View clinical trials related to Delayed Puberty.
Filter by:The goal of this study is to learn more about the genes that control puberty and reproduction in humans.
The absence of clinical signs of pubertal maturation, i.e. pubertal delay, is a relatively frequent reason for consultation in boys. In cases where it is necessary, the treatment to be established is the administration of testosterone with the aim of provoking the development of secondary sexual characteristics and optimizing growth. Currently, the most commonly used treatment is empirical, with im testosterone enanthate at increasing doses (from 50 mg every 4 weeks up to 250 mg every 4 weeks) over a period of 2 to 3 years. The pharmacokinetic profile has not been described to see if it mimics the physiological progressive increase in testosterone levels occurring during normal puberty. In adults, testosterone enanthate shows supraphysiological serum testosterone the first week after, with a progressive drop to subphysiological levels in the fourth week. Testosterone undecanoate is used in adults at a dose of 1000 mg im every 12 weeks, as equivalent to testosterone enanthate 250 mg every 4 weeks.Serum levels of testosterone show a profile within physiological ranges. Testosterone undecanoate im has not been tested in adolescents. Hypothesis: The hypothesis of this work is that the initial administration of 1 ml (~250 mg) of testosterone undecanoate (1000 mg/4 ml) via im every 12 weeks for 6 months, with a progressive increase of 1 ml (~250 mg) every 6 months until reaching 4 ml (1000 mg) per dose is safe and effective in causing normal progression of secondary sex characteristics and growth spurt in boys with pubertal delay. The primary specific objectives are to determine, in boys with pubertal delay: (a) if a treatment regimen of testosterone undecanoate (1000 mg/4 ml), with an initial dose of 250 mg every 12 weeks and subsequent increase up to 1000 mg every 12 weeks over 2 years (increasing 250 mg every 6 months) induces a progression in the development of secondary sexual characteristics and growth spurt commensurate with those of normal pubertal development, and (b) the safety of the administration of increasing doses of im testosterone undecanoate.
To evaluate the phenotype and biochemical characteristics of boys referred for delayed puberty, to describe the frequency of associated co-morbidities and diseases, to evaluate the diagnostic criteria and the effect of testosterone treatment.
Anorexia nervosa may be responsible for a catch- down or even an interruption of growth, delayed puberty and osteopenia with failure of acquisition of bone mass. The recovery of normal nutrition usually leads to a resumption of growth and pubertal development. However, despite a therapeutic nutritional and psychotherapeutic satisfactory approach, some patients have a significant short stature with reduced adult final height and a deficit of bone mass. The main objective is to evaluate the effect of growth hormone (hGH) treatment on the growth velocity in prepubertal children or children in early puberty with anorexia nervosa and significant reduction of height velocity. This is a single-center, controlled, randomized and double-blind clinical trial evaluating the efficacy of hGH treatment for 1 year against a placebo, on the growth velocity of prepubertal or children in early puberty with Anorexia nervosa and major catch-down.This period is followed by the evaluation of the hGH treatment in children receiving placebo and continued hGH treatment in the treatment arm for 1 year, in total 2 years of study for each child. This second period corresponds to an ethical consideration giving secondarily access to treatment for patients in the placebo group.
The goal of this study is to test whether the hormone kisspeptin has the potential to prospectively diagnose adolescents with self-resolving or permanent delayed puberty. Some children with delayed puberty will eventually enter puberty on their own. However, some children with delayed puberty have a permanent condition and require medical treatment to undergo puberty. Right now, there is no reliable diagnostic tool to tell whether a child's delayed puberty will be self-resolving or permanent. The hormone kisspeptin has the potential to prospectively diagnose adolescents with self-resolving or permanent delayed puberty.
The purpose of this study is to determine if the timing of the onset of puberty may be affected by FSH-regulatory peptides. We will determine how these peptides relate to FSH production in prepubertal and pubertal children by comparing the regulation of FSH control in children with precocious (early) puberty and delayed puberty. In this pilot study, we will stimulate the pubertal axis using an agonist of GnRH to determine the pubertal response of activin-A, inhibin-A and -B and follistatin. To determine baseline FSH secretion and FSH-regulatory peptide tone, we will block GnRH with a specific antagonist. These studies should lead to a better understanding of the role of FSH in controlling the onset of puberty and the pathogenesis of pubertal disorders.