample subcutaneous luteinizing hormone (LH)-releasing hormone (LHRH) stimulation test for monitoring LH suppression in children with central precocious puberty receiving LHRH agonists.

The effectiveness of LHRH agonist therapy in central precocious puberty depends upon suppression of LH secretion. The iv LHRH stimulation test is the gold standard for evaluating LH suppression, but is difficult to administer because it requires an iv line and multiple blood samples. We hypothesized that a sc LHRH test followed by a single LH measurement 40 min later would be as accurate in the assessment of LH suppression in children receiving LHRH analogs. Eleven children received the sc test 1 month before or after their regularly scheduled iv LHRH treatment. Each child was receiving Lupron to suppress central puberty. Twenty-five comparisons of the iv and sc LHRH tests were completed over 14 months. We developed a clinical score for pubertal suppression using Tanner staging, skeletal maturation, and growth velocity. The best correlation between this clinical score and the iv LHRH test was achieved when biochemical suppression was defined as peak LH less than 2 IU/L (100% sensitivity, 95% specificity). Using this definition, the sc LHRH test was 96% accurate (in 24 of 25 subjects), with a sensitivity of 75% and a specificity of 100% compared to the iv LHRH test. We conclude that the single sample sc LHRH test can accurately determine LH suppression and adequacy of LHRH agonist therapy in central precocious puberty.

Adolescent↗
PubMed1999

A limited repertoire of mutations of the luteinizing hormone (LH) receptor gene in familial and sporadic patients with male LH-independent precocious puberty.

Herein, we report mutation analysis of the LH receptor gene in 17 males with LH-independent precocious puberty, of which 8 were familial and 9 had a negative family history. A total of 7 different mutations (all previously reported) were detected in 12 patients. Among 10 European familial male-limited precocious puberty (FMPP) patients who had a LH receptor gene mutation, none had the Asp578Gly mutation, which is responsible for the vast majority of cases in the U.S. The restricted number of activating mutations of the LH receptor observed in this and other studies of FMPP strongly suggests that an activating phenotype is associated with very specific sites in the receptor protein. Clinical follow-up of the 5 patients who did not have LH receptor mutations shows that such cases most likely do not have true FMPP. LH receptor mutation analysis provides a sensitive tool for distinguishing true FMPP from other causes of early-onset LH-independent puberty in males.

Amino Acid Sequence↗
PubMed2000

High dose recombinant human growth hormone (GH) treatment of GH-deficient patients in puberty increases near-final height: a randomized, multicenter trial. Genentech, Inc., Cooperative Study Group.

GH production rates markedly increase during human puberty, mostly as an amplitude-modulated phenomenon. However, GH-deficient children have been dosed on a standard per kg BW basis similar to prepubertal children. This randomized study was designed to compare the efficacy and safety of standard recombinant human GH (rhGH) therapy (group I, 0.3 mg/kg x week) vs. high dose therapy (group II, 0.7 mg/kg x week) in GH-deficient adolescents previously treated with rhGH for at least 6 months. Ninety-seven children with documented evidence of GH deficiency (peak GH in response to stimuli, <10 ng/mL), with either organic or idiopathic pathology, were recruited. Both groups were matched for sex (group I, 42 males and 7 females; group II, 41 males and 7 females), age [group I, 14.0+/-1.6 (+/-SD) yr; group II, 13.7+/-1.6], standardized height (group I, -1.4+/-1.1; group II, -1.2+/-1.1), bone age (group I, 13.1+/-1.3 yr; group II, 13.1+/-1.3) etiology, maximum stimulated GH, previous growth rate, and midparental target height. All subjects were in puberty (Tanner stage 2-5) at study entry. Of the 97 subjects enrolled, 45 were treated for 3 yr or more; 48 completed the study. Of the subjects who discontinued the study, the most common reason was satisfaction with their height, although others discontinued for adverse events or personal reasons. The frequency of patients who discontinued was the same in both groups. The primary efficacy analysis was the difference between dose groups for near-adult height, defined as the height attained at a bone age of 16 yr or more in males and 14 yr or more in girls; all subjects who qualified were included in the analysis. This difference was statistically significant at 4.6 cm by analysis of covariance (ANCOVA; P < 0.001; n = 75). For subjects who received at least 4 yr of rhGH treatment, the difference between dose groups at that time point was 5.7 cm (by ANCOVA, P = 0.024; n = 20). The mean height SD score at near-adult height was -0.7+/-0.9 in the standard dose group and 0.0+/-1.2 in the high dose group. At 36 months the cumulative change in height (centimeters) was 21.5+/-5.3 cm (group I) vs. 25.1+/-4.9 (group II; P < 0.001, by ANCOVA); the change in Bayley-Pinneau predicted adult height was 4.8+/-4.2 cm (group I) vs. 8.4+/-5.7 (group II; P = 0.032). Median plasma IGF-I concentrations at baseline were 427 microg/L (range, 204-649) in group I and 435 microg/L (range, 104-837) in group II; at 36 months they were 651 microg/L (range, 139-1079) in group I vs. 910 microg/L (range, 251-1843) in group II (P = NS). No difference in change in bone age was detected between groups at any interval. High dose rhGH was well tolerated, with a similar safety profile as standard dose treatment and no difference in hemoglobin A1c or glucose concentrations between groups. In summary, compared to conventional treatment, high dose rhGH therapy in adolescents 1) increased near-adult height and height SD scores significantly, 2) did not increase the rate of skeletal maturation, and 3) appears to be well tolerated and safe. In conclusion, high dose rhGH therapy may have a beneficial effect in adolescent GH-deficient patients, particularly those who are most growth retarded at the start of puberty.

Adolescent↗
PubMed2001

Nocturnal application of transdermal estradiol patches produces levels of estradiol that mimic those seen at the onset of spontaneous puberty in girls.

The objective of pubertal induction in children with hypogonadism is to mimic spontaneous puberty in terms of physical and psychological development. In a clinical observation study, we induced puberty in 15 girls with hyper- or hypogonadotropic hypogonadism using low doses of transdermal estradiol patches attached only during the night and compared the estradiol concentrations obtained with those in healthy girls. Pubertal induction was started between the ages of 12.3 and 18.1 yr. A transdermal matrix patch of 17beta-estradiol (25 microg/24 h; Evorel, Janssen Pharmaceuticals-Cilag) was cut into pieces corresponding to 3.1, 4.2, or 6.2 microg/24 h initially and attached to the buttock. After 4-14 months, the dose was increased gradually. Serum 17beta-estradiol concentrations were measured every 2 h by RIA (detection limit, 6.0 pmol/L; 1.6 pg/mL). The results show that it is possible to mimic the spontaneous levels as well as the diurnal pattern of serum 17beta-estradiol in early puberty, by cutting a transdermal 17beta-estradiol matrix patch and attaching a part of it, corresponding to 0.08-0.12 microg estradiol/kg BW, to the buttock nocturnally. In most of the girls, breast development occurred within 3-6 months of the start of treatment.

Administration, Cutaneous↗
PubMed2001

Adrenocorticotropin-dependent precocious puberty of testicular origin in a boy with X-linked adrenal hypoplasia congenita due to a novel mutation in the DAX1 gene.

Primary adrenal insufficiency is a rare condition in pediatric age, and its association with precocious sexual development is very uncommon. We report a 2-yr-old Brazilian boy with DAX1 gene mutation whose first clinical manifestation was isosexual gonadotropin-independent precocious puberty. He presented with pubic hair, enlarged penis and testes, and advanced bone age. T levels were elevated, whereas basal and GnRH-stimulated LH levels were compatible with a prepubertal pattern. Chronic GnRH agonist therapy did not reduce T levels, supporting the diagnosis of gonadotropin-independent precocious puberty. Testotoxicosis was ruled out after normal sequencing of exon 11 of the LH receptor gene. At age 3 yr he developed clinical and hormonal features of severe primary adrenal insufficiency. The entire coding region of the DAX1 gene was analyzed through direct sequencing. A nucleotide G insertion between nucleotides 430 and 431 in exon 1, resulting in a novel frameshift mutation and a premature stop codon at position 71 of DAX-1, was identified. Surprisingly, steroid replacement therapy induced a clear decrease in testicular size and T levels to the prepubertal range. These findings suggest that chronic excessive ACTH levels resulting from adrenal insufficiency may stimulate Leydig cells and lead to gonadotropin-independent precocious puberty in some boys with DAX1 gene mutations.

Adrenal Gland Diseases↗
PubMed1994

Race, sex, and puberty influence onset, severity, and outcome in juvenile myasthenia gravis.

We assessed the influence of race, sex, and puberty upon clinical features and outcome in 115 patients with autoimmune juvenile myasthenia gravis (JMG). These demographic variables influenced not only disease incidence but also disease severity, response to therapy, and outcome, despite comparable therapeutic strategies. Among white patients, those with prepubertal onset had low incidence and equal sex ratio; the incidence in females increased during and after puberty; males had lesser disease severity than females during and after puberty (p < 0.05); spontaneous remissions were most frequent (44%, p = 0.001) and persistence of active JMG for more than 10 years was least frequent (p = 0.05) in patients with prepubertal onset; remissions were more frequent after early than late thymectomy (p = 0.03); and final disease severity was less after early than late thymectomy. Black patients had similar incidence, disease severity, and sex ratio (F:M = 2:1) with pre-, peri-, or postpubertal disease onset; infrequent spontaneous or treatment-induced remissions; and the same final disease severity after early or late thymectomy. These observations imply that race and sex hormones modify the clinical features and outcome of JMG; spontaneous remissions are common in white patients with prepubertal disease onset; early thymectomy may be more beneficial than late thymectomy in white patients; and the role of thymectomy in the youngest patients is uncertain. We suggest that demographic factors should be considered when evaluating past and future therapeutic strategies for JMG.

Adolescent↗
PubMed2006

Immunological changes in response to exercise: influence of age, puberty, and gender.

PURPOSE: This study tested the hypothesis that exercise-induced perturbation and recovery of the immune system would vary with age, puberty, and gender in healthy children and adolescents. METHODS: Twelve-year-old girls (YG; N = 14) and boys (YB; N = 20), and 14-yr-old girls (OG; N = 11) and boys (OB; N = 13) cycled for 60 min at 70% VO2max. Blood was collected before, at 30 and 60 min of exercise, and at 30 and 60 min of recovery to measure total leukocytes, leukocyte and lymphocyte subsets, and cytokines. Age and pubertal (Tanner stage) effects within genders and gender effects within age and pubertal groups were determined. RESULTS: Exercise-induced increases in lymphocytes, CD3-CD16+CD56+ counts, and IL-6 were approximately 83, 90, and 390% greater in OG versus YG (P < 0.05). Recovery leukocytosis and neutrophilia were approximately 56 and 35% greater in OB versus YB (P < 0.05). Pubertal stage did not have a statistically significant influence on responses in girls, but the lowest pubertal stage consistently showed smaller changes in lymphocytes and CD3-CD16+CD56+ counts. Recovery neutrophilia was approximately 120% greater in postpubertal boys versus prepubertal or pubertal boys (P < 0.05). Responses of lymphocytes and CD3-CD16+CD56+ counts, respectively, were approximately 120 and 82% greater in OG versus OB (P < 0.05), with no differences between YG and YB. Exercise-induced increases in total leukocytes, lymphocytes, and CD3-CD16+CD56+ counts were at least 35% greater in girls versus boys of similar pubertal status (P < 0.05). Regardless of age, puberty, or gender, IL-8 levels were significantly higher during recovery versus rest (P < 0.05). CONCLUSION: These results highlight the need to control for age, puberty, and gender when interpreting immunologic responses to exercise in a pediatric population.

Adolescent↗
PubMed2006

Puberty effects on NK cell responses to exercise and carbohydrate intake in boys.

UNLABELLED: Previous research has demonstrated that younger versus older animals and humans experience smaller perturbations in natural killer (NK) cells in response to physiological stress. PURPOSE: To determine whether the smaller perturbations in NK cells induced by strenuous exercise and carbohydrate (CHO) intake, previously reported in children, are influenced by puberty. METHODS: Twenty 12-yr-old boys, distinguished as prepubertal (Tanner (T) 1, N = 7), early pubertal (T2, N = 7), or pubertal (T3-5, N = 6), cycled for 60 min at 70% VO(2max) while drinking 6% CHO (CT) or flavored water (WT). Blood was collected at rest and during (30 and 60 min) and following (30 and 60 min) exercise to identify NK cells as CD3(-)CD56(dim) or CD3(-)CD56(dim). CD69 expression on CD3(-)CD56(+) cells was also determined. RESULTS: A puberty x CHO x exercise interaction was found for the proportion, but not number, of CD56(dim) cells (P = 0.06). CD56(dim) cell counts were lower in CT versus WT (P < 0.001). Responses of CD56(bright) proportions (P = 0.007) and counts (P = 0.03) depended on pubertal status, but not CHO. The CD56(bright):CD56(dim) ratio remained stable during exercise, but during recovery was higher in T1 and T3-5 versus T2 (P = 0.08) and in CT versus WT (P = 0.04). During recovery, CD3(-)CD56(+) cells expressed higher levels of CD69 (P = 0.01), with no change in the proportion of CD69(+) cells. CONCLUSION: These results confirm the influence of puberty on the distribution of NK cell subsets in response to exercise and CHO intake. Increased CD69 expression suggests that NK cells increase activation status during recovery from physiological stress.

Antigens, CD↗
PubMed1995

Idiopathic isosexual central precocious puberty: magnetic resonance findings in 30 patients.

The purpose of this prospective study was to define the incidence of magnetic resonance imaging (MRI) abnormalities in the brain in patients with idiopathic central precocious puberty without any additional neurological signs and symptoms, and to evaluate the routine use of gadolinium contrast in these patients. 30 patients (29 girls, one boy; age range 1.9-11.9 years) with idiopathic central precocious puberty were studied. MRI of the brain in axial, coronal and sagittal planes was performed before and after administration of gadopentetate dimeglumine, with special attention to the region of the third ventricle. There are three major findings: (1) the height of the pituitary gland is increased up to adult size compared with normal individuals; (2) in four patients (13%) major structural abnormalities were found; three hamartomas of the tuber cinereum and one gliomatous process extending from the chiasm to the optic tract; and (3) the routine use of gadopentetate dimeglumine did not reveal new abnormalities although the lack of enhancement made a positive contribution to diagnostic certainty. We conclude that contrast enhanced MR examination is a safe and reliable method for the exclusion of abnormalities in children with precocious puberty and for the follow-up of those patients in whom abnormalities are present.

Adolescent↗
PubMed2005

KiSS-1 and GPR54 as new players in gonadotropin regulation and puberty.

The recent identification of loss-of-function mutations in the gene encoding GPR54, the receptor for the KiSS-1-derived peptides, kisspeptins, has highlighted a previously unrecognized pathway in the physiologic regulation of puberty and reproduction. Patients with loss-of-function mutations in GPR54 have idiopathic hypogonadotropic hypogonadism, and mice lacking GPR54 similarly fail to undergo puberty and have immature reproductive organs and low levels of sex steroids and gonadotropins. These observations have led to the hypothesis that kisspeptins activate hypothalamic GnRH release, thereby serving as a pivotal factor in the pubertal activation of the reproductive cascade. This hypothesis is supported by subsequent studies in rodent and primate models that have demonstrated localization of KiSS-1 mRNA in the hypothalamus, colocalization of GPR54 in GnRH neurons, GnRH-dependent activation of LH and FSH release by intracerebroventricular or peripheral administration of kisspeptin, and increased hypothalamic KiSS-1 and GPR54 mRNA levels at the onset of puberty. Taken together, these findings weave a compelling case for a role of the kisspeptin-GPR54 system in the activation of GnRH neurons at the time of pubertal awakening of the reproductive axis.

Animals↗
PubMed1996

Management of puberty in growth hormone deficient children.

At puberty there occur marked increases in gonadotropin, gonadal steroid and GH secretion. An important physiological synergism exists between the gonadal and somatotropic axes to permit the growth spurt and adolescent development; however, epiphyseal maturation is also accelerated leading to cessation of long-bone growth. GH deficiency may be absolute, but often is not and the diagnosis may be complicated by a constellation of physical and hormonal findings that are along a spectrum from low normal GH sufficiency to absent GH secretion. Growth hormone therapy not only accelerates the growth velocity, but also promotes the redistribution of adipose tissue stores to more peripheral sites. Given the remarkable physiological alterations in the activities of the GH and gonadotropin gonadal axes during adolescence in normal children, how should the therapeutic plan for the treatment of prepubertal GH deficiency be altered at puberty? Evidence for efficacy has been reported for each of the following for the treatment of GH deficiency at adolescence: 1) GH alone at the usual dosage (approximately 0.3 mg.kg-1.day-1); 2) Double or triple the amount of GH to mimic the finding of increased GH release at puberty. 3) GH at the usual or moderately increased dose and gonadotropin releasing hormone agonist analog to halt pubertal development. The latter two plans are at present hypotheses that must withstand the rigor of proper controlled trials. The end point is more than merely adult height, because of the significant psychological and skeletal system dysregulation that accompany decrements in the gonadal steroid hormones during adolescence.

Adolescent↗
PubMed1980

In vitro steroidogenesis in testes of three infants, two with ambiguous external genitalia and one with true precocious puberty: Evidence for the presence of active 17 beta-hydroxysteroid oxidoreductase in immature human testes.

The present report investigated steroidogenesis in vitro in testis tissues obtained from two boys aged 8 months and 4 years with ambiguous external genitalia and male vagina, and a 4-year-old body with true precocious puberty. Histologically, testes of the former two boys are still immature and the testis of the last one contains differentiated Sertoli cells and primary spermatocytes, but no mature Leydig cells are recognized in any of them. In each testis, 17 beta-hydroxysteroid oxidoreductase is active for androstenedione in the presence of an excess amount of NADPH, while delta 5-3 beta-hydroxysteroid dehydrogenase and delta 4-steroid 5 alpha-reductase activities are limited. 17 alpha-Hydroxylase and C17--20 lyase are significantly active in each testis and are enhanced in the testis of the boy with precocious puberty. Although the testis tissue used in the present study may not be biologically normal and the number of cases investigated is still limited, the above results indicate that active 17 beta-hydroxysteroid oxidoreductase is present in immature human testes and that delta 5-3 beta-hydroxysteroid dehydrogenase may become active in the human testis at the advanced stage of the development of testicular function during the puberty.

17-Hydroxysteroid Dehydrogenases↗
PubMedDate not supplied

True precocious puberty associated with phenylketonuria.

We studied a girl with phenylketonuria who demonstrated signs of precocious puberty. At the age of 7.5 years she had premature telarche. Her height age was 7-9/12 years and her bone age was 9 years. Gonadotropin responses to LHRH administration were consistent with central precocious puberty. Elevated serum phenylalanine levels in this patient, due to poor compliance with the phenylalanine restricted diet, may be related to the early onset of puberty.

Body Height↗
PubMedDate not supplied

Long-acting gonadotropin-releasing hormone agonists in the differential diagnosis of male precocious puberty.

Male sexual precocity is defined as the development of secondary sexual characteristics before 9 years of age. It can be classified as gonadotropin-dependent precocious puberty (GnDP) or gonadotropin-independent precocious puberty (GnIP) and sometimes the differential diagnosis between these entities is difficult. To determine whether long-acting GnRH agonists (GnRH-a) are effective in differential diagnosis of male precocious puberty, we measured gonadotropins and testosterone levels 30 days after a single administration of depot GnRH-a (triptorelin, gosereline or leuprolide) in 10 boys with sexual precocity of different etiologies. Testosterone levels 30 days after depot GnRH-a were in the prepubertal range in patients with GnDP but not in GnIP. We conclude that measurement of testosterone levels 30 days after long-acting GnRH-a is effective in the differential diagnosis of male sexual precocity.

Child↗
PubMedDate not supplied

GH and GnRH analog treatment in children who enter puberty at short stature.

It is well known that height at the onset of puberty is closely related to final height. To improve final height of short children who enter puberty at short stature, twenty-one short boys and six short girls were treated with a combination of GH and GnRH analog. The boys started the combination treatment at a mean age of 12.0 years when their mean height was 128.5 cm (-2.74 SD) and the girls at a mean age of 10.68 years when their mean height was 126.4 cm (-2.23 SD). The boys discontinued GnRH at a mean age of 16.88 years after a mean treatment period of 4.89 years when their height was 153.7 cm (-2.75 SD), and the girls at a mean age of 13.89 years after a mean treatment period of 3.20 years when their height was 143.3 cm (-1.94 SD). Bone age maturation significantly decelerated during the combination treatment. Bone age rarely exceeded 14 years in boys and did not exceed 13 years in girls. Bone age maturation during combination treatment decelerated after bone age 12 years in boys and 10.5 years in girls. On average, bone age matured at a mean rate of 0.48 years a year in boys and 0.56 years a year in girls during the combination treatment. During the combination treatment, height velocity did not decelerate rapidly and remained at 3-5 cm/year for a longer duration because of the bone age deceleration, although a definite pubertal growth spurt was not observed. As a consequence, the mean projected height SDS for bone age increased 1.50 (+/- 0.76) SD in boys and 1.24 (+/- 0.49) SD during the combination treatment. Although most of the patients have not yet reached their final height, combined GnRH analog and GH treatment should increase the pubertal height gain and the adult height in short children who enter puberty early for height, when the post-GST growth is taken into account. The combination treatment seems more effective in boys than in girls. This improvement is attributed to the lengthening of the treatment period by slower bone maturation and maintained growth velocity.

Administration, Intranasal↗