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PubMedDate not supplied

The role of TRH-stimulated prolactin responses in distinguishing gonadotropin deficiency from constitutional delayed puberty.

LHRH and TRH tests were performed in 16 boys age 14.5-18.5 years with constitutional delayed puberty (CDP); 9 idiopathic hypogonadotropic hypogonadism (IHH) males, age 15.0-22.0 years; and 7 control subjects age 14.5-19.5 years. The responses of FSH and LH to LHRH stimulation overlapped so that it was difficult to differentiate IHH from CDP. Some patients with IHH had normal gonadotropin responses. Basal PRL levels were in the normal range in control, IHH, and CDP patients. We found a 6 to 25 times increment or a response of more than 22 ng/ml (normal response) with respect to basal levels in the control group. In the CDP group, we found 2 to 19 fold increments in basal PRL levels after TRH stimulation and the maximum response was more than 22 ng/ml in all the patients. In the IHH group, the increment in basal PRL levels was 2-9 times more after the TRH test and the maximum PRL response was more than 22 ng/ml in 6 of the 9 patients. Although the mean peak responses of PRL to TRH were significantly lower in the IHH group compared to CDP and controls (p < 0.001), the mean peak individual responses in all groups were in the normal range (minimum 2-fold increment) and the responses were more than 22 ng/ml in all cases except 3 of 9 patients in the IHH group. We conclude that PRL response to TRH may help in differentiating CDP from IHH if a "cut off" response level of 22 ng/ml is used.

Adolescent↗
PubMed1995

Delayed puberty in males with beta-thalassemia major: pulsatile gonadotropin-releasing hormone administration induces changes in gonadotropin isoform profiles and an increase in sex steroids.

Patients with beta-thalassemia major often have pubertal delay, the etiology of which has not been fully elucidated. We investigated the pituitary-gonadal response to short-term subcutaneous pulsatile gonadotropin-releasing hormone (GnRH) administration (150 ng/kg body weight every 120 min for 7 days) in five young males (aged 13.6-19.0 years) affected by beta-thalassemia major and presenting signs of delayed puberty. Immunoreactive and bioactive gonadotropin levels were determined and their isoform profiles were examined, before and after GnRH treatment, in a pool of samples collected every 15 min for 240 min. Testosterone, androstenedione, 17-hydroxyprogesterone, dehydroepiandrosterone and 17 beta-estradiol were measured as markers of gonadal function on days 0, 1, 3, 5 and 7 of treatment. Five patients (aged 16.9-26.8 years) with confirmed diagnosis of idiopathic hypogonadotropic hypogonadism who were starting pulsatile GnRH therapy were also studied in the same protocol. Increased sex steroid levels were observed in both groups as a result of treatment. On day 7, the thalassemic patients had increased bioactive luteinizing hormone (LH) and follide-stimulating hormone (FSH), although immunoreactive LH and FSH were comparable to day 0. Moreover, fewer acidic and more basic immunoreactive and bioactive isoforms were noted in LH profiles on day 7. Similar results were observed in hypogonadal patients, who also had increased immunoreactive LH and FSH values. We suggest that the early stage of delayed puberty in thalassemia might be characterized by a neuroendocrine dysfunction resulting in an impaired hypothalamic GnRH release, which is inadequate for a proper pituitary stimulation. Pulsatile GnRH treatment seems to re-establish partially the correct pituitary-gonadal function.

17-alpha-Hydroxyprogesterone↗
PubMed2005

IGF-1 administration to prepubertal female rats can overcome delayed puberty caused by maternal Pb exposure.

Because prepubertal female rats maternally exposed to lead (Pb) exhibit suppressed serum levels of insulin-like growth factor-1 (IGF-1) and delayed puberty, we investigated the ability of centrally administered IGF-1 to stimulate luteinizing hormone (LH) release in vivo and LH-releasing hormone (LHRH) release in vitro from maternally Pb-exposed prepubertal female rats. Additionally, we assessed whether IGF-1 replacement could affect the timing of female puberty. Results demonstrated that IGF-1 stimulated significantly LH release in both control and Pb-exposed animals. When median eminences from control and Pb-exposed females were incubated with rat IGF-1 in vitro, they responded similarly with significant peptide-induced LHRH release. Lastly, we showed IGF-1 replacement reversed the delay in puberty caused by Pb. These results indicate the central LHRH response to IGF-1 is intact and that Pb-induced delayed puberty is due, at least in part, to suppressed circulating IGF-1 available to the hypothalamus.

Animals↗
PubMed2006

[Delayed puberty with extreme uterine hypotrophy: do not conclude too early to the absence of the uterus].

OBJECTIVE: To emphasize the difficulties to distinguish between uterine agenesis and extreme uterine hypotrophy in the context of primary amenorrhoea with delayed puberty. PATIENTS AND METHODS: Among adolescents who consulted with our center because of primary amenorrhoea, from 1997 to 2005, three patients were referred for a suspicion of Mayer-Rokitansky-Kuster-Hauser Syndrome, after ultrasonography had failed to visualize the uterus. The 3 patients underwent endocrine and genetic evaluations. Transabdominal ultrasonography and MRI performed pelvic examination. Patients were placed under estrogen treatment. RESULTS: Endocrine evaluation indicated primary ovarian failure for patient 1, and hypogonadotrophic hypogonadism for patients 2 and 3. Karyotype was 46,XX in all patients. Initial pelvic ultrasonography revealed the absence of uterus. MRI allowed visualizing prepubertal uterus for patient 1, a hypotrophic uterus for patient 3 and concluded to uterine agenesis for patient 2. In all cases estradiol substitutive therapy induced uterine growth and confirmed retrospectively the diagnosis of extreme uterine hypotrophy. DISCUSSION AND CONCLUSION: Pelvic ultrasonography can be misleading in the evaluation of primary amenorrhoea. No visualization of uterus on ultrasonography can occur in the context of delayed puberty and should not induce a premature diagnosis of Mayer-Rokitansky-Kuster-Hauser syndrome. Indeed, such a diagnosis has therapeutic, reproductive and psychological consequences.

Adolescent↗
PubMed2005

Human chorionic gonadotropin therapy in adolescent boys with constitutional delayed puberty vs those with beta-thalassemia major.

We studied 12 adolescent boys with beta-thalassemia major and delayed puberty (age, 15.8 +/- 1 years) with Tanner I sexual development treated with a long-term low-transfusion regimen. Ten nonthalassemic adolescents (> 14 years) with constitutional delay of growth and puberty (CDGP) served as controls. Auxologic parameters and testicular size were measured, and bone age was determined. Measurement of basal gonadotropin (luteinizing hormone [LH] and follicle-stimulating hormone [FSH]) and testosterone (T) levels taken at 8 am revealed prepubertal levels in both groups of patients. Human chorionic gonadotropin (hCG, 2500 U/m(2)) was injected intramuscularly twice weekly for 6 months, and anthropometric data, testicular diameter, and serum T concentrations were remeasured after 1 and 6 months. The testicular diameter after 6 month of hCG therapy was significantly correlated with the testicular diameter and T level after 1 month of therapy (r = 0.93 and 0.39, respectively, P < .01). After 6 months of hCG therapy, the mean growth velocity (GV) increased from 4.1 to 8.6 cm/y in thalassemic patients and from 4.6 to 10.3 cm/y in those with CDGP during hCG therapy. In thalassemic boys, the mean T concentration increased from 0.93 to 2.7 nmol/L (mean increase = 1.8 nmol/L) vs an increase from 0.47 to 4.81 nmol/L (mean increase = 4.32 nmol/L) in those with CDGP. All adolescents with CDGP, but only 7 the 12 thalassemic adolescents, had T secretion above 2 nmol/L after 6 months of hCG therapy and maintained their growth and pubertal development for a year after stopping hCG. The 5 thalassemic patients with defective T secretion after hCG therapy had significantly higher ferritin level (1985 +/- 658 ng/mL) vs the other 7 patients (1100 +/- 425 ng/mL). These findings denoted significant testicular dysfunction in those patients with higher iron overload (testicular siderosis). Statural GV was significantly correlated with insulin-like growth factor 1 (IGF-1) concentrations and testicular diameter after hCG therapy (r = 0.5 and 0.43 respectively, P < .001). In summary, hCG therapy was effective in treating 7 of 12 (58%) of thalassemic adolescents with delayed puberty. In the rest of patients (5/12, 46%) with significantly higher iron overload, hCG therapy failed to stimulate testicular growth and adequate T. Proper iron chelation appears to protect against testicular dysfunction. In the first group of patients, hCG therapy can be used for the treatment of their hypogonadism, whereas T replacement remains the therapy of choice for the second group.

Adolescent↗
PubMed2002

The NOTOM hypothesis for idiopathic scoliosis: is it nullified by the delayed puberty of female rhythmic gymnasts and ballet dancers with scoliosis?

Nachemson suggested that there are more girls than boys with progressive adolescent idiopathic because of a different timing between skeletal maturation and postural maturation in the sexes during adolescence. We termed Nachemson's concept the neuro-osseous timing of maturation (NOTOM) hypothesis and used it to propose a possible medical treatment for idiopathic scoliosis by delaying puberty through the pituitary using gonadorelin analogues as in idiopathic precocious puberty. The prevalence of scoliosis is reported to be increased in rhythmic gymnasts (RGs) in Bulgaria and in ballet dancers (BDs) in the USA. Both groups exhibit delayed puberty, which, at first sight, nullifies the NOTOM hypothesis for idiopathic scoliosis. While constitutional and environmental factors may determine these scolioses, the different curve types in RGs and BDs suggest that the exercise pattern over many years determines which type of scoliosis develops, although not the curve severity. We support the view that scoliotic RGs should be included in a group of sports-associated scoliosis separate from idiopathic scoliosis. Hence the delayed puberty of RGs and BDs with scoliosis does not nullify the NOTOM hypothesis as their scolioses are not idiopathic. There is a need to focus research on such subjects who have defined constitutional and environmental factors related to their scolioses.

Adolescent↗
PubMed1995

[Delayed puberty and hypogonadotrophic hypogonadism: differential diagnosis with prolactin stimulation probe with chlorpromazine].

We studied the changes in plasma levels of prolactin after an intramuscular injection of 0.33 mg/kg chlorpromazine and changes in plasma levels of LH and FSH after the injection of 100 micrograms iv GnRH, in 16 patients with delayed puberty, 10 patients with hypogonadotrophic hypogonadism and 6 healthy controls. Prolactin response was significantly lower in patients with hypogonadotrophic hypogonadism compared to subjects with constitutional delayed and healthy controls (delta Prolactin 7.05 +/- 1.7, 28.9 +/- 2.7 and 22.0 +/- 3.4 ng/ml respectively). LH response to GnRH was also lower in patients with hypogonadotrophic hypogonadism, compared to the other two groups (delta LH 4.3 +/- 2.5, 13.4 +/- 5.4 and 17.2 +/- 4.8 mUI/ml respectively) however, there was a great overlapping of values. No differences between groups were observed in responses of FSH, testosterone and estrogens to GnRH. It is concluded that prolactin response to chlorpromazine is useful in the differential diagnosis of constitutional delayed puberty.

Adolescent↗
PubMed1991

A case of Parinaud's syndrome in a boy with delayed puberty.

The authors describe a case of Parinaud's syndrome in a 14-year-old boy with delayed puberty. The neurological examination and the neuroradiological work-up excluded the presence of cerebral pathological processes except for a pituitary microadenoma. As the sole presence of the microadenoma cannot justify gonadotropin deficiency, the authors in this case favor a form of isolated gonadotropin deficiency, and they suggest that the elevation paralysis can be put in the range of median line defects, such as labiopalatoschisis and hypoplasia of the olfactory bulbs, frequently associated with isolated hypogonadotropic hypogonadism.

Adenoma↗
PubMed2006

Pubertal evaluation of adolescent boys with beta-thalassemia major and delayed puberty.

OBJECTIVE: To examine the hormonal status of the hypothalamic-pituitary-gonadal axis in adolescent males with beta-thalassemia major. DESIGN: Controlled clinical study. SETTING: Tertiary referral teaching hospital. PATIENT(S): Thirty-three adolescent males with beta-thalassemia major. INTERVENTION(S): Basal LH, FSH, and T were examined. All individuals received 100 microg GnRH analogue. Four hours later the hormone levels were retested. Patients with beta-thalassemia and low T levels received hCG. MAIN OUTCOME MEASURE(S): The preintervention and postintervention levels of FSH, LH, and T were examined. RESULT(S): Of the 33 beta-thalassemia major adolescents, 17 had delayed puberty. The difference in basal LH, FSH, and T levels between delayed and normal puberty beta-thalassemia groups were statistically significant. These levels were significantly lower compared with the constitutional delayed puberty group and become even more significant after GnRH analogue administration. The T levels in the beta-thalassemia group were significantly lower than in the control group. After hCG administration, the T levels remained significantly lower in the delayed-puberty beta-thalassemia compared to the normal-puberty beta-thalassemia group. CONCLUSION(S): Despite recent therapeutic advances in the management of beta-thalassemia major, the risk of secondary endocrine dysfunction remains high. Hypogonadism is one of the most frequent endocrine complications.

Adolescent↗
PubMedDate not supplied

Leisure behavior of youth with short stature, delayed puberty and diabetes mellitus.

There is some evidence to suggest that adolescents with endocrinological disorders such as short stature (SS), delayed puberty (DP), or diabetes mellitus (DM) may display significant social or psychological problems. The purpose of our study was to examine the leisure behaviors and experiences of these adolescents. Of the 178 adolescents (all of whom had an endocrinological problem) 83 were male and 91 were female. We found the leisure behaviors and experiences of adolescents with SS, DP and DM (the group) were similar to adolescents with other endocrine disorders (comparison group) and to several other non-clinical groups (controls). The group spent the same amount of time in leisure activity as the comparison group. The characteristics of the group's leisure time in regard to boredom, self-determination, self-competence or parental control was the same as the comparison group and minimally different from the control groups. There were no differences among SS, DP, DM or comparison group in degree to which they were 'bothered' by their condition or the recency of the discovery of their condition. Neither botheredness nor recency were related to leisure time characteristics. Recency of the discovery of their endocrine problem was almost significantly related to increased parental control (p<0.062) which was slightly greater for those diagnosed with SS, DP and DM (p<0.080) than in the comparison group. Leisure time activity and behavior of adolescents with SS, DP, and DM was the same as that in other non-clinical adolescents and adolescents with other endocrine disorders.

Adolescent↗
PubMed1977

Differential response of serum LH in hypogonadotropic hypogonadism and delayed puberty to LH-RH stimulation before and after clomiphene citrate administration.

The differential diagnosis between hypogonadotropic hypogonadism and delayed puberty is facilitated by comparing the response of gonadotropins to LH-RH stimulation before and after administration of clomiphene citrate 200 mg daily during 7 days. Premedication of clomiphene citrate depresses peak values of LH and FSH on LH-RH in delayed puberty. In hypogonadotropic hypogonadism clomiphene citrate raises LH-RH induced peak LH while FSH does not change.

Adolescent↗
PubMed1997

Testosterone treatment in adolescents with delayed puberty: changes in body composition, protein, fat, and glucose metabolism.

Previously, we demonstrated decreased protein breakdown and insulin resistance in pubertal adolescents compared with prepubertal children. Puberty-related increases in sex steroids and/or GH could be potentially responsible. In the present study, the effects of 4 months of testosterone enanthate (50 mg in every 2 weeks) on body composition, protein, fat, and glucose metabolism and insulin sensitivity were evaluated in adolescents with delayed puberty. Body composition was assessed by H218O-dilution principle. Protein breakdown, oxidation, and synthesis were measured during primed constant infusion of [1-13C]leucine. Whole-body lipolysis was measured during primed constant infusion of [2H5]glycerol. Insulin action in suppressing proteolysis and lipolysis and stimulating glucose disposal was assessed during a stepwise hyperinsulinemic (10 and 40 mU-m2.min) euglycemic clamp. Fat and glucose oxidation rates were calculated from indirect calorimetry measurements. After 4 months of testosterone treatment, height, weight, and fat free mass (FFM) increased and fat mass, percent body fat, plasma cholesterol, high- and low-density lipoproteins, and leptin levels decreased significantly. Whole-body proteolysis and protein oxidation were lower after testosterone treatment (proteolysis, 0.49 +/- 0.03 vs 0.54 +/- 0.04 g.h.kg FFM, P = 0.032; oxidation, 0.05 +/- 0.01 vs. 0.09 +/- 0.01 g.h.kg FFM, P = 0.015). Protein synthesis was not different, and resting energy expenditure was not different. Total body lipolysis was not affected by testosterone treatment, however, fat oxidation was higher after testosterone (pre-: 2.4 +/- 0.7 vs. post-: 3.5 +/- 0.7 mumol.kg.min, P = 0.031). During the 40 mU.m2.min hyperinsulinemia, insulin sensitivity of glucose metabolism was not affected with testosterone therapy (59.1 +/- 8.8 vs. 57.1 +/- 8.2 mumol.kg.min per muU/mL). However, metabolic clearance rate of insulin was higher posttestosterone (13.6 +/- 1.1 vs. 16.7 +/- 0.8 mL.kg.min, P = 0.004). In conclusion, after 4 months of low-dose testosterone treatment in adolescents with delayed puberty 1) FFM increases and fat mass and leptin levels decrease; 2) postabsorptive proteolysis and protein oxidation decrease; 3) fat oxidation increases; and 4) insulin sensitivity in glucose metabolism does not change, whereas insulin clearance increases. These longitudinal observations are in agreement with our previous cross-sectional studies of puberty and demonstrate sparing of protein breakdown of approximately 1.2 g.kg.day FFM, wasting of fat mass, but no change in insulin sensitivity after short periods of low-dose testosterone supplementation.

Adolescent↗
PubMed1984

Chemical cues from families delay puberty in male California voles.

The role of chemical cues in the delay of puberty in male California voles (Microtus californicus) was investigated. Males that were raised from weaning in bedding from their families were delayed in attainment of adult androgen levels and seminal vesicle weights compared to males raised in clean bedding. In a second experiment, the source of the suppressive cues was examined by rearing males in bedding from unrelated adult males, their fathers, or their mothers. Males reared with bedding from their mothers showed delayed maturation of both androgen levels and seminal vesicle weights, whereas males exposed to bedding from unrelated males were not delayed. Males exposed to bedding from their fathers showed intermediate androgen levels but large seminal vesicles. Thus, chemical cues from the family, particularly the mother, suppress reproductive development in male California voles. These results are discussed in the context of the puberty delay which occurs in natural populations of this species; it is suggested that puberty delay is an adaptive strategy that may be employed by young voles in times of high density and limited resources.

Adaptation, Physiological↗
PubMed2001

Dihydrotestosterone treatment in adolescents with delayed puberty: does it explain insulin resistance of puberty?

Puberty is characterized by temporary insulin resistance, which subsides with the completion of pubertal development. This insulin resistance is manifested by lower rates of insulin-stimulated glucose metabolism and compensatory hyperinsulinemia in pubertal compared with prepubertal children. Whether or not pubertal insulin resistance is the result of sex steroids or GH or a combination of both has been investigated in our laboratory. Previously, we demonstrated that T treatment in adolescents with delayed puberty was not associated with the deterioration of insulin action. The present investigation evaluated the effects of 4 months of dihydrotestosterone administration (50 mg im every 2 wk) on body composition, glucose, fat, and protein metabolism, and insulin sensitivity. Ten adolescents with delayed puberty were evaluated before and after 4 months of DHT administration. Body composition was assessed by dual energy x-ray absorptiometry. Insulin-stimulated glucose metabolism was measured during a 3-h hyperinsulinemic (40 mU/m(2).min)-euglycemic clamp procedure. Lipolysis and proteolysis were evaluated by stable isotopes of [(2)H(5)]glycerol and [1-(13)C]leucine. After 4 months of dihydrotestosterone treatment, height, weight, and fat free mass increased and percentage of body fat decreased. IGF-I and nocturnal GH levels did not change. There was no significant change in insulin-stimulated glucose metabolism (57.2 +/- 3.9 vs. 58.3 +/- 3.9 micromol/kg.min). Total body proteolysis and lipolysis did not change. In summary, based on the present and past studies, we conclude that during puberty insulin resistance/hyperinsulinemia is not attributable to gonadal sex steroids in boys.

Adolescent↗
PubMed2004

Reversible kallmann syndrome, delayed puberty, and isolated anosmia occurring in a single family with a mutation in the fibroblast growth factor receptor 1 gene.

Kallmann syndrome (KS) is a clinically and genetically heterogeneous disorder. Recently, loss-of-function mutations in the fibroblast growth factor receptor 1 (FGFR1) gene have been shown to cause autosomal dominant KS. To date, the detailed reproductive phenotype of KS associated with mutations in the FGFR1 has yet to be described. We report a kindred comprising a male proband with KS and spontaneous reversibility, whose mother had delayed puberty and whose maternal grandfather isolated anosmia. The proband presented at age 18 yr with KS and was subsequently treated with testosterone (T) therapy. Upon discontinuation of T therapy, he recovered from his hypogonadotropic hypogonadism, as evidenced by a normal LH secretion pattern, sustained normal serum T levels, and active spermatogenesis. The three members of this single family harbor the same FGFR1 mutation (Arg(622)X) in the tyrosine kinase domain. This report demonstrates 1) the first genetic cause of the rare variant of reversible KS, 2) the reversal of hypogonadotropic hypogonadism in a proband carrying an FGFR1 mutation suggests a role of FGFR1 beyond embryonic GnRH neuron migration, and 3) a loss of function mutation in the FGFR1 gene causing delayed puberty.

Adult↗
PubMed1995

Treatment of constitutional delayed puberty with a combination of testosterone esters.

Thirteen boys who had constitutional delayed puberty (CDP) were treated with a combination of short- and long-acting testosterone esters (testosterone propionate, testosterone phenylpropionate, testosterone isocaproate). Mean age at the onset of treatment was 14.9 +/- 0.6 years and bone age delay was -2.7 +/- 0.9 years. An intramuscular dose of 200 mg testosterone was administered 4 times at 3-week intervals and the treated CDP boys were followed for 2 years. All boys with CDP entered puberty after the last dose (testicular volume > or = 4 ml) and growth rate increased from 4.5 +/- 0.5 cm/year pretreatment to 8.4 +/- 1.6 cm/year posttreatment after the 2-year follow-up period. Height for bone age SD score did not alter significantly from a mean of -1.1 pretreatment to -1.3 posttreatment as well as predicted height pretreatment (173.5 +/- 6.6 cm) and posttreatment (173.3 +/- 4.9 cm). A combination of testosterone esters in a given dose and schedule is a safe and effective treatment for prepubertal boys with CDP.

Adolescent↗