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Results for “Puberty, Delayed”

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PubMed1988

Prolactin response to metoclopramide does not distinguish patients with hypogonadotrophic hypogonadism from delayed puberty.

The prolactin response to metoclopramide (MCP) was studied in 23 sexually immature males, 14 with isolated hypogonadotrophic hypogonadism (IHH) and nine with constitutional delayed puberty. Six of the 14 IHH patients had not been treated prior to our study, whereas eight had received long term therapy with testosterone or hCG for variable periods ranging from 1 to 20 years. We also measured the prolactin response to chlorpromazine (CPZ) in the untreated IHH men. In these untreated subjects, we observed a greatly diminished prolactin response after CPZ by comparison to that measured following MCP administration (peak 15 ng/ml, areas 86 units vs peak 43 ng/ml, area 416 units, respectively) (P less than 0.01). Furthermore, prolactin levels following MCP were similar in untreated (peak 43 ng/ml, area 416 units) and treated (peak 55 ng/ml, area 545 units, NS) IHH males as well as in boys with constitutional delayed puberty (peak 50 ng/ml, area 532 units, NS). In addition, responses in the three groups of patients were about half (P less than 0.01) those measured in normal men (peak 81 ng/ml, area 845 units). These data indicate that, unlike CPZ, MCP is not useful in distinguishing patients with hypogonadotrophic hypogonadism from boys with constitutional delayed puberty.

Adolescent↗
PubMed2001

A specific aromatase inhibitor and potential increase in adult height in boys with delayed puberty: a randomised controlled trial.

BACKGROUND: The role of oestrogens in the closure of growth plates in both sexes is unequivocal. We postulated that inhibition of oestrogen synthesis in boys with delayed puberty would delay maturation of the growth plates and ultimately result in increased adult height. METHODS: We did a randomised, double-blind, placebo-controlled study in which we treated boys with constitutional delay of puberty with testosterone and placebo, or testosterone and letrozole. Boys who decided to wait for the spontaneous progression of puberty without medical intervention composed the untreated group. FINDINGS: Letrozole effectively inhibited oestrogen synthesis and delayed bone maturation. Progression of bone maturation was slower in the letrozole group than in the placebo group. In 18 months, bone age had advanced 1.1 (SD 0.8) years in the untreated group and 1.7 (0.9) years in the group treated with testosterone and placebo, but only 0.9 (0.6) years in the letrozole group (p=0.03 between the treatment groups). Predicted adult height did not change significantly in the untreated group and in the placebo group, whereas in the group treated with letrozole the increase was 5.1 (3.7) cm (p=0.004). INTERPRETATIONS: Our findings suggest that if oestrogen action is inhibited in growing adolescents, adult height will increase. This finding provides a rationale for studies that aim to delay bone maturation in several growth disorders.

Adolescent↗
PubMed1981

Clinical value of adrenal androgen measurement in the diagnosis of delayed puberty.

Serum levels of the adrenal androgens dehydroepiandrosterone (DHA), dehydroepiandrosterone sulphate (DHAS), and androstenedione (A) were measured in 90 males (age range 14 1/2--26 years) presenting with delayed puberty to an adult endocrine clinic over a period of 3 years. The results show that adrenal androgen levels are significantly lower (p less than 0.0005) in subjects with growth-hormone (GH) deficiency than in patients with simple and constitutional delayed puberty and other, less common, conditions. By contrast, subjects with hypogonadotropic hypogonadism had significantly raised values (p less than 0.0005). On initial presentation DHA and DHAS measurements correctly identified all GH-deficient subjects and in addition DHAS measurements identified 89% of subjects with hypogonadotropic hypogonadism. It is suggested that measurement of serum levels of DHA and DHAS may assist greatly in the early diagnosis of conditions causing delayed puberty, and thus may prevent unnecessary delay in treatment.

Adolescent↗
PubMed1992

Delayed puberty in uremia: pituitary-gonadal function during short-term pulsatile luteinizing hormone-releasing hormone administration.

Pubertal development is frequently delayed or disordered in children with chronic renal failure. Both neuroendocrine and peripheral alterations due to uremia have been hypothesized to explain the impairment in the pituitary gonadal axis. The aim of the present study was to evaluate quantitative (immunological) and qualitative (biological) LH secretion, as well as FSH and sex steroids, before and during 7 days of sc LHRH administration (136-150 ng/kg bw every 120 min) in 5 uremic children (13.1-14.8 yr) with delayed puberty. Six nonuremic children (13.2-17.8 yr) with delayed puberty underwent the same schedule and served as control group. On day 0 mean immunoreactive LH (I-LH) levels were higher in uremic (4.5 +/- 0.9 mIU/ml) than in nonuremic (1.9 +/- 03 mIU/ml; p < 0.05) subjects while no differences were observed in bioactive LH (B-LH) levels (2.9 +/- 0.7 mIU/ml vs 2.4 +/- 0.3 mIU/ml). In both groups of subjects testosterone was at prepubertal levels. Spontaneous I-LH and B-LH pulses were observed sporadically in both uremic and nonuremic subjects. Short-term pulsatile LHRH administration induced significant increases in B-LH, I-LH, FSH and testosterone. The B/I LH ratio increased from day 0 (0.7 +/- 0.2) to day 7 (1.3 +/- 0.4; p < 0.05) in uremics while it showed wide fluctuations in nonuremic subjects. On day 7, 4 uremic and 5 nonuremic subjects showed a pulsatile release of B-LH after exogenous LHRH pulses. Our data document that in uremia there are qualitative as well as quantitative abnormalities in pituitary gonadal secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2006

Delayed puberty due to pituitary stalk dysgenesis and ectopic neurohypophysis.

Hypopituitarism is not a common cause of delayed puberty. A 22 year old man was referred to our clinic because of the absence of the development of secondary sexual characteristics. The patient had no complaints of physical discomfort. Random serum testosterone and luteinizing hormone level were obtained and found to be low. The combined pituitary function stimulation test revealed a partial hypopituitarism. A pituitary magnetic resonance imaging (MRI) was obtained and showed decreased pituitary stalk enhancement and ectopic neurohypophysis. Therefore, we conclude that the delayed puberty was a result of hypopituitarism due to pituitary stalk dysgenesis and ectopic neurohypophysis. The patient was started on hormone replacement therapy and gradually developed secondary sexual characteristics.

Adult↗
PubMed1999

[Testosterone treatment of delayed puberty: a longitudinal study in relation to a control group].

OBJECTIVE: Delayed puberty is a very common clinical situation that affects a great number of adolescents. We analyzed the effects that testosterone therapy produces in this situation, including the start of puberty and, therefore, lessening the psychological effects that this delay causes. PATIENTS AND METHODS: We carried out a longitudinal study, in which we followed the growth and maturation of 32 boys from the age of 14 to 19 years. The sample was divided into a control group (n = 17) and a treatment group (n = 15). The treatment group received 50 mg/month of testosterone enantate depot during 6 months. None of the subjects, neither in the control group nor in the treatment group, had started puberty or if so, they had started it in an insufficient way for their age. RESULTS: The boys treated with testosterone developed a greater growth velocity compared to the control group during the first year of observation (9.07 +/- 1.11 cm/year vs 6.9 +/- 1.76, respectively, p < 0.0001). They had a higher increment in the muscular area of the arm (p < 0.005) and pubertal stage G changes occurred more quickly. On the other hand, the growth of the testicular volume was similar in both groups. At 19 years of age, no significant difference between the groups was observed in any of the clinical parameters studied. CONCLUSIONS: Treatment wit testosterone at the dose used promotes a significant response that leads to the start of puberty, but without stopping the maturation of the hypothalamic-pituitary axis that is produced in normal puberty, allowing a normal testicular evolution. The treatment does not show any long-term effects. It is, therefore, an effective treatment of delayed puberty.

Adolescent↗
PubMed2002

Use of GnRH agonist and human chorionic gonadotrophin tests for differentiating constitutional delayed puberty from gonadotrophin deficiency in boys.

OBJECTIVES: The differentiation of constitutional delayed puberty (CDP) from gonadotrophin deficiency (GD) in boys at referral poses a difficult challenge. The effectiveness of the GnRH agonist (GnRH-a) test in distinguishing between the two conditions was evaluated and compared with findings of the GnRH and hCG stimulation tests. PATIENTS, METHODS AND DESIGN: The study sample included 32 prepubertal boys aged 14 years or older. Thirteen entered spontaneous puberty within 1 year of referral (group A) and 19 remained prepubertal (group B). All underwent the GnRH test (Relefact, Hoechst AG, 0.1 mg/m2 i.v. in one bolus), GnRH-a test (Decapeptyl, Ferring GmbH, 0.1 mg/m2 s.c.) and hCG stimulation (Chorigon, Teva, 1500 units i.m. on three alternate days) at 1-week intervals. All tests were performed at referral at 0800 h. Blood samples were collected before testing and at 30 and 60 min (GnRH test) or 4 h (GnRH-a) for LH and FSH determination, and before testing and at 4 h (GnRH-a) or on the seventh day (hCG) after stimulation for serum testosterone measurement. RESULTS: The LH response to GnRH-a and the testosterone response to hCG stimulation were significantly higher in group A (LH, mean +/- SD 20.4 +/- 7.5 mIU/ml, range 10.8-32.6; testosterone, mean +/- SD 18.0 +/- 5.9 nmol/l, range 9.4-26, P < 0.0001) than in group B (LH, mean +/- SD 2.3 +/- 2.0 mIU/ml, range 0.7-6.9; testosterone, mean +/- SD 1.0 +/- 0.7 nmol/l, range 0.7-3.2), with no overlap between the groups. The cut-off for the LH response to GnRH-a was 8.0 mIU/ml, and for the testosterone response to hCG, 8 nmol/l. There were also significant differences between the groups in mean basal serum LH and FSH (LH, 1.1 +/- 0.5 vs. 0.6 +/- 0.2 mIU/ml, P < 0.05; FSH, 2.2 +/- 2.0 vs. 0.4 +/- 0.3 mIU/ml, P < 0.02) and their response to GnRH (LH, 11.4 +/- 4.4 vs. 2.7 +/- 1.1 mIU/ml, P < 0.0001; FSH, 5.1 +/- 3.4 vs. 2.5 +/- 2.4 mIU/ml, P < 0.0001), and mean serum testosterone level at 4 h after GnRH-a administration (1.9 +/- 1.0 vs. 0.9 +/- 0.4 nmol/l, P = 0.002), but all showed a great overlap in range. Mean age, testicular volume and basal serum testosterone levels were similar in the two groups at referral. One year later, the testicular volume of group A (5.0-12.0 ml) was significantly larger than that of group B (1.0-3.0 ml, P < 0.0001), which remained unchanged on re-examination 3.0 +/- 0.5 years later. CONCLUSIONS: The GnRH-agonist test and the repeated-injection hCG test are reliable diagnostic tools for differentiating CDP from GD in boys.

Adolescent↗
PubMed1983

Hyperprolactinemia and delayed puberty: a report of three cases and their response to therapy.

Delayed puberty occurred in three patients (aged 15 to 22 years) with elevated prolactin levels. Despite the varying etiologies, their clinical presentations were marked by absence of galactorrhea, prepubertal genitalia (2/3), and short stature (1/3). Except for hyperprolactinemia, endocrinologic evaluation was normal in two patients. Bromocriptine restored prolactin levels to normal in all three patients, two of whom had prior transsphenoidal surgery, and resulted in initiation of menses in one girl and pubertal development in both boys. The 22-year-old male patient with the empty sella syndrome has progressed through puberty after the addition of oral testosterone.

Adolescent↗
PubMed1990

[The role of pulsatile LHRH therapy in women: the treatment of delayed puberty and of hypothalamic amenorrhea].

The importance of gonadotropin pulsatility for normal hypothalamic-pituitary-gonadal axis function is well known. The most important aim of exogenous LHRH administration, given in females with delayed puberty or hypothalamic amenorrhea is to physiologically restore LH pulsatility to a more physiologic way as possible. In fact, a variable degree of LHRH endogenous defect is present in these conditions. Moreover, exogenous LHRH pulsatile administration is able to restore normal pubertal development until menarche appears and normal ovulatory cycles occur and pregnancy is induced. We reported our experience and review the literature regarding the importance and use of LHRH pulsatile therapy in delayed puberty and hypothalamic amenorrhea. We have also evaluated the data for various administration routes, the choice of patients, response to therapy and the possible diagnostic use of pulsatile LHRH with regard to the differential diagnosis of delayed puberty.

Adolescent↗
PubMed1995

Gonadotropin releasing hormone agonist (nafarelin) test to differentiate gonadotropin deficiency from constitutionally delayed puberty in teen-age boys--a clinical research center study.

The objective of this study was to determine whether the hormonal response to a GnRH agonist (nafarelin) challenge differentiates hypogonadotropinism from delayed puberty as well as the sleep test does. We studied boys ages 13.25-17.6 yr with prepubertal constitutional delay of puberty (CDP, n = 11), prepubertal gonadotropin deficiency (GnD, n = 10), pubertal CDP (PCDP, n = 11) and partial GnD (PGnD, n = 2). These disorders were defined on the basis of the following independent criteria: CDP = isolated delayed puberty with documentation of subsequent pubertal progression; GnD = panhypopituitarism or anosmia with absence of subsequent pubertal progression; PCDP = isolated delayed puberty in an early pubertal child; and PGnD = arrest of puberty in boys with partial hypopituitarism. CDP was compared with GnD and PCDP was compared with PGnD by analysis of variance and two-tailed t tests. Each patient had a nafarelin test with measurement of LH, FSH, and testosterone responses at intervals after nafarelin administration. Most patients had a sleep test with measurement of LH and testosterone levels at intervals overnight. CDP and GnD patients could not be distinguished by pubertal staging criteria. All but 1 patient with CDP had an LH response higher than that of GnD patients 4 h postnafarelin (P = 0.003). An incremental response to nafarelin of LH (delta LH at 4 h) below 4.8 IU/L was the best discriminant; it distinguished GnD from CDP in 95% of the cases and PGnD from PCDP completely. During the sleep test, all patients with CDP and 2 of 8 with GnD exhibited a significant increase in plasma LH. An incremental increase in LH during sleep (mean LH asleep minus mean LH awake) of less than 0.35 IU/L, near the limit of sensitivity of the method, differentiated GnD from CDP similarly to the nafarelin test. We conclude that the LH response to nafarelin distinguished gonadotropin deficiency from constitutional delay of puberty as well as the sleep test did and with certain advantages. The diagnostic reliability of the GnRH agonist test deserves to be determined prospectively in teen-agers with isolated GnD and partial hypopituitarism.

Adolescent↗
PubMed2003

Ascertainment and treatment of delayed puberty.

The majority of patients with pubertal delay, can be classified as having primary pubertal delay (constitutional delay of growth and puberty, CDGP), although any child with a chronic disease could present with delayed puberty. In contrast, children with hypogonadism, either hyper- or hypogonadotropic, exhibit a total absence of pubertal development. Hence, early evaluation of these patients should be performed. Delay of puberty leads to psychological problems, secondary to short stature and/or delay in the acquisition of secondary sex characteristics and the reduction of bone mass. Although the final height in patients with CDGP is usually normal, some of these patients do not reach the third percentile or remain in the lowest part of the growth chart according to familial height. The most common reason for treating CDGP patients, usually with sex steroids, is for psychological difficulties and for loss of bone mineralization. Treatment must be individualized. Therapeutic options and new drugs will be discussed. Appropriate treatment and adequate nutritional intake are indicated in patients with delayed puberty due to chronic illness. In patients with hypo- or hypergonadotropic hypogonadism, puberty must be induced or completed. Different treatments (GnRH analogues, gonadotropins and sex steroids), and the main objectives are discussed.

Adolescent↗