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PubMed1998

Androgen therapy in chronic renal failure.

Chronic renal failure, dialysis and transplantation have major effects on male reproductive health because of the impairment of spermatogenesis, steroidogenesis and sexual function. Hypothalamo-pituitary testicular dysfunction in uraemia is manifest clinically as delayed growth and puberty, sexual dysfunction, androgen deficiency, impaired spermatogenesis and infertility. Apart from renal anaemia, there are at present no proven indications for androgen therapy in chronic renal failure. This chapter reviews the basis and scope for various clinical applications of gonadotropin and androgen therapy as an adjunct to the standard medical care of chronic renal failure. The therapeutic possibilities implied by experimental and clinical findings suggesting that uraemic hypogonadism may be a functional state of gonadotropin deficiency are emphasized.

Anemia↗
PubMed1988

Growth and endocrine function in steroid sensitive nephrotic syndrome.

Longitudinal height data and physical development were assessed in 29 boys and 12 girls taking long term steroid treatment for steroid sensitive nephrotic syndrome. Growth in both boys and girls, assessed by changes in height standard deviation score (delta Ht SDS), worsened significantly with chronological age. There was a significant negative correlation between delta Ht SDS and duration of treatment in boys, but not in girls. There was no correlation between delta Ht SDS and relapse rate or the use of cyclophosphamide. In the boys, Ht SDS decreased significantly only after the age of 10 years and was associated with delay in the appearance of secondary sexual characteristics. Eight adolescent boys were assessed endocrinologically by an overnight hormone profile. Blunting of the pulsatility of growth hormone and gonadotrophins was seen in six. Normal profiles were seen in two subjects who were both off steroid treatment at the time of study. Abnormal endocrine function in adolescent boys treated long term for steroid sensitive nephrotic syndrome corresponded with the clinical picture of delayed onset of puberty, which accounted for severe growth retardation in a substantial proportion of subjects.

Adolescent↗
PubMed1980

The Cohen syndrome: clinical and endocrinological studies of two new cases.

This report concerns two new cases of the Cohen syndrome and gives further information on the variable phenotypical pattern of the disease. The frequency of major and minor clinical signs is reviewed from all the published reports. Among the minor signs we found previously undescribed skeletal abnormalities in one of our patients. The reported delay onset of puberty, which appears to be a frequent aspect of the syndrome, seems to occur without LH and FSH deficiency, as our patients show.

Adolescent↗
PubMedDate not supplied

Effect of nutritional stress on the hypothalamo-pituitary-gonadal axis in the growing male rat.

BACKGROUND/OBJECTIVE: Nutritional dwarfing (ND) consists of a decrease in weight and height gain and delayed onset of puberty. The aim of the present investigation was to study the modifications induced in male rats by the nutritional stress of a mere 20% reduction in food intake which, however, started immediately after weaning. MATERIALS AND METHODS: At weaning, male Wistar rats were divided into two groups: Control (C) and ND. C rats were fed ad libitum with a balanced rodent diet. ND received 80% of the diet consumed by C for 4 weeks (T4); then they were fed ad libitum for another 4 (T8) and 8 weeks (T12). The rats were studied at T0, T4, T8 and T12 for the effects of nutritional stress and refeeding on nutritional status, body composition, hypothalamic-pituitary-gonadal axis, and sperm morphology and concentration. RESULTS: ND body weight and length diminished vs. C (p < 0.001). ND body fat percentage decreased 40% (p < 0.001) without change in the percentage of body protein content. The hypothalamic content of LHRH did not change. However, FSH, LH and testosterone serum levels had significantly decreased (p < 0.001) at T4 in ND rats. A 48.4 % decrease in serum leptin in the ND group was observed at T4 (p < 0.05). The absolute testicular and seminal vesicle weight was significantly decreased by ND at T4 (p < 0.001). At T4 the percentage of anomalies of caudal spermatozoa increased in about 64% (p < 0.001) of ND vs. C rats, despite the unchanged sperm concentrations. All parameters normalized during refeeding. CONCLUSION: In this model, a decrease in leptin due to nutritional stress could be responsible, at least in part, for the inhibition of reproductive function. Refeeding normalized all parameters studied.

Animals↗
PubMed1993

Early morning plasma testosterone is an accurate predictor of imminent pubertal development in prepubertal boys.

In the management of constitutional delayed growth and/or puberty, there is a need for simple tests which can assess the overall developmental maturity of the hypothalamic-pituitary-testicular axis in clinically prepubertal patients. This would enable the physician to predict the likelihood or otherwise of an individual entering puberty spontaneously within subsequent months. Based on our previous physiological data on the sequential pattern of peripubertal pituitary-testicular activation by hypothalamic GnRH, we hypothesized that the nocturnal secretion of testosterone, in response to sleep-entrained LH secretion, may provide a basis for an in vivo bioassay of neuroendocrine sexual maturity. Overnight testosterone secretion by the testis in clinically prepubertal boys was assessed with respect to their subsequent clinical progress, the target being the attainment of testicular volumes of greater than or equal to 4 mL (a clinical landmark when puberty has assuredly begun and virilization will soon follow). Forty-five prepubertal (Tanner stage G1PH1 testicular volume < or = 2 mL) boys aged 10.0-15.3 yr (mean +/- SEM 11.8 +/- 0.2) with short stature had paired plasma T concentration measured at 2000 h and 0800 h the following morning. After the initial assessment, all patients were reviewed clinically at 3-month intervals for a minimum of 21 months (mean 26.0 +/- 1.1, range 21-50 months). During this period, 38 (84.4%) patients received treatment in the form of sc human GH 2-4 IU daily or oxandrolone 2.5 mg daily by mouth to improve short-term growth although this did not have any significant effect on the subsequent timing of pubertal onset. The patients were divided according to whether 1) there was a demonstrable increase in plasma T between 2000 and 0800 h and 2) morning plasma T concentration was less than or greater than or equal to 0.7 nmol/L at their initial assessment. In those with a significant overnight T increment, 58% and 89% achieved testicular volume of greater than or equal to 4 mL after 12 and 21 months, respectively. In contrast, only 12% and 56% of patients who had not shown a T increase went into puberty by these times. In patients who had morning plasma testosterone concentrations greater than or equal to 0.7 nmol/L, 77% entered puberty within 12 months and 100% within 15 months. However, in those with a morning testosterone of less than 0.7 nmol/L, only 12.5% and 25% entered puberty within 12 and 15 months, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1989

Pulsatile gonadotropin secretion in pubertal children with chronic renal failure.

We have examined physiological nocturnal secretion of gonadotropins in 6 boys and 2 girls with end-stage renal disease, who had either delayed or disturbed puberty. The 5 patients treated by dialysis had reduced gonadotropin pulsatility for their stage of pubertal maturation, whereas the 3 patients with successful kidney grafts demonstrated a higher nocturnal rise and increased amplitude of gonadotropin pulsatility. It is suggested that the improved gonadotropin pulsatility of transplanted patients is due to their restored renal function.

Adolescent↗
PubMed1984

Differential diagnosis of male central hypogonadism by short-term pulsatile LHRH administration.

UNLABELLED: In order to obtain a clinically valuable differentiation of central hypogonadism (CH), 18 male patients, including 13 with permanent gonadotropin deficiency (GD), age 14.3-41 yrs, bone age 8.5-19 yrs, and 5 with constitutional delay (CD) of puberty (age 15.3-20, bone age 12.5-15 yrs) were studied. Among the GD patients, there were 4 with anosmia (Kallmann's syndrome, KS), 6 with idiopathic hypopituitarism (HP) and 3 with isolated hypogonadotropic hypogonadism (HH). The spontaneous nocturnal plasma profile of LH and FSH was compared with that during pulsatile LHRH infusion (5 micrograms iv every 90 min) by a portable micropump (Zyklomat) for 36 hrs. The pituitary-gonadal response was evaluated by calculating the LH and FSH slopes during pulsatile LHRH and by comparing plasma testosterone (T) before and after. While spontaneous nocturnal FSH pulses were absent in all patients, between 1 and 4 significant LH pulses were seen in all CD but in none of the GD patients. In all patients, mean FSH was significantly higher during pulsatile LHRH than during sleep. During pulsatile LHRH administration, significantly increasing FSH responses were seen in all KS and HP patients, but in only 2 of the 5 CD and in none of the 3 HH patients. In all CD boys (mean testis vol, 8.6 ml), T rose markedly during pulsatile LHRH (mean, from 168 to 414 ng/dl), whereas in all GD patients (mean testis vol, 2 ml) it did not (19 vs 27 ng/dl). CONCLUSIONS: Pulsatile LHRH for 36 hrs differentiates CD and GD far more exact than was previously possible.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2000

A case of primary amenorrhea, diabetes and anosmia.

This case details a patient with primary amenorrhea with an unusual cause. She presented at age 16 with short stature, minimal sexual development and no prior menses. Her history was significant for poorly controlled type 1 diabetes. She had been evaluated previously for growth hormone deficiency, and had received a short course of growth hormone therapy. Of greatest significance was the fact that she had also had a decreased sense of smell since her youth. Although a previous computerized tomography scan had been reported as normal, follow-up magnetic resonance imaging demonstrated the absence of olfactory bulbs. Smell testing confirmed the absence of smell and testing of gonadotropin releasing hormone demonstrated an inadequate response. All of these features suggested Kallmann syndrome. This syndrome commonly presents with delayed onset of puberty and decreased or absent sense of smell. There are also many associated features, and the disease is remarkable for its great genotypic and phenotypic variability. Current understanding of its pathogenesis, the commonly associated features of Kallmann syndrome and the impact of diabetes on growth and sexual development are reviewed.

Adolescent↗
PubMed1992

Effect of implanting bull calves with testosterone propionate, dihydrotestosterone propionate or oestradiol-17 beta prepubertally on the pituitary-testicular axis and on postpubertal social and sexual behaviour.

Twelve non-implanted crossbred bull calves served as controls and 30 crossbred bull calves (10/treatment) were implanted for 82 days, beginning at 34 days of age, to determine the influence of testosterone propionate (TP), dihydrotestosterone propionate (DHTP) and oestradiol-17 beta (E2) on prepubertal and pubertal pituitary-testicular function and on postpubertal social and sexual behaviour. Compared with control bulls, concentrations of serum luteinizing hormone (LH), follicle-stimulating hormone (FSH) and inhibin concentrations were suppressed (P less than 0.01) in all implanted bulls. Testosterone (T) concentration increased (P less than 0.001) in TP-implanted, but decreased (P less than 0.01) in DHTP and E2 bulls during the implant period. LH response to gonadotrophin-releasing hormone (GnRH) challenge during the implant period (2.5 months of age) was less (P less than 0.01) in TP, E2 and DHTP bulls than in controls. A small but significant T response to GnRH occurred in control bulls at 2.5 months of age. LH and T responses to GnRH challenge at 7 months of age (100 days after implant removal) was similar (P greater than 0.20) in control and implanted bulls. Steroid implants administered prepubertally had no effect (P greater than 0.10) on postpubertal social and sexual behaviours, including number of flehmen responses, abortive mounts, services and competitive order score. Body weight did not differ (P greater than 0.10) between treatment groups, but testis size was reduced (P less than 0.01) during the implant period and up to 10 months of age in treated bulls compared with controls. Testes remained smaller in E2-treated bulls up to the end of the study (23 months of age), but daily sperm production and epididymal weight did not differ (P greater than 0.10) between treatment groups at slaughter. Control bulls reached puberty earlier (P less than 0.01; 270 +/- 11 days of age) than did TP (302 +/- 11 days), DHTP (309 +/- 11 days) or E2 (327 +/- 11 days) bulls. Although puberty was delayed in all implant groups, there was no difference in scrotal circumference at puberty (average 28.4 +/- 0.4 cm) between treatment groups. Our findings indicate that TP, DHTP and E2 implants administered prepubertally result in acute suppression of serum LH, FSH and inhibin during the implant period and in post-implant suppression of testis size and delayed puberty in bulls. The lack of treatment effect on behaviour suggests that steroidal programming of sexual behaviour occurs before 1 month of age in bulls.

Animals↗
PubMed1994

Oral treatment for constitutional delay of growth and puberty in boys: a randomised trial of an anabolic steroid or testosterone undecanoate.

Thirty three boys (mean 14.6 years old, range 12.8-16.2 years) with constitutional delay of growth and puberty were randomised into two groups to determine which form of oral treatment would give the better anthropometric response. The two drugs were administered by mouth (one tablet/day) for a mean of 3.5 months (range 3-7 months). At randomisation, 17 boys received testosterone undecanoate (40 mg/day) and 16 oxandrolone (2.5 mg/day). At the start of treatment they were prepubertal or in early puberty, their height SD score was -1.97 in boys treated with testosterone and -2.21 in those treated with oxandrolone, and their growth rates were 4.3 and 4.2 cm/year respectively. Both sex steroid and anabolic steroid treatments induced a significant growth acceleration in all patients except four (three treated with testosterone and one with oxandrolone). When treated with the alternative sex steroid, all four non-responders had a significant anthropometric response. In all boys the induced growth acceleration was sustained when treatment was interrupted. There was no significant difference in the induced growth spurt and bone maturation between the two groups. Spontaneous progress into puberty was achieved in all boys with an increase in testicular volume from a mean of 4.6 to 8.5 ml. The rate of development in secondary sexual characteristics was also similar in the two groups. These data suggest that oral testosterone and oxandrolone are equally effective in the treatment of growth delay in boys with constitutional delay of growth and puberty.

Administration, Oral↗
PubMed1982

Delay and acceleration of puberty in female mice by urinary chemosignals from other females.

A sequence of 7 experiments tested various aspects of the acceleration and delay of sexual maturation in young female mice as affected by cues from other females: Singly caged females produce the maturation-delaying chemosignal when exposed to urine from grouped females. Urine from females housed 3 or more/cage produces delays in puberty for young females. Urine from females in estrus accelerates puberty in young females relative to untreated controls or urine from non-estrous females. The delay-of-maturation phenomenon in female mice is not affected by reproductive history, cross-fostering of pups, or varying the cagemates according to whether they are sibs or nonsibs. Taken together these and previous findings suggest that female mice excrete, in their urine, a series of chemicals which act as signals regarding the adequacy of reproductive conditions.

Animals↗
PubMed1985

Constitutional delay of growth and puberty in boys: the effect of a short course of treatment with fluoxymesterone.

17 boys with delayed growth spurt, 9 of whom also had late puberty, were treated with 2.5 to 5.0 mg of fluoxymesterone daily for 0.23-0.58 years. Mean increment of growth velocity was 4.5 cm/year during treatment and this was maintained at 3.8 cm/year over a post-treatment observation period of 0.22-1.3 years. Mean testicular volume at the end of the treatment period was 9.9 ml. Mean height for bone age standard deviation score remained unchanged at -1.2 to -1.4 (not significant). We conclude that a low dose of fluoxymesterone may be used in safety for a short time to induce a growth acceleration in adolescent boys with constitutional delay of growth and puberty.

Adolescent↗
PubMed2006

Management of short stature with GnRH agonist and co-treatment with growth hormone: a controversial issue.

Adolescent growth is the focus of several interventions aimed at increasing the amplitude of the adolescent spurt. Favorable results with GnRH agonists in precocious puberty have encouraged attempts to increase the duration of the adolescent growth spurt by delaying normal puberty in short individuals using GnRH agonists with or without growth hormone. These approaches remain highly controversial, have not been validated and approved for use by regulatory authorities and were the topic of a session at the 6th International Conference on the Onset of Puberty. Here we review the available information on the efficacy and safety of this approach. GnRH agonists, when used outside the context of precocious puberty, induce a modest gain when used for extended periods of time. Several trials have now shown that growth hormone alone can modestly increase adult height in short adolescents with idiopathic short stature or in those born small for gestational age. The association of growth hormone and GnRH agonists still lacks a definite demonstration of its additional efficacy and available results do not allow firm conclusions. In conclusion, watchful waiting or sex steroids in delayed puberty are generally the best options in short children presenting around puberty. However, long-term and adequately powered clinical trials, focusing on efficacy, safety and clinical significance are needed to fully evaluate the combination of growth hormone and GnRH agonists in short adolescents. In the meanwhile, these approaches should be considered as experimental.

Adolescent↗
PubMed2005

Delayed but normally progressed puberty is more pronounced in artistic compared with rhythmic elite gymnasts due to the intensity of training.

CONTEXT: Elite gymnasts are subjected to intense training, which may alter pubertal development. OBJECTIVE: The objective of the investigation was to study the impact of gymnastics on pubertal development in rhythmic (RGs) and artistic gymnasts (AGs). DESIGN: Evaluation of somatometric parameters, pubertal stage, and intensity of training in the competition field were studied. SETTING: The study was conducted at European and world championships of years 1997-2004. SUBJECTS: Subjects included 433 elite RGs and 427 AGs, aged 11-23 yr. INTERVENTION: There were no interventions. MAIN OUTCOME MEASURES: Mean chronological and bone ages of each pubertal stage and their relation to the intensity of training were measured. RESULTS: AGs and RGs showed a delay in skeletal maturation (Delta age-bone age, 2.13 and 1.28, respectively; P < 0.001). AGs were subjected to higher levels of physical training. Thelarche occurred at 12.9 yr for RGs and 13.2 yr for AGs (P = 0.003) and pubarche at 12.5 and 12.9 yr, respectively (P = 0.002). Puberty was delayed but normally progressed. AGs entered each pubertal stage later than RGs. The delay was influenced by the amount of energy output. Menarcheal age was 14.6 yr for RGs and 14.9 yr for AGs. Menarche was influenced in AGs by bone age (b = 0.333; t = 2.521; P = 0.020), pubarche (b = 0.322; t = 2.401; P = 0.026), and body fat (b = -0.458; t = -3.412; P = 0.003) and in RGs by bone age (b = 0.378; t = 3.689; P < 0.001) and pubarche (b = 0.525; t = 6.017; P < 0.001). CONCLUSION: In RGs and AGs, pubertal development was shifted to a later age, maintaining a normal rate of progression, which followed the bone age. AGs, who were exposed to a greater and more sustained energy output than RGs, presented a more pronounced delay in both skeletal maturation and pubertal development.

Adolescent↗
PubMed1989

Essential fatty acid deficiency delays the onset of puberty in the female rat.

This study assessed the effect of a dietary deficiency in the essential fatty acids (EFA) linoleic and linolenic acids on the onset of female puberty. EFA deficiency was produced in female rats by means of a semipurified diet and was biochemically documented by analyzing serum and erythrocyte fatty acid levels of more than 30 fatty acids, including all members of the n-6 and n-3 series. Levels of linoleic acid (18:2 n-6) and all n-6 derivatives, particularly arachidonic acid, were strikingly reduced. A less pronounced but clear-cut decrease in n-3 fatty acids, including docosahexaenoic acid (22:6 n-3) was also found. The times of puberty and first ovulation, as assessed by the ages at vaginal opening and first diestrus, were significantly delayed in EFA-deficient rats. The mechanisms underlying this delay appear to reside at both hypothalamic and ovarian sites. Simulation of preovulatory plasma estradiol (E2) levels via implantation of E2-containing Silastic capsules evoked a LH surge 30 h later in control juvenile rats, but not in EFA-deficient animals, indicating a delay in the development of the hypothalamic component of E2-positive feedback in the latter group. This delay appears to be due at least in part to reduced prostaglandin E2 (PGE2) synthesis, as the ability of the neurotransmitter norepinephrine to induce PGE2 release from median eminence nerve terminals was markedly reduced in EFA-deficient rats compared with that in controls. The decrease in hypothalamic PGE2 release was related to the EFA deficiency and not to reduced PG synthase activity, as determined by HPLC analysis of PG synthase products derived from exogenous [14C]arachidonic acid. Basal and hCG-stimulated PGE2 synthesis was also compromised in ovaries from EFA-deficient rats. Depressed gonadal function resulting from the EFA deficiency was further evidenced by a reduced gonadotropin receptor content, a blunted E2 response to hCG in vitro, and an increase in mean serum FSH levels. These results suggest that the delay in puberty resulting from EFA deficiency is due to a reduced availability of arachidonic acid for synthesis of bioactive metabolites. This results in delayed development of both the hypothalamic and ovarian components of the reproductive axis.

Animals↗
PubMed1991

Constitutional delay of growth and puberty: do they really reach their target height?

We compared the final adult height (FH) of patients with classic constitutional delay of growth and puberty with their target height (TH) and with the height prediction by the Bayley-Pinneau method (BP). 20 patients and their parents were included in our study: 6 females (mean age 19.1 years) and 14 males (mean age 20.6 years). No significant difference could be detected between TH, FH and BP prognosis. This is in contrast to recent studies using height data partly obtained by self-estimation. We measured our patients and their parents ourselves and were accurately able to calculate their genetically determined TH. This proceeding could explain our results. Our study shows that adolescents with true constitutional delay do not need treatment and that height prediction seems to be accurate.

Adolescent↗