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PubMed1986

Growth and childhood asthma.

Height and weight were measured every six months in a long term prospective study of 66 children with chronic perennial asthma for a mean 13.1 years. There was no evidence of growth retardation on entry into the study. Growth developed along normal lines in all 66 children until about 10 years, and in 35 of these children growth continued along normal lines throughout the whole period of follow up. Thirty children showed the physiological decelerating growth velocity pattern seen in children with delay in the onset of puberty, and one child had an early menarche. The tendency for delay in the onset of puberty was significant for both boys and girls and was noted to be independent of severity of asthma. Once puberty finally began in these children, complete catch up growth resulted in the attainment of the predicted adult height. Long term prophylactic inhalation of beclomethasone dipropionate in 26 children in a dosage up to 600 mcg/day before puberty and 400 mcg/day during puberty was shown not to affect growth. It is concluded that asthma had no direct influence on growth in height but was associated with delay in the onset of puberty. The pre-adolescent physiological deceleration of growth velocity that occurs in these children gives the impression of growth retardation.

Asthma↗
PubMed1982

Pubertal development: normal, precocious and delayed.

The present concepts on the neuroendocrine mechanisms which trigger pubertal development and modulate the progression towards sexual maturity have been reviewed. Essentially, puberty is presented as a continuum, the programming of which is initiated prenatally and which ends in adult life when all hormonal secretions become autoregulated. This continuum is dependent on a delicate equilibrium between CNS neurohormones (GnRH), neurotransmitters (biogenic amines), pituitary gonadotrophin (FSH, LH) secretion and the end-organ response (testis or ovary) through the activation of specific membrane receptors. The gonadal sex steroids (T, OE2) will activate specific cytoplasmic and nuclear receptors of target tissues and exert their biological action. Initially, the activity of the HPGA is manifested by nocturnal LH peaks, followed by increased gonadal secretion of T or OE2. Extremely sensitive to negative feedback by circulating androgen and/or oestrogen in prepuberty, an hypothalamic regulatory system called the gonadostat increases its threshold of sensitivity and eventually becomes autoregulated at a higher feedback level. Progressively, the hypothalamus becomes sensitive to positive feedback action of gonadal hormones, this phenomenon being important for the onset of ovulation. It is likely also that adrenal androgens play a permissive and supportive role in the onset and progression of pubertal development. Finally, full maturity is reached, with final adult height through fusion of the epiphysis, and fertility is achieved. The clinical manifestations of each developmental stage of puberty are described and abnormalities of sexual development reviewed. While over 90 per cent of cases of precocious pubertal development are idiopathic in girls, a space-occupying lesion in the hypothalamic-pituitary region is frequent in boys. Dissociated pubertal signs (premature adrenarche, pubarche, thelarche, menarche) are discussed, together with diagnosis and treatment of precocious puberty, whether it is idiopathic or occurring independently of the activation of the HPGA. In addition to delay of puberty on a constitutional basis, or related to chronic endocrine or non-endocrine diseases, the main clinical entities with gonadal insufficiency, primary (hypergonadotrophic) or secondary (hypogonadotrophic), are reviewed in boys and girls and their investigation and treatment discussed.

Adolescent↗
PubMed2003

Usefulness of the free alpha-subunit to diagnose hypogonadotropic hypogonadism.

OBJECTIVE: Differentiating constitutional delay of growth and puberty from hypogonadotropic hypogonadism is still a problem in clinical practice. Our previous study demonstrated that the peak/basal ratio of the free alpha-subunit of the glycoprotein hormones is higher in normal prepubertal boys than in male adults with hypogonadotropic hypogonadism. The objective of this study was to assess the performance of this ratio in normal male patients at different ages and levels of pubertal development, and in patients with hypogonadotropic hypogonadism, both isolated and combined with other pituitary hormone deficiencies. DESIGN: Cohort study. PATIENTS: Twenty-eight normal prepubertal males between 6 and 8 years; 20 normal prepubertal males between 9 and 13 years; 18 males with constitutional delay of growth and puberty; 26 normal pubertal males; 13 adult men with isolated hypogonadotropic hypogonadism; 21 adult men with complete hypogonadotropic hypogonadism combined with other hormone deficiencies; and 11 adult men with partial hypogonadotropic hypogonadism combined with other hormone deficiencies. MEASUREMENTS: Serum levels of free alpha-subunit immediately before (basal), and 30 and 60 min after 100 micro g intravenous GnRH were measured by immunofluorimetry. Median and P25-P75 range of the peak/basal ratio of the free alpha-subunit was determined for each group. A receiver operating characteristics curve was calculated. Results were compared using the Kruskal-Wallis test. RESULTS: The peak/basal ratio of the free alpha-subunit was higher in patients with constitutional delay of growth and puberty (7.46) than in those with isolated hypogonadotropic hypogonadism (2.73), complete combined hypogonadotropic hypogonadism (1.58), and partial combined hypogonadotropic hypogonadism (2.61; P < 0.001). A peak/basal ratio < 3.26 identified hypogonadotropic hypogonadism with 93.2% sensitivity and 94.4% specificity when compared to constitutional delay of growth and puberty. There was no statistical difference between the peak/basal ratio of prepubertal patients between 6 and 8 years (7.20), patients between 8 and 13 years (8.71), normal pubertal males (8.10) and those with constitutional delay of growth and puberty (7.46). In a group of boys with delayed puberty, a cut-off point of 3.69 defined hypogonadotropic hypogonadism with 95.6% sensitivity and 94.4% specificity. A cut-off point of 4.81 gave 100% sensitivity (88.9% specificity), and 3.09 gave 100% specificity (86.7% sensitivity). CONCLUSIONS: The peak/basal ratio of the free alpha-subunit can be used for the differential diagnosis of constitutional delay of growth and puberty and hypogonadotropic hypogonadism, irrespective of age. This distinction allows early investigation and treatment of patients with hypogonadotropic hypogonadism and reassurance for those with constitutional delay of growth and puberty.

Adolescent↗
PubMed2004

In boys with abnormal developmental tempo, maturation of the skeleton and the hypothalamic-pituitary-gonadal axis remains synchronous.

The primary mechanism that initiates puberty is unknown. One possible clue is that pubertal maturation often parallels skeletal maturation. Conditions that delay skeletal maturation also tend to delay the onset of puberty, whereas conditions that accelerate skeletal maturation tend to hasten the onset of puberty. To examine this relationship, we studied boys with congenital adrenal hyperplasia (n = 13) and familial male-limited precocious puberty (n = 22), two conditions that accelerate maturational tempo, and boys with idiopathic short stature (n = 18) in which maturational tempo is sometimes delayed. In all three conditions, the onset of central puberty generally occurred at an abnormal chronological age but a normal bone age. Boys with the greatest skeletal advancement began central puberty at the earliest age, whereas boys with the greatest skeletal delay began puberty at the latest age. Furthermore, the magnitude of the skeletal advancement or delay matched the magnitude of the pubertal advancement or delay. This synchrony between skeletal maturation and hypothalamic-pituitary-gonadal axis maturation was observed among patients within each condition and also between conditions. In contrast, the maturation of the hypothalamic-pituitary-gonadal axis did not remain synchronous with other maturational processes including weight, height, or body mass index. We conclude that in boys with abnormal developmental tempo, maturation of the skeleton and the hypothalamic-pituitary-gonadal axis remains synchronous. This synchrony is consistent with the hypothesis that in boys, skeletal maturation influences hypothalamic-pituitary-gonadal axis maturation.

Adolescent↗
PubMed1987

Effect of exercise on the onset of puberty, gonadotropins, and ovarian inhibin.

Swimming 6 h/day from 11 days of age led to a significant delay of the onset of puberty of female rats compared with the sedentary group. Rats who were in contact with water but without the energy expenditure due to exercise (paddlers) had their vaginal opening in a middle point between control and exercising rats. Vaginal opening occurred at different ages but at a same body weight. Exercise and stress led to a marked decrease of the body weights between 19 and 40 days of age. Serum luteinizing hormone and follicle-stimulating hormone were increased with the exercise program at 30 days of age, whereas no significant differences between groups in serum gonadotropins were observed at 50 days of age. Only the anterior pituitary luteinizing hormone content was increased by exercise in adult rats. Total ovarian proteins were significantly reduced by stress and to a greater degree by exercise. Ovarian inhibin activity is not modified by exercise at 30 days of age, whereas it increased significantly in the exercising group at 50 days of age and to a lesser degree in paddlers. It is therefore suggested that the onset of puberty in rats is dependent on a critical weight and that exercise and stress can delay the onset of puberty. This delay could be explained by a deficiency of hormonal maturational process while exercising until sexual maturity alters the inhibin activity, which suggests that inhibin could play a major role for the normal reproductive function and this could possibly explain the menstrual disturbances in the female athlete.

Animals↗
PubMed1995

Testosterone treatment in adolescent boys with constitutional delay of growth and development.

Administration of androgens to adolescent boys with constitutional delay in growth has been highly controversial. One hundred forty-eight adolescent boys with constitutional delay of growth and puberty with a mean age of 14.3 +/- 0.7 years were treated with testosterone enanthate 100 mg intramuscularly each month for 6 months. Growth parameters, sexual maturation, and circulating concentrations of testosterone and insulin-like growth factor-I (IGF-I) were compared with those for 50 age-matched adolescent boys with constitutional delay of growth and puberty with a mean age of 14.1 +/- 0.9 years who did not receive any treatment. The mean height growth velocity, height standard deviation score, weight gain, and IGF-I concentration were significantly greater in the treatment group after 1 year of follow-up evaluation. The advancement in bone age equaled that in chronologic age in the treatment group, with no significant change in the bone age to chronologic age ratio (BA/CA) before versus after therapy. All subjects in the treatment group had clearly entered puberty by the end of 1 year. Testicular size increased significantly in the treatment group and they had significantly higher serum testosterone concentrations 6 months after the end of testosterone therapy as compared with the control group, denoting activation of the hypothalamic-pituitary testicular axis. All subjects in the treatment group were psychologically satisfied with the enhanced growth and increased muscle mass, versus only 40% of those in the control group. In conclusion, our regimen appears to be efficacious and safe for treatment of boys with constitutional delay of growth and puberty and has no deleterious effect on skeletal age.

Adolescent↗
PubMed1992

Evaluation of the wap-ras transgenic mouse as a model system for testing anticancer drugs.

Transgenic mouse models have provided many valuable insights into the molecular mechanisms of tumorigenesis; unfortunately, there is a paucity of published information on the utility of these models for evaluating potential anticancer therapeutics. Line 69 wap-ras transgenic mice have an activated, human c-Ha-ras gene on their Y chromosome. Adult males develop salivary and/or mammary adenocarcinomas. Both tumor types express high levels of human ras oncoprotein. Two new sublines, designated wap-ras/F, were created by selective breeding. Subline 69-2 wap-ras/F males developed multiple mammary tumors at puberty. Tumor onset was delayed by cyclophosphamide treatment prior to puberty. Mammary tumors from cyclophosphamide-treated mice weighed 0.57 +/- 0.09 g/mouse (SD +/- SEM; n = 8), while tumors from control mice weighed significantly more at 2.36 +/- 0.25 g/mouse (n = 8; P less than or equal to 0.001; SD +/- SEM). These results suggest that subline 69-2F mice will be valuable for testing therapeutic regimes designed to interfere with processes occurring early in tumorigenesis, before palpable tumor presentation. Tumor sensitivity to several clinically relevant cytotoxins was also tested in adult wap-ras males with palpable tumors. Both salivary and mammary tumors were sensitive to cyclophosphamide and 5-fluorouracil, but not methotrexate. This suggests that wap-ras transgenic mice will indeed be useful in the discovery of novel therapeutics against neoplasia.

Animals↗
PubMed2002

Mechanisms of abnormal puberty in coeliac disease.

Coeliac disease (CD) is one of the most frequent chronic diseases in childhood. The clinical spectrum has changed; in addition to the classical gastrointestinal form, other clinical manifestations have been described, such as hypogonadism and the consequent delay in onset of puberty. Recent studies reported not only a significantly retarded menarche in untreated CD girls as compared with girls following a gluten-free diet, but also in treated CD a negative effect on pregnancy, resulting in lower birth weight and shorter duration of pregnancy. In boys, there is a reduced serum level of dihydrotestosterone and an increased serum level of luteinizing hormone, an abnormality pattern suggesting androgen resistance. The pathogenesis of CD-related reproductive disorders is still unclear. Some hypotheses may be tried; for example, in CD there is a high level of autoantibodies directed against self-antigens, so there could be antibodies directed against hormones or organs critical for pubertal development. Moreover, in CD there could be a selective malabsorption of micronutrients essential for the metabolism of carrier or receptor proteins for sex hormones.

Autoantibodies↗
PubMed1984

Sex hormone profiles of premenarcheal athletes.

Female gymnasts have a delayed onset and probably retarded progression of puberty. The aim of this study was to test the hypothesis that the delay in onset of puberty in gymnasts as compared to girl swimmers is modulated by a lower estrone level due to a smaller amount of body fat. The sex-hormone and gonadotropin levels of 46 gymnasts and 37 girl swimmers of the same biological maturation (breast development: M = 1 or M = 2) were studied. In each subject the following hormones were measured in plasma: estrone, 17-beta-estradiol, DHEAS, testosterone, androstenedione, LH, and FSH. In prepubertal children (M = 1) the levels of estrone, testosterone, and androstenedione were lower in the gymnastic group as compared to the swimming group. In the early pubertal (M = 2) gymnastic and swimming groups these hormone levels were no longer different. The other hormone levels were not significantly different in either the prepubertal groups or the early pubertal ones. Within the total prepubertal group there is a clear relationship between the estrone levels and the levels of testosterone and androstenedione, but not between estrone and 17-beta-estradiol, nor between the calculated fat mass and any of the hormone levels. It appears that the androstenedione and testosterone levels are responsible for the difference in estrone level, rather than the amount of body fat.

Adolescent↗
PubMed1982

Acceleration and delay of sexual maturation in female mice via chemosignals: circadian rhythm effects.

Two experiments tested whether the male urinary chemosignal that accelerates puberty in female mice or the urinary chemosignal from grouped females that delays puberty are affected by circadian rhythms. The experiments also tested whether there is a circadian component for the response system(s) of the young recipient female mice for the onset of first vaginal estrus. Male urine collected at 0600 h was more effective in inducing earlier maturation than urine collected at 0000, 1200 or 1800 h. Urine from grouped females collected at all four times produced significant delays in first estrus, but urine collected at 0000 h produced longer delays than urine from 0600, 1200 or 1800 h. For male urine, application at 0600 h produced significant acceleration relative to urine treatment at 0000, 1200 or 1800 h. No differences were recorded in age of puberty in females treated with urine from grouped females when urine was applied at the four different time points. Possible interpretations of these results involve circadian variations for various hormones and related physiological processes in both donor and recipient mice.

Animals↗
PubMed1982

Dietary arginine and sexual maturation of the female rat.

The effects of dietary arginine deficiency on sexual maturation were examined in the female rat. Consumption of a diet devoid of arginine since weaning delayed the onset of puberty. Weight at vaginal opening and weight at first estrus were significantly greater in the arginine-deficient rat than in the control rat. Arginine deficiency appeared to have a specific effect on the development of reproductive function since puberty in arginine-deficient animals was delayed more than could be accounted for by impairment of growth. The specific effect of arginine deficiency was also indicated by reduced weights of the reproductive tissues after 15 weeks of experimental feeding when compared with the growth-matched controls. Sexual maturation was also examined in rats fed diets containing graded levels of arginine (1.12, 0.84, 0.56, 0.28 or 0%). Vaginal opening and first estrus were delayed by feeding diets containing 0.28 or 0% arginine. Uncoupling of these two events also occurred in the majority of the rats fed these two diets. In spite of normal timing of puberty, maturing rats fed a diet with 0.56 of 0.84% arginine had reduced ovarian weight and first ovulation rate when compared with rats fed the control diet (1.12% arginine). It is concluded that more than 0.84% dietary arginine was required for growing rats to support normal sexual maturation.

Animals↗
PubMed1994

Treatment of growth delay in boys with isolated growth hormone deficiency.

We report our experience in treating growth delay in boys with isolated growth hormone deficiency (IGHD) receiving biosynthetic human growth hormone. The study was performed in 15 boys with IGHD receiving GH. At the chronological age of 13.1 (1.1) years (SD), 13 were prepubertal, two were in early puberty and there was a mean bone age delay of 2.5 (1.4) years. A growth spurt was induced by either depot testosterone or oxandrolone. There was an increase in growth rate from 5.7 (1.6) cm/year, occurring the year before anabolic or sex steroid therapy, to 8.1 (1.2) cm/year during treatment (p < 0.05), followed by 7.3 (1.9) cm/year the year after the cessation of treatment (p < 0.05). There was no significant change in height SD score for bone age, which was -0.69 (0.97) at the commencement of anabolic or sex steroid therapy and -0.53 (0.84) at the end of treatment. Before the induced growth spurt, there was equal body proportion between sitting height and subischial leg length, which had no significant change following androgen treatment. Spontaneous progress in pubertal development was achieved by all patients with an increase in testicular volume from a mean of 2.9 (2-8) to 6.1 (4-10) ml. The pattern of growth presented by patients treated with oxandrolone or those with testosterone was similar. Our data suggest that growth delay and delayed puberty, in patients with IGHD during concomitant growth hormone therapy, can be treated without deterioration in height prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Evolution of polycystic ovaries in a girl with delayed menarche. A case report.

A 17-year-old girl had delayed growth secondary to low birth weight. Although she entered puberty at 12.5 years, she had delayed menarche. She underwent serial ovarian ultrasound scans, and a change in ovarian morphology was observed, from a normal multicystic appearance to one typical of polycystic ovaries (PCOs). We hypothesize that normal ovarian morphology may change to PCOs during the peripubertal period because of a change in the endocrine milieu.

Adolescent↗
PubMed2001

Growth response, pubertal growth and final height in Greek children with growth hormone (GH) deficiency on long-term GH therapy and factors affecting outcome.

The growth data of 156 children (100 boys, 56 girls) with growth hormone deficiency (GHD), treated with human growth hormone (GH) for 5.7+/-3.7 years, from 1970-1997, were retrospectively analyzed to assess the efficacy of GH treatment and the factors involved. 62.2% of the studied population had idiopathic GHD (IGHD) and 35.2% had organic GHD (OGHD). At initiation of treatment, chronological age (CA) was 10.1+/-4.0 years in children with IGHD and 9.7+/-4.0 years in those with OGHD, while bone age (BA) was 7.0+/-3.7 and 7.7+/-3.2 years, respectively. The SDS of the growth velocity during the first year of therapy (GV1) was negatively related to CA at start of therapy (r = -0.53, p = 0.01). 109 children have reached final height (FH): 67 boys (FH = 165.3+/-6.3 cm) and 42 girls (FH = 153.9+/-5.4 cm). FH SDS was not significantly different from target height (TH) SDS. In the total group, FH SDS was positively related to height SDS for CA and BA at start of therapy (p = 0.01, p = 0.001, respectively), to TH SDS (r = 0.40, p = 0.001), and to GV1 (r = 0.33, p = 0.001). TH SDS was not different between the IGHD and OGHD groups (-1.02+/-0.8 vs. -0.94+/-6.9). The height gain at puberty did not differ between the groups with induced or spontaneous puberty in boys (23.7+/-8.6 vs. 25.4+/-6.9, not significant), while in girls it was higher in the group with spontaneous puberty (12.7+/-7.3 vs. 20.0+/-9.0, p = 0.008). The age and height at start of puberty was higher in girls and boys with induced puberty. In the total group, the FH SDS of children with induced puberty was higher in comparison with those with spontaneous puberty (-1.0+/-0.8 vs. -1.7+/-0.9, p = 0.001) and it was positively related to the height at start of puberty. When the two sexes were analyzed separately, the difference reached significance only in boys. In conclusion, children with GHD on GH treatment achieved a final height which was comparable to their genetic potential. The FH of children with OGHD was not different from those with IGHD. The age and height at start of puberty were the most significant determining factors for FH. Hence, a better FH might be expected by delaying or arresting puberty.

Adolescent↗
PubMed1975

Delayed adolescence.

Delayed adolescence has several causes. Most frequent is the physiological or constitutional (hereditary) delay of growth and adolescence. This is a normal variation of growth and development, with growth, bone age and puberty retarded in a harmonious way. It carries a good prognosis with late but normal puberty and late catch-up growth leading to normal adult height. It manifests itself long before puberty by short stature and retarded bone age. True endocrine defects with permanent hypogonadism (hypothalamic-pituitary deficiency of the gonadotropinds and primary gonadal failure) are rare. Differential diagnosis before puberty is not always possible on clinical grounds alone. The most useful laboratory test consists of the LH-RH test. The i.v. injection of the recently introduced hypothalamic LH-releasing hormone, LH-RH, is followed by an age-dependent increase of the plasma gonadotropinds LH and FSH. This test allows differentiation, before puberty, between constitutional delay of growth and adolescence with a normal response for bone age, true hypothalamic-pituitary insufficiency with no response, and primary gonadal failure with an increased response. True hypogonadism requires permanent sex hormone replacement therapy. Constitutional delay of growth and adolescence in boys may present a psychosocial indication for temporary hormone therapy with testosterone.

Adolescent↗
PubMed1992

Stimulated growth hormone (GH) secretion in children with delays in pubertal development before and after the onset of puberty: relationship with peripheral plasma GH-releasing hormone and somatostatin levels.

A reduced GH secretion has often been shown in prepubertal children with delays in pubertal development. In order to study the mechanism underlying this finding, we evaluated peripheral circulating levels of GH, GHRH, and somatostatin (SRIH) before and after the onset of sexual development in a group of eight late maturing children (six boys, two girls), comparing the results with those obtained in two groups of five prepubertal and four pubertal short children with familial short stature. GH was measured by a two-site immunoradiometric assay. Both GHRH and SRIH were assayed by specific RIAs after an acetone-petrolether extraction from plasma. Our data showed a significant increase (P less than 0.001) in GH, GHRH, and SRIH levels (peak vs. basal values) in response to L-dopa administration in all groups. In pubertal children with delays in pubertal development GH and GHRH peak values (15.8 +/- 2.2 micrograms/L and 120 +/- 18 pg/mL, respectively) were significantly greater (P less than 0.001) than in the same subjects before puberty (8.2 +/- 0.9 micrograms/L and 79 +/- 9 pg/mL, respectively), whereas SRIH peak values did not significantly change (41 +/- 6 vs. 41 +/- 5 pg/mL; P = NS). Furthermore, prepubertal subjects with delays in pubertal development showed GH and GHRH peak values lower (P less than 0.001) than those of prepubertal subjects with FSS (13.3 +/- 1.8 micrograms/L and 120 +/- 13 pg/mL, respectively), whereas no statistical difference was present between the two groups of subjects after pubertal development (18.2 +/- 2.9 micrograms/L and 128 +/- 11 pg/mL, respectively). In conclusion, these findings support the assumption that in late maturing subjects during prepubertal period the decreased GH secretion may be ascribed to a reduced GHRH secretion, reversible with the onset of puberty, without change in circulating SRIH levels.

Adolescent↗
PubMed1982

[Gonadotropic insufficiency associated with the cytomegalic type of congenital adrenal hypoplasia (author's transl)].

Two adolescents with chronic adrenal insufficiency, presumably secondary to the cytomegalic type of congenital adrenal hypoplasia, developed a gonadotropin deficiency at puberty, which was both delayed and incomplete. Endocrine studies demonstrated in plasma low LH levels which failed to increase after LH-RH, higher levels of FSH, low basal testosterone concentration but increasing normally after HCG stimulation. Azoospermia was demonstrated in one case. In parallel with those previously reported, these two new cases show that the association between gonadotropin deficiency and congenital adrenal hypoplasia is not accidental, even if the relationship between the two components of the syndrome is still unclear.

Adrenal Insufficiency↗
PubMedDate not supplied

[Endocrinologic problems of the male adolescent].

The male adolescent may present several endocrinological problems, the most frequent of which is the retardation or absence of puberty due to constitutional delay of growth and development. This form does not require therapy and must be distinguished from other forms of hypogonadism (primitive or secondary) by endocrine tests (LHRH test, nightly pulses LH secretion, plasmatic basal level of testosterone and after HCG, cerebral NMR). Hypogonadism treatment consists of replacement therapy with testosterone or testes stimulation with HCG or LHRH. Another frequent disease is gynecomastia, usually due to physiological enlargement of mammary gland during pubertal development, sometimes it may be secondary to hypogonadism, tumors, liver function abnormalities. Severe or psychologically disturbing gynecomastia can be corrected by reductive mammoplasty. Very often, adolescents may present diseases related to incorrect food habits. Obesity is common and anorexia is becoming an important problem also in males.

Adolescent↗