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PubMed1976

A study of seasonally delayed puberty in the male hare, Lepus Europaeus.

The brown hare, Lepus europaeus, has a mating season which extends from January to September. Adult males exhibit pronounced seasonal changes in the reproductive tract which are associated with changes in LH secretion. Maximum plasma levels of immunoreactive LH occur between March and June and minimal levels in the autumn non-mating period from September to December; this seasonal cycle in gonadotrophin output is reflected by the appropriate changes in the secretion of testosterone from the testes and in the activity of the accessory sex glands. Juvenile animals reach puberty only during the adult mating season, and the age of puberty thus varies with the date of birth. Males born before May reach puberty and become fertile at 3 months of age, while those born from May to July grow to a mature body size during the autumn non-mating season but puberty is delayed for several months. Since some animals experiencing delayed puberty were found to have elevated plasma levels of LH and testosterone, it is concluded that puberty is not completely suppresed by the environmental effects of the autumn, but that the developmental process is prolonged, resulting in the juveniles being synchronized with the adults in their reproductive activity.

Age Factors↗
PubMed2003

Pitfall in diagnosing growth hormone deficiency in a hypochondroplastic patient with a delayed puberty.

Hypochondroplasia is a clinically and genetically heterogeneous skeletal dysplasia with less obvious disproportion in childhood and a reduced pubertal growth spurt. We report on a young hypochondroplastic man who had been misdiagnosed and treated as being growth hormone (GH) deficient in the early phase of puberty. The delay of his puberty which is unusual in hypochondroplasia might have confused the results of provocative GH testing. At the age of 17 years measurement of body proportions revealed an increased upper to lower body segment ratio. Skeletal radiographs showed a lack of increase in the interpedicular distance from the first to the fifth lumbar vertebra, anteroposterior shortening of the lumbar pedicles, short femoral necks, a fibula longer than the tibia, and short tubular bones. As the clinical and radiographic features suggested the diagnosis of a skeletal dysplasia, a DNA sequence analysis of the fibroblast growth factor receptor 3 gene on chromosome 4 p16.3 was performed, which identified the missense mutation C1620 G in the tyrosine kinase domain resulting in an Asn540Lys substitution. Hypochondroplastic children with this common mutation (N540K) were previously found to respond to GH treatment with an increase in sitting height compared to leg length, which accentuated the existing disproportion. We want to emphasise that in children with normal serum IGF-I and IGFBP-3 levels accurate measurements of body proportions and skeletal radiographs in disproportionate cases are more important than reiterative GH stimulation tests, which prepubertally and in the early phase of puberty often show subnormal responses.

Child↗
PubMed2006

Impact of body mass index on growth in boys with delayed puberty.

It is unclear whether overweight but otherwise healthy boys with delayed puberty have a variation of constitutional delay of growth and maturation (CDGM) or a different etiology for their pubertal delay. To characterize better this group of boys and investigate whether their growth pattern distinguishes them from boys with typical CDGM, growth data were analyzed in eight overweight (BMI SDS > or = 85th percentile) and 37 non-overweight (BMI SDS <85th percentile) boys with delayed puberty. Primary outcome measures included predicted height (PH) and adult height (AH). At diagnosis of delayed puberty, the overweight boys had less delayed bone ages (chronological age [CA] - bone age [BA] = 1.2 +/- 1.0 vs 2.5 +/- 1.1 years, p <0.01), greater height SDS for CA (-0.5 +/- 0.7 vs -2.4 +/- 0.8, p <0.001), and greater height SDS for BA (0.6 +/- 0.9 vs -0.4 +/- 1.1, p <0.05). PH for the overweight boys exceeded their mid-parental height (MPH) by 5.0 +/- 7.2 cm while non-overweight boys were predicted to fall below their MPH by 2.8 +/- 6.3 cm (p <0.01). Available AH data corroborated the differences in PH, with a trend for overweight boys to have greater height relative to their MPH than the non-overweight boys. These observations suggest that in the context of delayed puberty, being overweight may modulate adult height and/or that the etiology of delayed puberty in overweight boys may differ from typical CDGM.

Adolescent↗
PubMed2006

[Primary amenorrhea: constitutional delayed puberty or hormonal disturbance].

Investigations were carried out in 2 women of 17 and 18 years with primary amenorrhea, normal external female genitalia and delayed secondary sexual characteristics, for the reasons for delayed puberty. The 17-year-old patient had reduced values of FSH, LH and oestradiol. This disturbance in the hypothalamo-hypophysary axis was caused by hydrocephalus. Menarche occurred following drainage of the fluid. The 18-year-old patient had raised values ofFSH and LH and a lowered oestradiol value. There was therefore a disfunction existing at ovarian level, which appeared to be caused by an XX-gonadal dysgenesis. The patient was treated with hormones which led to breast development and menarche taking place. The cause ofprimary amenorrhea can mainly be divided into three categories: constitutional delayed puberty, delayed puberty due to hypogonadotropic hypogonadism, or delayed puberty due to hypergonadotropic hypogonadism. A carefully taken medical history, together with determination of the serum levels of FSH and LH, is helpful in differentiating between these categories. Subsequently, structured clinical management must be performed in order to approach the differential diagnosis of each of these categories, which will then be followed by the final diagnosis.

Adolescent↗
PubMed1996

A longitudinal evaluation of bone mineral density in adult men with histories of delayed puberty.

We have previously demonstrated that men with histories of constitutionally delayed puberty have significantly lower spinal and radial bone mineral density than normal men. Because these men were in their mid-twenties, it is possible that bone density was decreased because bone development was still incomplete. In addition, there is no information on the bone density of the proximal femur, the most important clinical site for osteoporotic fractures, in men with histories of delayed puberty. To address these issues, we performed repeat measurements of radial and spinal bone mineral density 2 yr after the initial evaluations in 18 men with histories of delayed puberty. Bone mineral density of the femoral neck was also measured at the time of follow-up evaluations. The mean radial bone mineral density at the time of the repeat evaluations was similar to the mean value from the initial evaluations (0.74 +/- 0.08 vs. 0.74 +/- 0.07 g/em2) and the mean change was 0.00 +/- 0.04 g/cm2. Similarly, the mean spinal bone mineral density at the time of the repeat evaluations was similar to the mean value from the initial evaluations (1.02 +/- 0.10 vs. 1.01 +/- 0.10 g/cm2) and the mean change was -0.01 +/- 0.04 g/cm2. Bone mineral density of the femoral neck was significantly lower in the men with histories of delayed puberty than in normal men (0.88 +/- 0.11 vs. 0.98 +/- 0.14 g/cm2 P < 0.02). These data indicate that bone accretion is complete by the mid-twenties in men with histories of constitutionally delayed puberty and that their bone mineral density does not improve with time. In addition, these men have decreased bone density of the femoral neck, which might increase their risk for hip fractures when they are older.

Adult↗
PubMed1999

Serum leptin levels in males with delayed puberty during short-term pulsatile GnRH administration.

Leptin may be a possible trigger for puberty. In normal males, it has been shown that leptin increases from the pre-pubertal to the early pubertal stage, and then declines in the late pubertal stage. We examined leptin levels in six male adolescents (mean age 16.3+/-0.6 yr; range 14.2-17.6 yr) with delayed puberty (constitutional delay of puberty no.=2; idiopathic hypogonadotropic hypogonadism no.=4) during 120 days of subcutaneous pulsatile GnRH administration. A group of subjects in pre-puberty (no.=11), early-puberty (n=10) and mid-puberty (no.=7) were evaluated as controls. Morning blood samples were taken for determination of leptin, testosterone, LH and FSH levels. In delayed puberty subjects blood samples were taken every 30 days after the start of GnRH administration. At each examination BMI and testicular volume were evaluated. A follow-up examination was performed in the 6 patients 1.3-7.5 yr after the end of the 120 days of GnRH therapy. At baseline evaluation in delayed puberty mean leptin levels were 11.3+/-2.0 microg/l (median 11.3 microg/l; range 4.7-17.3 microg/l) and were higher than those found in pre-puberty (p=0.04) and mid-puberty (p=0.001). During GnRH administration there was no change in BMI and leptin levels but there was an increase in gonadotrophin levels, testosterone and testicular volume. One hundred and twenty days after, mean serum leptin were 10.1+/-2.1 microg/l (median 9.1 microg/l; range 3.4-16.8 microg/l). At the end of the study, leptin levels were higher in delayed puberty than in mid-puberty (p=0.002). At the follow-up examination leptin levels were 4.3+/-1.3 microg/l (median 3.4 microg/l; range 1.4-9.1 microg/l) (p=0.03 vs end of 120 days GnRH therapy) while testosterone and BMI were not changed. In conclusion 120-day pulsatile GnRH administration induced in males with delayed puberty physiological-like pubertal changes but not the decline in leptin levels reported during the progression of puberty. Therefore, in males with delayed puberty an impairment in the phenomenon of leptin decline associated with progression of puberty could be suggested. However after retrospective diagnosis of pubertal delay and long-term therapy in subjects with idiopathic hypogonadotropic hypogonadism leptin levels declined. These data seem to indicate that time more than increase in testosterone levels and testicular volume is the determinant of leptin decline at puberty.

Adolescent↗
PubMed2002

Delayed puberty: analysis of a large case series from an academic center.

Despite the clinical importance of delayed puberty, the understanding of this condition is hampered by the lack of studies evaluating etiologies and predisposing factors among large case series. We performed a retrospective study of clinical and laboratory data from adolescents (< or =18 yr of age) with delayed puberty who had been seen in our clinic between 1/96 and 7/99 (n = 232 subjects; 158 males and 74 females). Family histories of pubertal timing among primary relatives were classified as negative, having at least a tendency to pubertal delay (development > or =1 SD beyond the mean), or diagnostic of delay (development > or =2 SD beyond the mean). The most common cause of delayed puberty was constitutional delay of growth and maturation (CD), which affected 53% of the subjects (63% of males and 30% of females). The remaining subjects could be divided into four categories: those with an underlying condition associated with delayed, but spontaneous, pubertal development [functional hypogonadotropic hypogonadism (FHH)], 19% of subjects; those with permanent hypogonadotropic hypogonadism, 12% of subjects; those with permanent hypergonadotropic hypogonadism, 13% of subjects; and those without clearly classified disorders, 3% of subjects. Like CD, FHH was male predominant, whereas the other categories either affected both genders equally or were predominantly female. In total, 50 different etiologies led to pubertal delay within our case series. Data permitted classification of family histories of pubertal timing among primary relatives in 95 of 122 of the CD and in 25 of 45 of the FHH cases. Analysis revealed at least a tendency to pubertal delay in 77% of the CD and in 64% of the FHH families and a diagnosis of delay in 38% of the CD and 44% of the FHH families. Both parents contributed to the positive family histories. The rates of positive family histories among the CD and FHH groups were approximately twice those seen among the other subjects in our case series. Among all subjects, those with FHH had the most marked growth delay, and girls had the greater bone age delay. Among the boys and at comparable chronological ages, CD and FHH were characterized by greater delays in pubic hair development and bone age than in the other diagnostic groups. Although CD is typically associated with leanness, 22% of our subjects had a BMI SD score at the 85th percentile or above for chronological age. These overweight subjects differed from the rest of the CD group: bone age was less delayed, and height was less affected. Finally, our analysis suggested a possible association between attention deficit disorder with or without hyperactivity and pubertal delay in our CD and FHH subjects. Our study provides valuable data regarding the variety and frequency of diagnoses that lead to delayed puberty. The results underscore the importance of performing a thorough evaluation and family history in adolescents with delayed puberty. Moreover, the data from our case series provide clues for unraveling the mechanism(s) of idiopathic pubertal delay and lead to the hypothesis that the pubertal delay seen among some subjects with FHH and CD may stem in part from similar underlying physiology.

Academic Medical Centers↗
PubMed1994

[The status of the gonadotropin releasing hormone test in differential diagnosis of delayed puberty in adolescents over 14 years of age].

BACKGROUND: In patients with delayed puberty with a bone age less than 11 years in girls or 12 years in boys, the clinical and endocrinological examination allows the differentiation of patients with the various forms of hypergonadotropic hypogonadism, but not of patients with hypogonadotropic hypogonadism from more prevalent constitutional delay in puberty. Therefore, watchful waiting is generally recommended for differential diagnosis in patients with delayed puberty. On the other hand, the late onset of sexual hormone replacement in patients with hypogonadism will worsen their outcome. PATIENTS AND METHOD: Therefore, we decided to carry out a retrospective study in 105 adolescents who were examined because of short stature or delayed puberty, who were aged 14 to 22 years at first visit and in whom the differential diagnosis of delayed puberty was documented after an at least one-year follow-up in order to find out which endocrinological parameters could have effectively predicted the final diagnosis already at the first visit. RESULTS: Patients with hypogonadotropic hypogonadism differed from patients with constitutional delay in puberty by lower responses of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels to gonadotropin-releasing hormone stimulation (GnRH, 100 micrograms iv) (p < 0.01) as well as by smaller testicular volume (p < 0.05) and by lower testosterone levels (p < 0.01). Stimulated LH < 10 mU/ml differentiated patients with hypogonadotropic hypogonadism from constitutional delay in puberty with a sensitivity of 82% and a specificity of 98%. CONCLUSION: In patients with delayed puberty aged 14 years and older bone age usually exceeds 11 years in girls or 12 years in boys. It thus is in the range, in which normal adult responses of LH to GnRH can be expected. In contrast to patients aged less than 14 years, therefore, measuring GnRH-stimulated LH levels in these patients allows the rapid and effective differential diagnosis of delayed puberty.

Adolescent↗
PubMed1986

Pituitary response to LHRH, LH pulsatility and plasma melatonin and prolactin changes in ewe lambs treated with melatonin implants to delay puberty.

Prepubertal ewe lambs were treated with empty or filled melatonin implants. The implants were placed s.c. at birth and pituitary responsiveness to various doses of LHRH, LH/FSH pulsatility and prolactin and melatonin secretion were examined at 10, 19, 28, 36 and 45 weeks of age. Control animals (N = 10) showed no consistent alteration in pituitary responsiveness to LHRH during development. Ewes treated with melatonin (N = 10) had puberty onset delayed by 4 weeks (P less than 0.03) but no effect of melatonin on LH or FSH response to LHRH injection was observed at any stage of development. In the control and melatonin-treated ewe lambs the responses to LHRH injection were lower during darkness than during the day at all stages of development. No consistent differences in LH or FSH pulsatility were observed between treatment groups or during development. Prolactin concentrations, however, failed to decrease at the time of puberty (autumn) in the melatonin-treated group. Melatonin-treated ewe lambs maintained normal rhythmic melatonin production which was superimposed on a higher basal concentration and showed the same increase in melatonin output with age as the control ewes. These results indicate that the delayed puberty caused by melatonin implants is not due to decreased pituitary responsiveness to LHRH or to dramatic changes in basal LH or FSH secretion.

Animals↗
PubMed1995

Increased nocturnal melatonin secretion in male patients with hypogonadotropic hypogonadism and delayed puberty.

Hypogonadotropic hypogonadism (IGD) and constitutional delayed puberty (DP) share a common pathophysiologic process, i.e. GnRH deficiency. Both conditions are heterogenous and exhibit different grades of GnRH deficiency. To discern whether these disorders of GnRH deficiency are associated with altered melatonin secretion profiles, we compared untreated young males IGD (n = 7) and DP (n = 7) to normal pubertal male controls (n = 6). Serum samples for melatonin, LH, and prolactin concentrations were obtained every 15 min from 1900 h to 0700 h in a controlled light-dark environment with simultaneous sleep recordings. Mean (+/- SD) darktime nocturnal melatonin levels were significantly higher in IGD (259 +/- 73 pmol/L) and DP (217 +/- 29 pmol/L) compared with 182 +/- 69 pmol/L in controls (P < 0.02). So were the mean (+/- SD) peak melatonin levels (410 +/- 117, 327 +/- 97 and 298 +/- 95 pmol/L in IGD, DP, and controls, respectively (P < 0.05). Integrated nocturnal melatonin secretion values (AUC) were also higher in IGD and DP (168 +/- 45 and 134 +/- 28) compared with 119 +/- 45 pmol/min.1 x 10(3) in controls (P < 0.02). The time of melatonin peak and the time of onset of the nocturnal melatonin rise were observed earlier in IGD and DP. Light-time mean (+/- SD) serum melatonin levels were similar in all three groups. No correlations were found between melatonin and LH levels, nor between melatonin and prolactin levels. These data indicate that melatonin secretion is increased in male patients with GnRH deficiency. The lack of correlations between melatonin and LH suggest that circulating sex steroids, rather than LH, modulate melatonin secretion in a reverse fashion.

Activity Cycles↗
PubMed1995

Use of the gonadotropin-releasing hormone agonist triptorelin in the diagnosis of delayed puberty in boys.

To differentiate gonadotropin deficiency from delayed puberty in teenage boys, 0.1 mg/m2 of triptorelin, a gonadotropin-releasing hormone agonist, was administered subcutaneously at 4 AM. Serum gonadotropins and testosterone levels were determined at baseline and 4 hours after the injection. The increase in blood gonadotropin and testosterone levels was significantly greater in patients with delayed puberty than in those with gonadotropin deficiency.

Adolescent↗
PubMed1997

Relationship between the thymus and neurochemical changes in the hypothalamus-preoptic area and prefrontal cortex in female rats with delayed puberty.

In female rats, aged 55-58 days with delayed puberty due to deficient growth and environmental stress, 5-hydroxyindoleacetic acid levels and serotonin turnover rate in the hypothalamus-preoptic area as well as body weight, body weight gain and relative weight of ovaries, uterus, adrenals and preputial glands were lower while serotonin and 5-hydroxyindoleacetic acid levels in the prefrontal cortex were higher when compared to normal rats with the latest onset of puberty aged 42-52 days. In rats with delayed puberty, multiple regression analysis revealed a significant negative dependence on dopamine turnover in the hypothalamus-preoptic area for body weight gain and, of all organs, for the relative weight of the thymus. A similar negative significant dependence on serotonin turnover rate in the prefrontal cortex was also found for the relative weight of thymus and spleen. The same analysis in the opposite direction revealed a significant negative dependence of 3,4-dihydroxyphenylacetic acid levels and dopamine turnover rate in the hypothalamus-preoptic area as well as serotonin turnover rate in the prefrontal cortex only on thymus weight. After separation of delayed pubertal rats into two groups, based on absolute ovarian weight, the rats in the low ovarian weight range and no signs of puberty exhibited: lower body weight gain, lower body weight, and lower relative weight only of thymus, ovaries and preputial glands in parallel with an increased dopamine turnover rate in the hypothalamus-preoptic area and serotonin turnover rate in the prefrontal cortex compared to the delayed pubertal rats in the high ovarian weight range and early signs of puberty. The results suggest that in rats with delayed puberty: (1) serotonergic activation in the hypothalamus-preoptic area is lower compared to normal puberty rats; (2) dopaminergic activation in the hypothalamus-preoptic area negatively affects body weight gain, thymus weight and initiation of puberty and (3) thymus weight is negatively implicated in dopaminergic activation in the hypothalamus-preoptic area and serotonergic activation in the prefrontal cortex and positively related to ovarian weight and early signs of puberty.

Animals↗
PubMed2003

Delayed puberty and amenorrhea.

The ability to diagnose and manage disorders that cause delayed puberty requires a thorough understanding of the physical and hormonal events of puberty. Wide variation exists within normal pubertal maturation, but most adolescent girls in the United States have begun to mature by the age of 13. Delayed puberty, a rare condition in girls, occurs in only approximately 2.5% of the population. Constitutional delay, genetic defects, or hypothalamic-pituitary disorders are common causes. Amenorrhea, often found as a symptom of delayed puberty, may be due to congenital genital tract anomalies, ovarian failure, or chronic anovulation with estrogen presence or with estrogen absence.

Adolescent↗
PubMed2005

Management of boys with short stature and delayed puberty.

OBJECTIVE: To review the management of boys with short stature and delayed puberty and the testosterone priming protocol. METHODS: In 148 boys aged > 14 years seen for height < -2 SDS and constitutional delayed puberty we evaluated growth hormone (GH) secretion and final height (80 boys). RESULTS: The GH peak was < 10 microg/l after arginine-insulin tests performed with testosterone heptylate priming in 8/32 (25%) and without in 62/153 (41%), including first and second evaluations. It was low in 7/11 boys given 2 x 100 mg testosterone (14.7 +/- 1.7 microg/l) and in 1/21 given 4 x 100 mg (21.3 +/- 2.0 microg/l, p = 0.04). It was low during sleep in 4/29 (14%) boys, all having basal plasma testosterone below 3.5 nmol/l. The basal insulin-like growth factor (IGF)-I concentration was below -2 SDS in 22% of the boys evaluated. Final height was -0.8 +/- 0.1 SDS. It was similar in those with low (n = 9) and normal (n = 71) GH peak, and in those treated (n = 22) or untreated (n = 58) with testosterone. It was over 1 SDS lower than the target height in 20% and than the predicted height at the initial evaluation in 14% of the boys. Pubertal growth was not correlated with the GH peak or plasma IGF-I. CONCLUSIONS: The GH peak during the sleep is more frequently normal than the peak after stimulation. The number of testosterone doses influences the quality of priming. The medical problems involved in treating boys with delayed puberty are excluding disease and deciding on testosterone treatment.

Adolescent↗
PubMed1979

Effect of puberty on rates of bone growth and mineralisation: with observations in male delayed puberty.

The bone mineral content (BMC) and body height were measured in 301 normal children and adolescents aged 7--20 years, and in 8 boys with constitutional delayed puberty aged 14--17 years. Serum testosterone was measured in the last group as well as in a subpopulation of the normal children and adolescents. The growth spurt, which coincided with a steep increase of serum testosterone in boys, indicated a great change in skeletal growth and mineralisation in both sexes. After the growth spurt, linear growth slowed down considerably while bone mineralisation rose steeply. When low levels of serum testosterone were maintained, as in delayed puberty, these combined changes of skeletal growth and mineralisation did not occur. It is suggested that gonadal hormones are the true initiators of the short-lived growth spurt as well as of prolonged acceleration of bone mineralisation.

Adolescent↗