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PubMed2006

A wider perspective on puberty.

The mechanisms that control the onset of puberty remain within the purview of the neurobiologists who first recognised the concept of removal of a restraint factor to permit reawakening of puberty. The discovery of a ligand-activated G protein receptor-signalling pathway upstream of the GnRH pulse generator adds further weight to the role of the hypothalamus in the central regulation of puberty. The physical pointers to puberty are the mainstay of assessing timing and tempo in a clinical setting but non-invasive and indirect methods of assessment only are appropriate for population studies in normal children. That puberty can be regarded as a sensor recognises the observation of secular changes in pubertal timing and perhaps qualitative aspects of tempo. The influences on the sensor include marked changes in nutrition and an environmental exposure to low-dose chemical mixtures interacting with a polygenic background.

Breast↗
PubMed1997

Girls diagnosed with premature pubarche show an exaggerated ovarian androgen synthesis from the early stages of puberty: evidence from gonadotropin-releasing hormone agonist testing.

OBJECTIVE: To assess the gonadotropin and ovarian steroid responses to the GnRH agonist (GnRH-a) leuprolide acetate (LA) in premature pubarche girls and in Tanner stage- and bone age-matched controls to ascertain whether the ovarian 17-hydroxyprogesterone (17-OHP) hyper-response to GnRH-a challenge present in some subsets of adolescent premature pubarche girls is detectable during puberty and whether these patients have a distinct pattern of pituitary-ovarian maturation. DESIGN: Cross-sectional study. SETTING: A university teaching hospital. PATIENT(S): Seventy-six premature pubarche girls (early pubertal [B2; n = 31], midpubertal [B3; n = 15], late pubertal [B4; n = 12], and postmenarcheal [B5; n = 18]) and 45 controls. INTERVENTION(S): Gonadotropins and plasma steroid hormones (17-OHP, 17-OH-pregnenolone [17-Preg], androstenedione [A], T, DHEA, DHEAS, E2, and cortisol) were measured before and 3 and 24 hours, respectively, after LA challenge (500 micrograms SC). MAIN OUTCOME MEASURE(S): Ovarian-steroidogenic responses to GnRH-a challenge. RESULT(S): Luteinizing hormone responsiveness increased significantly during puberty in all subjects whereas FSH levels changed less consistently. Peak E2 levels differed among pubertal stages and were significantly higher in premature pubarche girls than in controls at B4 and at B5. Both peak and incremental increases of 17-Preg and DHEA throughout puberty and of 17-OHP and A at B4 were significantly higher in premature pubarche girls than in controls. This pattern of ovarian-steroidogenic response was most evident during midpuberty and late puberty and resembled the adrenal hyper-response to ACTH of exaggerated adrenarche, suggestive of increased ovarian activity of both the 17 alpha-hydroxylase and the 17,20 lyase functions of cytochrome P450c17 alpha. CONCLUSION(S): Pubertal girls with a history of premature pubarche show a distinct pattern of ovarian maturation characterized by an exaggerated ovarian androgen synthesis throughout puberty.

17-alpha-Hydroxypregnenolone↗
PubMed1980

Bioactive LH: a test to discriminate true precocious puberty from premature thelarche and adrenarche.

Since luteinizing hormone levels by radioimmunoassay (I-LH) have rarely been useful in distinguishing true isosexual precocity from other less serious disorders of puberty, we have studied bioassayable B-LH in 17 prepubertal girls, seven girls with premature adrenarche, 12 girls with premature thelarche, and six girls with true isosexual precocity. The I-LH levels were three times higher in the girls with true precocious puberty than in the other groups but there was overlap between those with premature thelarche and true precocious puberty. The B-LH levels were 16 times higher in the girls with isosexual precocity than in the others, and there was no overlap. We conclude that B-LH better discriminates between true isosexual precocity and other disorders of puberty and may be a very useful laboratory test for the early diagnosis of true precocious puberty.

Adrenal Cortex↗
PubMed1987

Precocious puberty after traumatic brain injury.

After traumatic brain injuries in 33 prepubertal children, precocious puberty was observed in seven. Precocious puberty developed significantly more frequently in girls than in boys (54.5 versus 4.5%, P less than 0.01). Six children with precocious puberty were in coma for greater than or equal to 2 weeks. Follow-up computed tomography revealed cerebral atrophy or focal encephalomalacia in all children with and 69% of children without precocious puberty. There were no striking differences in incidence of motor or cognitive deficits or posttraumatic epilepsy in children with and without precocious puberty. In four of five children, basal sex steroid levels were elevated, and the response to luteinizing hormone releasing hormone stimulation revealed a pubertal pattern after the appearance of secondary sex characteristics.

Brain Injuries↗
PubMed1995

Spontaneous serum gonadotropin concentrations in the evaluation of precocious puberty.

OBJECTIVE: We assessed the utility of spontaneous and gonadotropin-releasing hormone (GnRH)-stimulated serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels measured by new immunochemiluminometric assays in the evaluation and monitoring of precocious puberty. METHODS: We evaluated serum gonadotropin values from intravenous GnRH stimulation tests in 49 girls with clinical signs suggesting central precocious puberty (CPP). Because GnRH-stimulated LH has been considered the standard for diagnosing CPP, we used it as the basis for comparison with GnRH-stimulated FSH levels and spontaneous LH and FSH measured by immunochemiluminometric assay. RESULTS: Twenty-six patients had a peak serum LH value above the +2 SD threshold for normal prepubertal female subjects (LH > 5 IU/L). The GnRH-stimulated FSH values had a narrow range and did not discriminate patients with CPP. In contrast, elevations in spontaneous LH and FSH were found to be specific for CPP. Spontaneous LH levels correlated strongly with peak stimulated LH levels in subjects with precocious puberty (r = 0.79) or in control subjects (r = 0.93, both p (0.0001). Spontaneous LH levels in excess of 0.1 IU/L detected true puberty with 94% sensitivity and 88% specificity. Random LH levels in excess of 0.3 IU/L had 100% specificity for CPP. CONCLUSIONS: The GnRH-stimulated FSH levels do not adequately differentiate children with and without CPP and have limited utility in the evaluation of precocious puberty. Spontaneous FSH levels are elevated in CPP with fair sensitivity and marked specificity. Elevated random LH, measured by third-generation assay such as immunochemiluminometric assay, is strongly correlated with and highly predictive of elevated peak GnRH-stimulated LH, and is a useful screening tool for CPP.

Adolescent↗
PubMed1995

Progression of premature thelarche to central precocious puberty.

To evaluate whether girls with premature thelarche progress to central precocious puberty (CPP) and to analyze their clinical and hormonal characteristics, we retrospectively examined 100 girls with premature thelarche who were followed for several years. Fourteen of the patients with characteristics diagnostic of premature thelarche (isolated breast development before age 8 years, bone age advancement within 2 SD of normal, normal growth velocity, follicle-stimulating hormone-predominant response to luteinizing hormone-releasing hormone) progressed during follow-up to precocious or early central puberty (progressive breast size increase, bone age acceleration, and significant decrease in predicted adult height). The chronologic age of this group of 14 girls was 5.1 +/- 2.0 years at the onset of premature thelarche and 7.8 +/- 0.6 years (mean +/- SD) after progression to central early or precocious puberty. Pelvic ultrasonography showed significant differences in measurements between the time of diagnosis of premature thelarche and progression to CPP. Nine of these patients required treatment, three with cyproterone acetate and six with luteinizing hormone-releasing hormone analogs, and all responded as expected for classic CPP. At baseline evaluation, no clinical or hormonal characteristics could be established that separated the 14 children who progressed to precocious or early puberty from the 86 girls who did not. We conclude that premature thelarche is not always a self-limited condition and may sometimes accelerate the timing of puberty.

Age Determination by Skeleton↗
PubMed2001

[Treatment with LHRH analogues in girls with precocious puberty does not improve final height. Longitudinal study compared with a control group].

BACKGROUND: We analysed the effectiveness of therapy with LHRH analogues in girls with a puberty onset at age 8 years. PATIENTS AND METHOD: We performed a non-randomised clinical study of 32 girls with advanced puberty. These included 16 treated with triptorelin LHRH analogue(3.75 mg/month during 1 year) and 16 control subjects. We carried out anthropometric measurements and determined the pubertal height growth (gain in height from the puberty onset up to the final height) and the pubertal duration (time in years from the puberty onset up to the age at which final height is attained). RESULTS: Treatment with LHRH analogue delayed the menarche age (11.5 [1.46]vs 10.37 [0.67] years of age; p = 0.03), led to an involution in secondary sexual characteristics and a temporary decrease ingrowth rate, and delayed skeletal maturation. However, pubertal duration, pubertal height growth and final height were all similar in both groups. In addition, no significant differences in body fat mass were observed. CONCLUSIONS: Treatment with LHRH analogues in advanced puberty modifies pubertal development, without modifying pubertal duration or pubertal height growth. Furthermore, this treatment does not improve final height.

Adolescent↗
PubMed2002

Microsurgical treatment for hypothalamic hamartoma in children with precocious puberty.

BACKGROUND: We review the surgical treatment of hypothalamic hamartoma causing precocious puberty. METHODS: Six children (three girls and three boys) with precocious puberty secondary to hypothalamic hamartoma were recruited for our study. The mean age of the patients was 30 months old (range 13 months to 5 years), and the mean age of the onset of puberty was 7.3 months. All patients were treated by microsurgery. RESULTS: All patients had higher then normal stature, body weight, bone growth, and serum levels of sexual hormones. The boys presented with mature external genitalia, pubic hair, frequent erection, and acne, while the girls presented with growth of breasts and menarche. Magnetic resonance image (MRI) revealed an isointense mass below the tuber cinereum extending into the supersellar and interpeduncular cistern, ranging from 4 to 12 mm in diameter, consistent with pedunculate hamartoma. The hamartoma was removed completely via a right pterional approach. The symptoms and signs of precocious puberty resolved completely, and sexual hormone levels decreased to the pre-pubertal range in all six patients without any postoperative complications. CONCLUSION: We report a series of six children with hypothalamic hamartoma-induced precocious puberty who underwent microsurgical treatment. All of them recovered completely to their age-appropriate state. Microsurgery is a good choice of treatment for pedunculate hypothalamic hamartoma.

Brain Neoplasms↗
PubMed1987

Induction of puberty by pulsatile gonadotropin releasing hormone.

15 girls and 17 boys with delayed or arrested puberty were treated with gonadotropin releasing hormone (GnRH) for a mean of 1.04 years. GnRH was administered subcutaneously in a pulsatile fashion at 90 min intervals, and the dose was increased as required to maintain progression of puberty, initially only at night and subsequently over 24 h. Initial GnRH dose was 1-2 micrograms per pulse in the girls and 2-4 micrograms per pulse in the boys. The effect of treatment was monitored by serial overnight gonadotropin profiles in all patients and with pelvic ultrasound in the girls. The clinical features, growth acceleration, endocrinology, and ovarian ultrasound morphology of puberty were those seen in normal children. Measurement of spontaneous gonadotropin pulsatility after treatment had been discontinued allowed the distinction between 20 patients with hypogonadotropic hypogonadism and 12 who had constitutional delay of growth and puberty. 2 girls and 6 boys did not respond to the treatment regimen. These findings indicate that normal puberty is GnRH dependent.

Adolescent↗
PubMed2001

Puberty and prognosis of asthma and bronchial hyper-reactivity.

It is a commonly held view that pediatric asthma frequently abates during puberty. However, little data are available that associate the stage of puberty with the prognosis of asthma and bronchial hyper-reactivity (BHR). In this study, 155 children with active asthma at 10 years of age (60 girls [38.70%], 95 boys [61.3%]) were followed-up until they reached 14 years of age. The stage of puberty was assessed by parental questionnaire; in addition, serum 3-alpha-androstanediolglucuronide, as an endocrinological marker for peripheral androgen status, was measured in 107 subjects. Persistence of asthma was determined via questionnaire, lung function testing, and bronchial provocation (hyperventilation of cold, dry air). At 14 years of age, 73.3% of girls were reported to have had menarche and 40.8% of boys a voice change, and only 35.5% of the subjects had experienced acute asthma symptoms during the last 12 months, with an almost unchanged gender ratio (19 girls [34.5%], 36 boys [65.5%]) vs. that recorded at 10 years of age. The level of androstanediolglucuronide was higher in the children who reported puberty (mean+/-SD): 3.03+/-2.13 nmol/l vs. 1.89+/-1.26 nmol/l, p = 0.003. No statistically significant relationship was found between the reported signs of late puberty and loss of asthma or BHR. Likewise, no significant association was found between asthma persistence and the level of androstanediolglucuronide (2.39+/-1.75 nmol/l vs. 2.44+/-1.82 nmol/l, p = 0.84), or BHR and the level of androstanediolglucuronide (3.02+/-1.97 nmol/l vs. 2.28+/-1.67 nmol/l, p = 0.13), at 14 years of age, in girls or boys. At 14 years of age, no change in the gender ratio of children with active asthma had occurred. These results may indicate that the change in gender predominance of asthma through the second decade of life is not caused by increased loss of established asthma in boys between 10 and 14 years of age.

Adolescent↗
PubMed1979

Melatonin, the pineal gland and human puberty.

Animal experiments have suggested that the pineal gland produces an anti-gonadotropic hormone. The hamster, for example, undergoes reproductive collapse when kept in short-day periods, an effect which is abolished by pinealectomy. Although there is little direct evidence about the endocrine role of the pineal gland in man, it has been noted that tumours of the pineal gland in young boys are associated with precocious puberty and the human pineal gland has been suggested to produce a substance that holds sexual maturation in check. This observation has been extended by Kitay, who has shown that destructive tumours are associated with precocious puberty whereas hyperactive tumours are associated with delayed puberty. However, no studies have described any change of pineal function with normal puberty. Because two pineal indoles, melatonin and methoxytryptophol, have been shown to be antigonadotropic when administered to animals, we have now measured them in schoolchildren. Our findings show that in young boys there is an abrupt fall in the concentration of melatonin with advancing development suggesting that it may play an important physiological role in the control of human puberty.

Adolescent↗
PubMed1998

Final height after combined growth hormone and gonadotrophin-releasing hormone analogue therapy in short healthy children entering into normally timed puberty.

OBJECTIVE: Combined gonadotrophin-releasing hormone analogue and recombinant human growth hormone therapy has been used in an attempt to improve the final height of short non-GH deficient adolescents with normally timed puberty; its use, however, is still controversial as only short-term studies in a very limited number of patients have been undertaken, with either improvement in height prognosis or no beneficial effect on predicted growth. We have treated a group of extremely short healthy children with very low predicted adult heights entering into normally timed puberty with combined therapy, in order to determine whether we could improve their final height above their pretreatment predicted adult height. PATIENTS: We treated 10 healthy adolescent short children (7 girls and 3 boys) simultaneously for 30.0 +/- 5.2 months with the GnRH analogue leuprolide acetate (0.3 mg/kg im every 28 days) and with rhGH (0.1 U/kg/day, sc, 6 days a week). The mean chronological age of our patients was 11.8 +/- 1.3 years, with a mean bone age of 11.2 +/- 0.9 years, height of 128.9 +/- 7.5 cm (-2.4 +/- 0.4 SD below the mean) and a predicted adult height of 150.7 +/- 9.8 cm; they were all in Tanner stage II-III of puberty. Ten healthy short children (7 girls and 3 boys) in the early stages of puberty with a mean chronological age of 11.4 +/- 1.0 years, a mean bone age of 11.0 +/- 0.8 years, height of 128.9 +/- 7.8 cm (-2.3 +/- 0.4 SD below the mean) and a mean adult predicted height of 151.8 +/- 10.1 cm served as controls and were simultaneously followed without therapy for the same study period. MEASUREMENTS: Height and pubertal status were followed every 3 months during combined therapy and until final height of our patients was reached; bone ages were obtained every 6 months. Growth hormone deficiency was ruled out in all our subjects prior to beginning of the study by a normal response to oral clonidine and normal IGF-1 levels. Basal serum testosterone and/or oestradiol levels, as well as LH and FSH following administration of LH-releasing hormone were obtained before treatment and after 6 weeks and 4 months of combined therapy and every 6 months thereafter. Routine biochemistry as well as thyroid function tests were obtained at each visit. RESULTS: Combined treatment resulted in an interruption of pubertal development with a suppression of gonadal steroids and of the LH response to LH-releasing hormone. Growth velocity decreased from 6.5 +/- 1.6 cm/year before treatment to 5.5 +/- 1.5 cm/year and 3.9 +/- 1.3 cm/year during the first and second year of treatment (P < 0.02 and P < 0.05, respectively) resulting in a height Z score reduction, declining from -2.4 +/- 04 to -2.6 +/- 0.7 SD. Bone age maturation declined averaging 0.75 bone age year/year of treatment but height SDS for bone age declined from -1.7 +/- 0.7 to -2.2 +/- 0.5 at the end of the second year of therapy with no improvement in predicted adult height (150.7 +/- 9.8 cm before and 150.0 +/- 8.0 after 2 years of therapy). After discontinuing treatment growth velocity did not improve and bone maturation advanced more rapidly (averaging 2.0 +/- 0.4 year/year of follow up) and the mean final height of our patients was 151 +/- 2.4 cm (-2.6 +/- 0.6 SD below the mean) which was not greater than the mean pretreatment predicted adult height and well below their target height; these results were also similar to those of the control population in whom the predicted adult height at the beginning of the study and after 2 years of follow up, was not different from their final height and well below their target height. CONCLUSIONS: We conclude that combined rhGH and GnRH analogue therapy in short adolescents with normally timed puberty does not contribute to increase their final height above their pretreatment predicted adult height; we can therefore not recommend this form of therapy for this group of patients given the poor results obtained, as well as the cost of these medications and the

Body Height↗
PubMed1999

Constitutional delay in growth and puberty (CDGP) is associated with hypoleptinaemia.

OBJECTIVE: Serum leptin concentrations are higher in early adolescence compared with childhood and may play a facilitatory role in pubertal development. Constitutional delay in growth and puberty (CDGP) is a disorder of the tempo of physical maturation and may be associated with relative hypoleptinaemia. We have therefore compared serum leptin concentrations in normal boys with those in boys exhibiting constitutional delay of growth, controlling for pubertal status, age and body mass index (BMI). PATIENTS: 23 boys with constitutional delay in growth (n = 17, prepubertal) and puberty (n = 6, early pubertal) and 88 normal boys (n = 64 prepubertal, n = 24 Tanner stage 2). MEASUREMENTS: Serum leptin was measured in a single, non-fasted morning serum sample by radioimmunoassay. Using the data from normal boys, leptin standard deviation scores (sds) were calculated, to account for the independent influences of age and body mass index (BMI) sds. Both chronological age and bone age were used in the calculation of leptin sds in those with delay. RESULTS: BMIsds was significantly lower in prepubertal delays compared with controls but was not different in pubertal subjects. Leptin concentrations were higher in early puberty compared with prepuberty (P < 0.001) in normal boys but were not significantly elevated in pubertal boys with delay compared with prepubertal delays. Although leptin sds, for both chronological age and bone age, was similar in prepubertal controls and delays, it was significantly lower in the pubertal delay group (P < 0.05). In controls leptin sds did not correlate with age. However, in delays leptin sds was negatively correlated with both chronological age (r = - 0.43, P < 0.05) and bone age (r = - 0.68, P < 0.01), indicating that in the older delays leptin levels were lower than expected given their age and BMIsds. CONCLUSIONS: These data indicate that significantly higher leptin levels in Tanner stage 2 compared with prepuberty are not a prerequisite for progression into puberty. However, the absence of elevated leptin concentrations may be associated with delayed puberty in boys.

Biomarkers↗
PubMed2000

Serum levels of growth hormone binding protein in children with normal and precocious puberty: relation to age, gender, body composition and gonadal steroids.

AIM: To study the regulation of GHBP serum levels by gonadal steroids in normal and precocious puberty. STUDY PROTOCOL: We studied GHBP levels in relation to age, sex, pubertal maturation, body composition as well as to circulating IGF-I and gonadal steroid levels in 320 healthy children. Furthermore, we studied the regulation of circulating GHBP in 33 girls with central precocious puberty before and during gonadal suppression with GnRH agonist. METHODS: GHBP was determined by a time-resolved fluoroimmunoassay (GHBP TR-FIA) based on a commercially available immunoassay for GH, the DELFIA GH assay. RESULTS: In healthy children GHBP levels were significantly higher in normal girls compared with boys, and there was no significant increase in GHBP in puberty in both sexes. GHBP levels did not correlate with height (SDS), age, pubertal stage, IGF-I or testosterone/oestradiol levels in boys and girls, respectively. There were significant correlations between BMI and GHBP in boys and girls (R 2 = 0.14 and R 2 = 0.12, both P < 0.0001). Furthermore, GHBP correlated highly significantly with the percentage body fat, determined by BIA in 43 healthy girls (R 2 = 0. 40, P < 0.0001). GHBP levels were significantly higher in girls with central precocious puberty (CPP) (1.31 SDS (1.26), mean (SD)) compared to prepubertal controls (P < 0.0001), and above + 2 SD in 10 out of 33 patients. In girls with CPP, GHBP correlated inversely with oestradiol before treatment (R 2 = 0.26, P < 0.01) and there was a tendency towards a positive correlation with BMI (R 2 = 0.13, P = 0.078). By contrast, there were no signficant correlations between GHBP and IGF-I or height SDS. Gonadal suppression with GnRH agonist treatment caused a transient significant increase of 0.57 SD after 2 months of treatment (P < 0.001), but decreased to baseline levels hereafter. CONCLUSION: We conclude that in children, as in adults, body fat is the primary determinant for the circulating level of GHBP, and that the difference in body fat is probably the main factor for the higher levels of serum GHBP in girls compared with boys, as well as for the negative influence of testosterone levels in boys and of oestrogen levels in girls. The elevation in GHBP levels observed in girls with central precocious puberty is probably due their higher body fat content.

Adolescent↗
PubMed2002

Timing of puberty and fetal growth.

Children born small for gestational age (SGA: birth weight or birth length more than 2 standard deviations below the mean score) are at a higher risk of perinatal morbidity and mortality and of a number of chronic diseases in later life such as hypertension, decreased insulin sensitivity, diabetes mellitus type 2 and an increased risk of cardiovascular disease. The programming of the endocrine axes occurs during critical phases of fetal development and might thus be affected by intrauterine growth retardation. Studies in Northern Spanish adolescent girls have indicated associations between reduced fetal growth and the occurrence of precocious adrenarche, pubarche, hyperandrogenism, polycystic ovary syndrome (PCOS) and hyperinsulinism. These findings have attracted much attention because it might have serious consequences in later life. However, hyperandrogenism and precocious pubarche were not confirmed in a large Dutch study in short children born SGA. Two studies reported a lower number of follicles in the ovaries in girls born SGA, which might have an impact on fertility. Clearly, further studies are required before definite conclusions can be drawn. There are still only limited data concerning the timing of puberty in children born SGA. Most studies indicate that these children start their puberty at a normal age but relatively early within the normal range. Age at menarche seems comparable with controls. Data on duration of puberty, influence of puberty on attainment of adult height, peak height velocity during puberty and fertility are not yet known.

Animals↗
PubMed2000

Do all girls with apparent idiopathic precocious puberty require gonadotropin-releasing hormone agonist treatment?

OBJECTIVE: To evaluate prospectively pubertal and predicted adult height progression until final height (FH) or near FH in girls with apparent idiopathic precocious puberty who were not treated. STUDY DESIGN: The decision not to treat at the time of initial evaluation was based on evidence of slowly progressive puberty as shown by bone age (BA) advancement <2 years above the chronologic age, whatever the hypothalamic pituitary ovarian axis activation, or no evidence of hypothalamic pituitary ovarian axis activation, whatever the BA advancement. During follow-up, patients who showed a significant decrease in predicted FH were treated with gonadotropin-releasing hormone agonist. RESULTS: Twenty-six girls with idiopathic precocious puberty were studied at a mean chronologic age of 7.4 +/- 0.9 years during a follow-up period of 6.6 +/- 2.2 years until FH or near FH. During the first 2 years of follow-up, most of the patients (group 1, n = 17; 65% of the cases) showed no substantial changes in predicted FH. They never required treatment, and menarche occurred at a mean chronologic age of 11.9 +/- 0.6 years. Their mean FH (or near FH) at 160.7 +/- 5.7 cm was close to their target height (161.3 +/- 4.7 cm). On the other hand, after a mean follow-up period of 1.4 +/- 0.8 years, 9 patients (group 2) had acceleration of bone maturation and deterioration of their predicted FH (from 162.1 +/- 6. 2 cm to 155.3 +/- 5.6 cm; P <.01), which was at that time significantly lower than their target height (P <.05) (mean target height = 159.8 +/- 4.6 cm). They received a gonadotropin-releasing hormone agonist for 2.1 +/- 0.7 years, resulting in a restoration of growth prognosis (mean FH or near FH = 160.2 +/- 6.7 cm). CONCLUSIONS: This study demonstrates that not all patients with apparent idiopathic precocious puberty require medical treatment, notably when there is no evidence of hypothalamo-pituitary ovarian activation or no significantly advanced BA to impair height potential. Most show a slowly progressing puberty. However, careful follow-up of these patients is necessary up to at least 9 years of age, because until then height prediction may deteriorate, necessitating gonadotropin-releasing hormone agonist treatment in one third of the cases.

Child↗
PubMed2005

Current wheezing, puberty, and obesity among mexican adolescent females and young women.

BACKGROUND: Studies suggest an association between obesity and asthma. This may be modified by the physiological changes of puberty. We aim to explore the relation between overweight and current asthma among Mexican adolescent females and young women and evaluate how puberty may modify this association. METHODS: Adolescent females (n=6944) and young women aged 11-24 years provided data. Current asthma was defined as wheezing in the last 12 months and obesity by body mass index (BMI). Puberty was defined by age at menarche. The association of obesity and current wheezing was evaluated by using logistic regression adjusting for confounders. The impact of puberty was studied by using stratified analysis by age at menarche. RESULTS: The prevalence of current wheezing was 16.2% (95% CI 15-17). Compared with girls of normal weight (BMI 15 to >or=85 percentile), obese girls (BMI>or=95 percentile) had an increased risk of current wheezing of 19% (OR=1.19; 95% CI 0.97-1.46). After stratifying by age at menarche, we observed that this increased risk was only present in girls with menarche at 11 years old or younger (1.31%; 95% CI 1.01-1.73). CONCLUSIONS: The association between obesity and asthma seems to be greater among girls with early puberty, suggesting the role of female hormones.

Adolescent↗
PubMed2003

Puberty does not induce serum antisperm surface antibodies in patients with previously operated cryptorchidism.

PURPOSE: We investigated serum antisperm surface antibody (ASA) prevalence at puberty, which is reported to be as high as 38% in the sera of males with cryptorchidism operated on before puberty. Operative technique impact, dartos pouch orchiopexy or testis fixation, was also examined. MATERIALS AND METHODS: We examined a total of 61 pubertal males (Tanner stage 2 or greater) divided into 3 groups. Group 1 consisted of 24 males with cryptorchidism 10 to 17.9 years old who underwent unilateral dartos pouch orchiopexy before puberty (median age 5.85). All of these cases were known to be negative for ASA preoperatively, and 20 before puberty. Group 2 consisted of 22 males with cryptorchidism 12.1 to 17.7 years old operated on previously (median age 10.35) by testicular fixation among other techniques. Group 3 consisted of 15 healthy males 12.2 to 17.3 years old. Prepubertal ASA status was unknown for groups 2 and 3. Operated testis was compared with counterpart before serum collection in group 1 and during operation in group 2. IgG IgM and IgA ASA were studied by the indirect Immunobead (BioRad, Clinisciences S.A., Montrouge, France) test. RESULTS: All sera tested were found negative in the 3 groups. Dartos pouch operation, testis fixation or even consecutive operations did not induce ASA production. Alterations in size or consistency were observed in operated testes in 10 patients in group 1, and in 8 patients in group 2. CONCLUSIONS: Our results suggest that dartos pouch orchiopexy, testicular fixation and/or intrinsic developmental alterations of the cryptorchid testis does not elicit an autoimmune response against sperm surface antigens at puberty.

Adolescent↗