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PubMed1998

Effect of restricted nutrition on timing of puberty in female Soay sheep.

Ovariectomized, oestradiol-implanted Soay ewe lambs from 21 September (aged 21 weeks) had restricted (liveweight maintenance) (n = 4) or unrestricted food (n = 4); ovary-intact lambs had unrestricted food (n = 8). LH activation in ovariectomized lambs on restricted and unrestricted food and onset of ovulatory cycles in ovary-intact lambs all occurred on 7 December (SED 8.8 days) (32 weeks), but at different liveweights (24.2, 17.9 and 18.3 kg, respectively, SED 1.22). LH pulse frequency was similar in ovariectomized lambs on restricted and unrestricted food. From 29 August (aged 18 weeks), Soay ewe lambs in seasonally advanced decreased artificial daylength were given restricted food, unrestricted food, or food was restricted for 8 weeks and then unrestricted (n = 8 per group). Ovarian cycles started 3 weeks earlier than in lambs in natural photoperiod on similar dates for all three groups (14, 18 and 19 November, respectively, SED 5.5 days) (29 weeks), but at different liveweights (16.2, 20.7, and 18.4 kg, respectively, SED 0.87). From 1 August, Suffolk x Greyface ewe lambs (aged 16 weeks) had restricted food, unrestricted food, or food restricted for 8 weeks and then unrestricted (n = 8 per group). By 1 November (29 weeks), 0/8 lambs on restricted food (29.3 +/- 0.92 kg) but 8/8 lambs on unrestricted food an 5/8 lambs on 8 weeks of restricted food had ovulated (mean dates: 16 October +/- 2.5 days (27 weeks, 40.1 +/- 1.02 kg), and 1 November +/- 3.0 days (29 weeks, 35.5 +/- 1.23 kg), respectively. Thus, nutritional growth restriction during the 11 weeks preceding normal puberty delayed pubertal data in the improved breed but did not influence the timing of puberty in the unimproved Soay breed within the weight range studied.

Animal Nutritional Physiological Phenomena↗
PubMed2002

[Beta-thalassemia major in children and adolescents in Denmark].

INTRODUCTION: Beta-thalassemia major occurs with increasing frequency among Danish children as a result of immigration. The aim of the study was to estimate the occurrence of beta-thalassemia major in Denmark, analyse the treatment and organ functions, and identify areas for an improved treatment strategy. MATERIAL AND METHODS: During 1998-99 all Danish pediatric departments were contacted for identification of children aged 0-18 years with beta-thalassemia major. Blood transfusions and chelation therapy were registered, and for Eastern Denmark clinical, endocrine, cardiac, and serologic parameters were performed. RESULTS: Twenty-six children had beta-thalassemia major. Out of these, 20 received blood transfusions, and 17 patients were chelated. Eight patients were not chelated owing to previous bone marrow transplantation, treatment with hydroxyurea or ferritin < 2000 micrograms/l and young age. One patient had died. The body height was between 1.5 and -5.4 SDS (median -1.7) and the sitting height was -0.6 to -5.6 SDS (median -2.3). The bone age was delayed 1-5 years (median -2.5) in six out of ten examined patients, and puberty delayed in four out of five. A dilated left ventricle was documented in one out of eight patients examined. All patients were HIV and hepatitis C negative. For 75% of the children, the parents were related. DISCUSSION: Children and adolescents with beta-thalassemia major in Denmark experience major heterogenicity with regard to treatment and late effects. An earlier and more effective iron chelation therapy together with improved patient support may reduce growth disturbances and endocrine and cardiac late effects.

Adolescent↗
PubMed1977

Delay of sexual maturation in female house mice by exposure to grouped females or urine from grouped females.

The experiments examined the timing, duration and possible enhancement effects of group contact on the delay of sexual maturation produced in prepubertal female house mice by urine from grouped females. One or three days of pheromone stimulation at specified ages during the first 2 weeks after weaning was not sufficient to delay puberty in females caged singly. However, pheromone treatment for 7 days, beginning during the first week after weaning, did significantly delay the onset of first vaginal oestrus relative to control females treated with water. Both the timing and duration of pheromone stimulation appear to be critical factors affecting pheromone-induced delay of sexual maturation. Mean ages at first oestrus for females housed with a group of 7 other females, for 3 or 7 days at specified ages during the first 2 weeks after weaning, did not differ from mean ages recorded with urine stimulation only. Contact with other females does not appear to alter or enhance the delay-of-maturation effect achieved with urine stimulation. In all these respects the maturation-delay pheromone of grouped female mice appears to differ from the puberty-accelerating pheromone of male mice.

Aging↗
PubMed2001

Alcohol and female puberty: the role of intraovarian systems.

Alcohol consumption during early adolescence may suppress the secretion of specific female reproductive hormones, thereby delaying puberty and adversely affecting the maturation of the reproductive system. These effects occur through several mechanisms, including altered production and secretion by the ovaries of estradiol, a key steroid hormone involved in the timing and regulation of female reproductive events. Alcohol can affect estradiol production by interfering with the normal function of regulatory hormones produced by the brain and the pituitary gland. Recent research has demonstrated additional potential mechanisms for alcohol's effects on female reproductive capability, including interference with specific regulatory systems located entirely within the ovary. Such "intraovarian" systems include the insulin-like growth factor-1 (IGF-1) and nitric oxide (NO) systems. Alcohol can dampen the stimulatory effects of the ovarian IGF-1 system and can increase the inhibitory effects of the ovarian NO system. These effects combine to decrease estradiol secretion. Thus, alcohol impairs ovarian function not only by interfering with hormonal communication between the brain, pituitary gland, and ovaries but also by directly altering the function of regulatory systems within the ovaries themselves. These results provide further evidence of the risks of underage drinking and the importance of its prevention.

Adolescent↗
PubMed1985

Pathogenesis and management of abnormal puberty.

In the prepubertal child, the hypothalamic-pituitary-gonadal (H-P-G) axis is functional and extremely sensitive to negative feedback inhibition by low circulating levels of sex steroids. This feedback system may be under the control of unknown CNS inhibitory mechanisms. Clinical signs of puberty are preceded by increased pulsatile secretion of hypothalamic gonadotropin-releasing hormone (GnRH) followed by increased pituitary responsiveness to GnRH. Gonadotropin secretion, particularly LH, increases in both sexes, especially during sleep, resulting in gonadal stimulation, secretion of sex steroids, and progressive physical maturation. When any phase of the H-P-G axis malfunctions, abnormal puberty can result. Abnormal puberty may be precocious or delayed. When puberty is precocious it may be isosexual or heterosexual, complete or partial, intermittent (unsustained), or progressive. True (central) precocious puberty is usually progressive, and hormonally reflective of normal puberty, although occurring at an earlier age, whereas intermittent or unsustained precocious puberty usually is associated with immature patterns of gonadotropin secretion, or with complete gonadotropin suppression as in precocious pseudopuberty (ovarian or adrenal tumors). Cranial axial tomography, gonadotropin response to GnRH, and pelvic ultrasound in girls are useful tools to aid in the differential diagnosis of these conditions. Intermittent, or unsustained, puberty in girls is usually self-limited, requiring no medical or surgical intervention. True progressive central precocity may now be managed with GnRH analogues, which effectively arrest pubertal changes as well as slow rapid linear growth and skeletal maturation. Although a maturation lag usually explains most patterns of delayed puberty, it is often challenging to exclude other conditions that may contribute to slow pubertal progression, such as chronic illness, excessive exercise, emotional stress, anorexia, or drug use. Elevated serum gonadotropin levels direct further evaluation toward etiologies of gonadal failure, including gonadal dysgenesis, Klinefelter syndrome, and chemotherapy/irradiation damage. Both low gonadotropins and absence of or immature gonadotropin response to GnRH administration after a bone age of 11 years in girls and 13 years in boys point toward hypopituitarism or isolated hypogonadotropic hypogonadism. Management with administration of gradually incremented amounts of sex steroids at an appropriate psychologic age usually leads to enhanced linear growth, physical maturation, and improved self-esteem.

Adrenal Gland Neoplasms↗
PubMed2001

Multiple pituitary hormone deficiency: management of puberty for optimal auxological results.

The overview in this paper focuses on ways of achieving optimal auxological results in puberty, principally in idiopathic and congenital multiple pituitary hormone deficiency (MPHD), suggested by the co-authors. We agreed that diagnosing gonadotrophin insufficiency/deficiency is difficult in young children and should be repeated in late prepuberty, but a firm diagnosis of MPHD helps avoid endocrine re-testing at the end of growth. The hypothalamic-pituitary axis must be reassessed periodically in evolving endocrinopathies, though current practice varies widely. Optimum age to induce puberty is 11-12 years in girls and 13-14 boys, and sex steroids are the preferred agents. Short-course testosterone to increase micropenis size is advantageous, but inducing early testicular maturation is not known to improve later fertility. There is also little evidence for increasing the dose of GH during puberty, though therapy should continue to final height, and possibly until peak bone mass is achieved. Delaying puberty is an option in septo-optic dysplasia, and minimising the dose of hydrocortisone is crucial in treating ACTH/cortisol insufficiency. Many unresolved questions remain in this difficult area.

Adolescent↗
PubMed1991

Insulin-like growth factor I as an intraovarian regulator: basic and clinical implications.

Although much remains to be learned with respect to the possible relevance of IGF-I to ovarian physiology, it may be possible at this time to tentatively formulate possible functions of IGF-I in this connection: 1. Amplification of gonadotropin hormonal action--a key requirement given the exponential nature of follicular development. 2. Integration of follicular development--an essential facet concerned with the coordination of granulosa-theca cooperation. 3. Selection of dominant follicle(s)--a speculative proposition assuming timely and selective activation of the IGF-I system in "chosen" follicles. Aside from its possible role(s) in the course of established follicular cycles, IGF-I (and/or IGF-II) may also participate in the very formation of the follicular apparatus during the late fetal/early neonatal period. Although the ovary is gonadotropin-independent at that time, we previously showed that IGF-I may well interact with VIPergic input now implicated in the morphodifferentiation of the follicular apparatus. Similarly, IGF-I may be concerned with the promotion of juvenile and early pubertal follicular gonadotropin (FSH) levels; ovarian IGF-I may have a bearing on the puberty-promoting effect of growth hormone. Indeed, an association appears to exist between isolated growth hormone deficiency and delayed puberty in both rodents and human subjects, a process reversed by systemic growth hormone replacement therapy. Given that ovarian IGF-I and its receptor may be growth hormone-dependent, it is tempting to speculate that the ability of growth hormone to accelerate pubertal maturation may be due, at least in part, to the promotion of ovarian IGF-I production and reception with the consequent local potentiation of gonadotropin action.

Animals↗
PubMed1998

Short-term therapy with recombinant growth hormone in polytransfused thalassaemia major patients with growth deficiency.

Growth failure is commonly described in polytransfused thalassaemia major patients (Th) with or without growth hormone (GH) releasing hormone-GH axis impairment. We have investigated the efficacy of short-term recombinant GH (rhGH) therapy (Saizen [Serono] 0.1 IU/kg/day 6 evenings/week administered s.c. for 12 months) on growth and predicted final height in 28 (19M, 9F) regularly transfused Th with growth deficiency (aged 14.8 +/- 2.0 yr) on long term desferrioxamine s.c. therapy. All Th had no evidence of congestive heart failure, hypothyroidism or impaired glucose tolerance; in all patients the GH peak (evaluated during both insulin and clonidine test) was < or = 20 mIU/l; hypergonadotropic hypogonadism was excluded in Th with delayed puberty. At the start of therapy height age (HA)/bone age (BA) ratio was 0.92 +/- 0.12. Bone age delay was positively correlated to chronological age (CA), serum ferritin levels (mean of the last three years), the age at the start of chelation therapy, growth velocity calculated for CA during the last year; a positive correlation was also found between circulating IGF-I levels and age at the start of chelation therapy. After 1 year on rhGH therapy there was a significant increase of height calculated for CA (not for BA), of growth velocity calculated for both CA and BA and of circulating IGF-I levels; the HA variation/BA variation ratio was 1.85 +/- 1.71, without any significant difference between predicted final height at the start (-1.08 +/- 1.28 SDS) and at the end of rhGH therapy (-0.88 +/- 1.13). The variation of height calculated for CA was positively correlated to both CA and growth velocity during the last year before rhGH therapy (calculated for CA) and negatively to the height at the start (calculated for CA). There were no side effects and haematological parameters did not show significant changes. In conclusion, our data, obtained in a relatively large group of Th, confirm the emerging results of short-term (12 months) rhGH therapy on growth, as shown by the increase of both growth velocity and height calculated for CA. With regard to final height, although the mean variation of HA/variation of BA ratio was 1.85, no significant increase of the predicted final height was found between the start and the end of rhGH therapy. We are evaluating the effect of long-term rhGH therapy on growth in these patients.

Adolescent↗
PubMed1985

Effect of conspecifics on sexual maturation in female European pine voles (Pitymys subterraneus).

Using the number of large ovarian follicles (Type 8) as an indicator of sexual maturation we found that urinary compounds released by adult males accelerated puberty while urine from females suppressed hormonal activity in juvenile female European pine voles. The release of chemosignals that delayed puberty of juvenile females was not influenced by ovarian hormones; urine from ovariectomized females was as effective as urine from unoperated animals.

Animals↗
PubMed1980

Puberty in Laron type dwarfism.

The onset and progress of puberty was followed in 18 patients (7 males and 11 females) with Laron-type dwarfism (LTD). The boys had delayed puberty, testicular enlargement occurring between 12--14 years being the first sign. The first conscious ejaculation occurred between 17--21 years and full maturity was reached after the age of 22. In girls menarche occurred between 13--14 years and full maturity was reached between 16-19 years. Two patients--one male and one female--have children.

Adolescent↗
PubMed1985

Female reproductive development is not activated by male California voles exposed to family cues.

Reproductive development of male California voles (Microtus californicus) is delayed when voles are raised in bedding taken from their family. In these experiments the effects of this chemically mediated puberty delay on male reproductive potential were examined. Males were paired with females for a 4-day period; the resultant uterine weights constituted a measure of male potency. In Experiments 1 and 2, 45-day-old males raised in clean or family bedding were paired with females. Regardless of whether cohabitation occurred in a clean, novel cage or in the male's home cage, only males reared in clean bedding caused significant growth of the female reproductive tract. In Experiment 3 the stimulus males were adults, either castrated or intact. Only cohabitation with an intact male stimulated female reproductive development. These data show that chemical cues present in family bedding impair the ability of young males to stimulate reproductive development in females and suggest that this effect is due to low circulating androgen levels in reproductively delayed males. Since chemical cues in bedding from solitary males did not activate uterine growth, the androgen-dependent deficit in delayed males may be behavioral. The relevance of these phenomena to animals living in a natural environment is discussed.

Animals↗
PubMed1993

Environment, human reproduction, menopause, and andropause.

As the hypothalamic gonadotropin-releasing hormone (GnRH) pulse generator is an integrator of hormonal, metabolic, and neural signals, it is not surprising that the function of the hypothalamogonadal axis is subject to the influence of a large array of environmental factors. Before puberty, the central nervous system (CNS) restrains the GnRH pulse generator. Undernutrition, low socioeconomic status, stress, and emotional deprivation, all delay puberty. During reproductive life, among peripheral factors that effect the reproductive system, stress plays an important role. Stress, via the release of corticotropin-releasing factor (CRF), eventually triggered by interleukin 1, inhibits GnRH release, resulting in hypogonadism. Effects of CRF are probably mediated by the opioid system. Food restriction and underweight (anorexia nervosa), obesity, smoking, and alcohol all have negative effects on the GnRH pulse generator and gonadal function. Age and diet are important determinants of fertility in both men and women. The age-associated decrease in fertility in women has as a major determinant chromosomal abnormalities of the oocyte, with uterine factors playing a subsidiary role. Age at menopause, determined by ovarian oocyte depletion, is influenced by occupation, age at menarche, parity, age at last pregnancy, altitude, smoking, and use of oral contraceptives. Smoking, however, appears to be the major determinant. Premature menopause is most frequently attributable to mosaicism for Turner Syndrome, mumps ovaritis, and, above all, total hysterectomy, which has a prevalence of about 12-15% in women 50 years old. Premature ovarian failure with presence of immature follicles is most frequently caused by autoimmune diseases or is the consequence of irradiation or chemotherapy with alkylating cytostatics. Plasma estrogens have a physiological role in the prevention of osteoporosis. Obese women have osteoporosis less frequently than women who are not overweight. Early menopause, suppression of adrenal function (corticoids), and thyroid hormone treatment all increase the frequency of osteoporosis. Aging in men is accompanied by decreased Leydig cell and Sertoli cell function, which has a predominantly primary testicular origin, although changes also occur at the hypothalamopituitary level. Plasma testosterone levels, sperm production, and sperm quality decrease, but fertility, although declining, is preserved until senescence. Stress and disease states accelerate the decline on Leydig cell function. Many occupational noxious agents have a negative effect on fertility.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed1984

Effects of adrenalectomy with hormone replacement therapy on the presence of a sexual maturation-delaying chemosignal in the urine of grouped female mice.

When grouped, adult female mice excrete in their urine a chemosignal that delays sexual maturation of young females. This effect does not occur if the adult females have been adrenalectomized. In this report we test whether hormone replacement therapy affects the production and/or excretion of this chemosignal in adrenalectomized females. Injections of two glucocorticoids, corticosterone and hydrocortisone acetate, restored the delay chemosignal in excreted urine from grouped females. In subsequent dose-response experiments, we determined that daily injections of at least 125 micrograms corticosterone or 80 micrograms hydrocortisone acetate were needed to bring about the reappearance of the maturation-delaying substance in the urine of grouped adrenalectomized females. Injections of varying doses of a mineralcorticoid, deoxycorticosterone, did not produce restoration of the delay chemosignal in excreted urine from grouped females. Two additional tests revealed that injections of either glucocorticoid would restore the puberty-delaying activity to the bladder urine of both grouped and singly caged adrenalectomized females.

Adrenalectomy↗
PubMed1978

[The deficiency of 17-hydroxylase: a cause of growth and puberty retardation in the girl. One case].

A case of 17-hydroxylase deficiency in a 14 years old girl is reported. She presented with the unique association of hypertension, hypokaliemia, delayed puberty and growth failure. It is suggested that the reduced statural growth starting between 7 and 10 years of age and accompanied by a markedly reduced bone maturation was, at least in part, the consequence of the absence of adrenarche. The secretion rate of cortisol was very low while an increased production of D.O.C. and corticosterone was demonstrated by the elevated levels of their urinary tetrahydroderivatives. A good feminisation and a growth spurt were observed under ethinyl oestradiol substitutive therapy. A progressive normalization of the kaliemia and the blood pressure was obtained with hydrocortisone treatment but long term hydrocortisone therapy appears less satisfactory with easy clinical manifestations of overdosage on the one hand and incomplete maintenance of normal blood pressure of the other hand.

Adolescent↗
PubMed2006

Deletion of the Ttf1 gene in differentiated neurons disrupts female reproduction without impairing basal ganglia function.

Thyroid transcription factor 1 (TTF1) [also known as Nkx2.1 (related to the NK-2 class of homeobox genes) and T/ebp (thyroid-specific enhancer-binding protein)], a homeodomain gene required for basal forebrain morphogenesis, remains expressed in the hypothalamus after birth, suggesting a role in neuroendocrine function. Here, we show an involvement of TTF1 in the control of mammalian puberty and adult reproductive function. Gene expression profiling of the nonhuman primate hypothalamus revealed that TTF1 expression increases at puberty. Mice in which the Ttf1 gene was ablated from differentiated neurons grew normally and had normal basal ganglia/hypothalamic morphology but exhibited delayed puberty, reduced reproductive capacity, and a short reproductive span. These defects were associated with reduced hypothalamic expression of genes required for sexual development and deregulation of a gene involved in restraining puberty. No extrapyramidal impairments associated with basal ganglia dysfunction were apparent. Thus, although TTF1 appears to fulfill only a morphogenic function in the ventral telencephalon, once this function is satisfied in the hypothalamus, TTF1 remains active as part of the transcriptional machinery controlling female sexual development.

Animals↗
PubMed1992

Influence of season of birth on onset of gonadotrophic and ovarian functions in young doe hares (Lepus europaeus).

The pituitary and ovarian responses to a monthly i.v. injection of 5 micrograms luteinizing-hormone-releasing hormone (LHRH) were studied in three groups of young doe hares, born in January-February (group I), in April (group II) or at the end of the breeding season (August-September, group III). The LHRH injection was always followed by a release of LH and progesterone, which did not differ among the three groups at 3 months of age. The pituitary and ovarian responses to LHRH increased gradually from the age of 3 months in groups I and III and from the age of 9 months in group II. One female of the ten born in January-February ovulated and reached puberty in June, at the age of 4 months, but with a weak pituitary response. The females born in April displayed a seasonally delayed puberty, at 9 months of age (two of five females ovulated in the next January). Four of the five females born at the end of the breeding season ovulated after LHRH when 5 months old (in February), with a full pituitary-ovarian response. The low pituitary response of group I in June-August, even if 10-20% of females ovulated after LHRH, suggests a need for a period of short days. Then, the most favourable conditions for the hare to reach puberty would be a period of short decreasing daylengths during the fall, followed by increasing daylengths after the winter solstice.

Age Factors↗
PubMed1994

Use of leuprolide acetate response patterns in the early diagnosis of pubertal disorders: comparison with the gonadotropin-releasing hormone test.

The effects of a single injection (500 micrograms sc) of the GnRH agonist leuprolide acetate on gonadotropin secretion and those induced by a GnRH test were analyzed in 32 children (11 males and 21 females) referred for possible pubertal developmental disorders and in 9 prepubertal controls [group C; 4 males and 5 females; chronological age (CA), 7.4 +/- 1.2 yr]. The pituitary-gonadal secretory responses to the GnRH agonist were characterized in all subjects and in a control group in early puberty [10 females (Tanner breast stage II; CA, 11.3 +/- 1.1 yr) and 6 males (Tanner pubertal stage II; CA, 13.5 +/- 0.4 yr); group D]. Twelve girls (CA, 7.1 +/- 0.7 yr) presented with precocious breast development, 11 patients [6 boys (CA, 10.9 +/- 0.4 yr) and 5 girls (CA, 9.3 +/- 0.5 yr)] had advanced puberty and predicted adult heights below -2.0 SD score, and 9 patients [5 boys (CA, 14.6 +/- 0.3 yr) and 4 girls (CA, 14.4 +/- 1.1 yr)] had delayed puberty. Less than 6 months had elapsed since the appearance of pubertal signs in all patients with pubertal development. After a follow-up period of 12.9 +/- 2.0 months, 20 patients showed progression of pubertal signs (group A, progressive puberty), and in 12, puberty regressed or did not progress (group B, nonprogressive puberty). The results of hormonal tests in all patients were analyzed retrospectively according to their clinical outcome. Patients in group A had a mean plasma peak LH response significantly higher after leuprolide acetate stimulation than after GnRH challenge (13.1 +/- 0.2 vs. 7.3 +/- 0.9 IU/L; P < 0.003). Those in groups B and C had similar peak LH responses after both tests (3.3 +/- 0.2 vs. 3.1 +/- 0.4, and 1.5 +/- 0.1 vs. 1.8 +/- 0.4 IU/L, respectively). No differences in basal and poststimulated LH levels were found between boys and girls in the same group. In patients in groups A and D, LH consistently peaked 3 h postleuprolide acetate challenge; in those in groups B and C, the LH peak occurred 3-6 h postinjection. Maximal gonadal responses were elicited 24 h poststimulation. No overlap in poststimulated estradiol or testosterone values occurred between patients in groups A and D and those in groups B and C.(ABSTRACT TRUNCATED AT 400 WORDS)

Child↗
PubMed2006

Use of aromatase inhibitors to increase final height.

During puberty in both sexes, the mechanism involved in epiphyseal fusion is mediated by the action of estrogen through a cascade of events including proliferation, differentiation, and apoptosis of chondrocytes. The enzyme P450 aromatase catalyzes the aromatization of C19 androgens (androstenedione and testosterone) to C18 estrogens (estrone and estradiol). Inhibition of estrogen action by aromatase inhibitors (AIs) appears to decelerate the process of growth plate fusion, and thus AIs may be used therapeutically to increase adult height. The clinical experience with AIs in the pediatric setting is limited to testolactone, fadrozole, letrozole, and anastrozole. Testolactone, a nonselective steroidal AI, has been used successfully as an adjunct to antiandrogen and gonadotropin-releasing hormone analogue (GnRHa), therapy for children with familial male-limited precocious puberty (FMPP) and congenital adrenal hyperplasia (CAH), and with some success in girls with McCune-Albright syndrome. The limitations of testolactone include its relatively low potency and the need for frequent dosing. Results of a randomized placebo-controlled trial in boys with delayed puberty treated with letrozole, a selective nonsteroidal AI, found that boys treated with letrozole + testosterone experienced delayed bone maturation and good growth response and achieved an increase in predicted adult height. In this study, only minor differences in bone density were seen between the placebo and letrozole treatment groups, both of which were receiving concomitant testosterone therapy. No adverse effects on testis size or inhibin B concentration were noted. The therapeutic value of AIs in growth promotion now remains to be substantiated in future controlled clinical trials.

Aromatase Inhibitors↗