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PubMed1998

Bone mineral status in prepubertal children with constitutional delay of growth and puberty.

OBJECTIVE: We wished to clarify whether the osteopenia reported in adult men with a history of constitutional delay of growth and puberty (CDGP) could be due to the delayed puberty or an independent predisposition to osteoporosis in this condition. DESIGN: Short prepubertal children with CDGP and children with familial short stature (FSS) were matched for height and other auxological variables. The FSS children served as a control group. METHODS: We measured spinal (L1-L4) bone mineral content (BMC) and bone mineral density (BMD) by dual energy X-ray absorptiometry (Hologic QDR 1000/w) in 56 children aged 5-11 years. All children had height below the 10th percentile for chronological age (CA), and bone age (BA) less than 10 years, 29 of them with clinical diagnosis of possible CDGP and 27 of them with FSS. The BMD standard deviation scores (SDS) relative to the values for normal height children were obtained. RESULTS: The mean (+/-S.D.) spinal BMD was significantly lower in the children with CDGP than in the FSS group (0.534+/-0.059 vs 0.623+/-0.060 g/cm2, P< 0.001). Both groups had negative mean lumbar BMD SDS, but in the CDGP group it was significantly lower than in the FSS group as well when the SDS was based on the CA (-1.41+/-0.61 vs -0.38+/-0.51, P< 0.001) and when it was related to BA (-0.78+/-0.64 vs -0.17+/-0.52, P< 0.01). BMC was significantly lower in the CDGP than in the FSS group, when multiple regression analysis was performed by using scanned bone area, body weight and height, sex and BA as independent variables (P = 0.0005). CONCLUSION: The finding of decreased mineralization in prepubertal children with CDGP before the age of puberty suggests that they may have an inherent predisposition to osteopenia.

Absorptiometry, Photon↗
PubMed2003

The human chorionic gonadotropin test is more powerful than the gonadotropin-releasing hormone agonist test to discriminate male isolated hypogonadotropic hypogonadism from constitutional delayed puberty.

OBJECTIVE: The effectiveness of biological investigations aiming at discriminating isolated hypogonadotropic hypogonadism (IHH) from constitutional delayed puberty (CDP) in male patients is still controversial. We revisited the diagnostic power of the basal serum testosterone level, the Triptorelin test and the human chorionic gonadotropin (hCG) test in a cohort of 33 boys with delayed puberty. DESIGN: Boys were aged 14.2 to 26.2 Years at referral. A 5-Year-long clinical follow-up after the initial study allowed confirmation of the diagnosis. At the end of the follow-up period, IHH was found in 13 patients while the other 20 had normal spontaneous pubertal development (CDP). RESULTS: At referral, a basal morning testosterone level >1.7 nmol/l was observed in 55% of patients with CDP exclusively (predictive positive value (PPV)=100%; predictive negative value (PNV)=59%). For CDP, the PPV of the LH peak 3 h after Triptorelin was 100% by setting the upper threshold at 14 IU/l and the PNV was 72%. However, no lower threshold could discriminate IHH from CDP in the remaining patients with an LH peak 3 h after Triptorelin <14 IU/l. In CDP patients, the PPV of the serum testosterone increment after hCG stimulation (deltaT/hCG) was 100% for values >9 nmol/l (PNV=72%). In IHH patients, the PPV of deltaT/hCG was 100% for values <3 nmol/l (PNV=82%). Only 29% of the studied population had a deltaT/hCG between these lower and upper thresholds and therefore could not have been classified initially. CONCLUSIONS: (i) Dynamic testing for the diagnosis of delayed puberty is useful only when the basal testosterone level is lower than 1.7 nmol/l; (ii) in that case, the hCG test has better discriminating power than the Triptorelin test and appears as the best cost-effective investigation. It prevents useless and expensive investigations in about one-half of CDP patients with a basal morning testosterone level lower than 1.7 nmol/l.

Adolescent↗
PubMed2004

Classic congenital adrenal hyperplasia and puberty.

Congenital adrenal hyperplasia (CAH) is a group of autosomal recessive disorders resulting from deficiency of one of the five enzymes required for synthesis of cortisol in the adrenal cortex. The most common form of the disease is classic 21-hydroxylase deficiency, which is characterized by decreased synthesis of glucocorticoids and often mineralocorticoids, adrenal hyperandrogenism and impaired development and function of the adrenal medulla. The clinical management of classic 21-hydroxylase deficiency is often suboptimal, and patients are at risk of developing in tandem iatrogenic hypercortisolism and/or hyperandogenism. Limitations of current medical therapy include the inability to control hyperandrogenism without employing supraphysiologic doses of glucocorticoid, hyperresponsiveness of the hypertrophied adrenal glands to adrenocorticotropic hormone (ACTH) and difficulty in suppressing ACTH secretion from the anterior pituitary. Puberty imposes increased difficulty in attaining adrenocortical suppression despite optimal substitution therapy and adherence to medical treatment. Alterations in the endocrine milieu at puberty may influence cortisol pharmacokinetics and, consequently, the handling of hydrocortisone used as replacement therapy. Recent studies have demonstrated a significant increase in cortisol clearance at puberty and a shorter half-life of free cortisol in pubertal females compared with males. Furthermore, children with classic CAH have elevated fasting serum insulin concentrations and insulin resistance. The latter may further enhance adrenal and/or ovarian androgen secretion, decrease the therapeutic efficacy of glucocorticoids and contribute to later development of the metabolic syndrome and its complications.

Adolescent↗
PubMed2006

The role of KiSS-1 in the regulation of puberty in higher primates.

Puberty in higher primates is triggered by resurgence in the pulsatile secretion of hypothalamic GnRH after a hiatus in the robust release of this hypophysiotropic signal during childhood and juvenile development. Interestingly, the prepubertal decline in GnRH release is not associated with a marked reduction in the expression of either the gene that codes for GnRH (GnRH-1) or the decapeptide itself, and the network of GnRH neurons in the hypothalamus of the juvenile may by activated prematurely and with surprising ease by intermittent neurochemical stimulation with N-methyl-d-aspartate (NMDA), a glutamate receptor agonist. KiSS-1, a gene that encodes for kisspeptin-121, which is proteolytically cleaved to a 54 amino acid peptide, metastin, was initially studied in the context of tumor suppression. In 2003, however, inactivating mutations in the metastin receptor, GPR54, were reported to be associated with hypogonadotropic hypogonadism and absent puberty in man. Subsequent studies in the rhesus monkey have shown that GPR54 and KiSS-1 are expressed in the mediobasal hypothalamus (MBH), KiSS-1 expression in the MBH increases at the time of the pubertal resurgence in GnRH release and pulsatile, but not continuous, i.v. administration of metastin 45-54 in the juvenile male monkey elicits sustained GnRH release precociously. The significance of these findings in the context of the initiation of the onset of puberty is discussed.

Animals↗
PubMed2004

Puberty and the onset of substance use and abuse.

OBJECTIVE: Substance abuse remains one of the major threats to adolescent health in Western cultures. The study aim was to ascertain the extent of association between pubertal development and early adolescent substance use. METHODS: The design was a cross-sectional survey of 10- to 15-year-old subjects in the states of Washington, United States, and Victoria, Australia. Participants were 5769 students in grades 5, 7, and 9, drawn as a 2-stage cluster sample in each state, and the questionnaire was completed in the school classrooms. The main outcomes of the study were lifetime substance use (tobacco use, having been drunk, or cannabis use), recent substance use (tobacco, alcohol, or cannabis use in the previous month), and substance abuse (daily smoking, any binge drinking, drinking at least weekly, or cannabis use at least weekly). RESULTS: The odds of lifetime substance use were almost twofold higher (odds ratio [OR]: 1.7; 95% confidence interval [CI]: 1.4-2.1) in midpuberty (Tanner stage III) and were threefold higher (OR: 3.1; 95% CI: 2.4-4.2) in late puberty (Tanner stage IV/V), after adjustment for age and school grade level. Recent substance use was moderately higher (OR: 1.4; 95% CI: 1.0-1.9) in midpuberty and more than twofold higher (OR: 2.3; 95% CI: 1.7-3.3) in late puberty. The odds of substance abuse were twofold higher (OR: 2.0; 95% CI: 1.2-3.2) in midpuberty and more than threefold higher (OR: 3.5; 95% CI: 2.2-5.4) in late puberty. Reporting most friends as substance users was more likely in the later stages of pubertal development, a relationship that accounted in part for the association found between later pubertal stage and substance abuse. CONCLUSIONS: Pubertal stage was associated with higher rates of substance use and abuse independent of age and school grade level. Early maturers had higher levels of substance use because they entered the risk period at an earlier point than did late maturers. The study findings support prevention strategies and policies that decrease recreational substance use within the peer social group in the early teens.

Adolescent↗
PubMed2005

The histrelin implant: a novel treatment for central precocious puberty.

OBJECTIVE: Standard treatment of central precocious puberty (CPP) consists of intramuscular or subcutaneous administration of a gonadotropin-releasing hormone (GnRH) agonist (GnRHa) at 3- to 4-week intervals. Although generally effective in suppressing clinical and laboratory parameters of puberty, GnRHa injections are painful, and the need for monthly clinic visits may contribute to poor compliance. Recently, a subcutaneous implant was developed that releases the GnRHa histrelin at an average rate of 65 microg/day. The aims of this study were to determine if a histrelin implant would suppress gonadotropin and estradiol (E2) in girls with CPP for 1 year and to compare the suppression to standard treatment. METHODS: We studied 11 girls with CPP to determine if the histrelin implant can maintain long-term gonadotropin suppression. Mean age at diagnosis was 6 years (range: 2-9 years). GnRH (100 microg intravenously) stimulation tests (GnRH-STs) showed peak luteinizing hormone and follicle-stimulating hormone responses of 23 +/- 28 (mean +/- SD) and 20 +/- 25 mIU/mL, respectively. All subjects were initially treated with depot intramuscular GnRHa triptorelin embonate. Implants were inserted subcutaneously under local anesthesia, and depot GnRHa treatment was discontinued. Six girls were followed for 15 months after insertion (group A). For the remaining 5 girls, the implant was removed after 9 months, and a new implant was inserted at the same incision site (group B). GnRH-STs were performed before depot GnRHa treatment, immediately before implant insertion, at the 6- and 9-month visits for each patient and the 12- and 15-month visit for those girls followed for 15 months. RESULTS: In all girls, breast development regressed, growth velocity decreased, and bone-age advancement was slowed. Basal gonadotropins and their responses to GnRH-STs and E2 levels were suppressed. Peak luteinizing hormone and follicle-stimulating hormone responses to GnRH-STs at preinsertion versus 9 months were 1.30 +/- 1.34 vs 0.25 +/- 0.08 and 1.68 +/- 1.08 vs 1.13 +/- 0.55 mIU/mL, respectively. Basal and stimulated gonadotropin levels and E2 level remained suppressed in all 6 patients followed for 15 months after implant insertion. Patients and parents reported less pain and discomfort and less interference with school activity and work with the implant compared with standard monthly injections. CONCLUSIONS: The histrelin implant consistently suppresses clinical and laboratory parameters of puberty for 1 year and is a promising new technique for treating CPP without the pain and inconvenience of monthly injections.

Child↗
PubMed2005

[Idiopathic central precocious puberty in girls in Bahia, Brazil].

INTRODUCTION: Although the therapeutic effects of GnRH analogues (GnRHa) in central precocious puberty (CPP) have been established, clinical aspects may vary according to racial groups. OBJECTIVE AND METHODS: To describe the profile of 175 girls from Bahia, Brazil, treated with GnRHa for idiopathic CPP. RESULTS: The mulatto racial group predominated in the sample. The chronological age at puberty was 6.3 +/- 0.1 years. At diagnosis, height was 2.2 +/- 0.1 SD and body mass index (BMI) was 1.5 +/- 0.1 SD (> 2 SD in 32%), this one, inversely associated with age at onset of puberty (R = -0.20, p = 0.008). At treatment, chronological and bone ages were 8.4 +/- 0.1 years and 10.3 +/- 0.1 years, respectively. At the end of treatment (n = 52) age, BMI and height were 10.6 +/- 0.1 years, 1.6 +/- 0.2 SD and 1.9 +/- 0.2 SD, respectively. CONCLUSION: Clinical presentation and evolution were similar to other studies, independently of racial characteristics. In this sample, treatment with GnRHa was not associated to significant weight gain.

Brazil↗
PubMed2004

Growth and puberty after treatment for acute lymphoblastic leukemia.

UNLABELLED: Over the last 20 years, after combining treatment of chemotherapy and radiotherapy, there has been an improvement in the survival rate of acute lymphoblastic leukemia patients, with a current cure rate of around 70%. Children with the disease have been enrolled into international treatment protocols designed to improve survival and minimize the serious irreversible late effects. Our oncology unit uses the international protocol: GBTLI LLA-85 and 90, with the drugs methotrexate, cytosine, arabinoside, dexamethasone, and radiotherapy. However, these treatments can cause gonadal damage and growth impairment. PATIENTS AND METHOD: The authors analyzed 20 children off therapy in order to determine the role of the various doses of radiotherapy regarding endocrinological alterations. They were divided into 3 groups according to central nervous system prophylaxis: Group A underwent chemotherapy, group B underwent chemotherapy plus radiotherapy (18 Gy), and group C underwent chemotherapy plus radiotherapy (24 Gy). Serum concentrations of LH, FSH, GH, and testosterone were determined. Imaging studies included bone age, pelvic ultrasound and scrotum, and skull magnetic resonance imaging. RESULTS: Nine of the patients who received radiotherapy had decreased pituitary volume. There was a significant difference in the response to GH and loss of predicted final stature (Bayley-Pinneau) between the 2 irradiated groups and the group that was not irradiated, but there was no difference regarding the radiation doses used (18 or 24 Gy). The final predicted height (Bayley-Pinneau) was significantly less (P = 0.0071) in both groups treated with radiotherapy. Two girls had precocious puberty, and 1 boy with delayed puberty presented calcification of the epididymis. CONCLUSION: Radiotherapy was been responsible for late side effects, especially related to growth and puberty.

Adolescent↗
PubMed1988

An evaluation of hormonal changes at puberty in man.

The pulsatile nature of the secretion of gonadotrophins, sex steroids and growth hormone are important in both the onset and maintenance of sexual maturation. The night-time is intimately related to the endocrine events which result in puberty, such that hormone measurements during the daytime have little meaning. This relationship between the night-time and gonadal function is not restricted to puberty but continues in adult life; the onset of the preovulatory LH surge occurs in the early hours of the morning. Girls seem more sensitive to small changes in GnRH concentrations than boys, which is why the physical signs of puberty appear slightly earlier in them. Low levels of oestradiol appear to assist growth hormone secretion, whereas higher levels of testosterone are required for the same effect. This probably explains the sex differences in the timing of the pubertal growth spurts.

Adolescent↗
PubMed1989

Levels of the small insulin-like growth factor-binding protein are strongly related to those of insulin in prepubertal and pubertal children but only weakly so after puberty.

We have looked at the relationship between fasting levels of insulin and a small insulin-like growth factor (IGF)-binding protein (IBP-1) in a cross-sectional study of 116 normal subjects aged 5-48 years. The relationship between IBP-1 and insulin was also examined within individual normal children in overnight profiles of IBP-1 and insulin obtained from two children at each stage of puberty (Tanner stages 1-5). In the cross-sectional study high levels of IBP-1 were found in early childhood and these fell throughout puberty as fasting levels of insulin rose. Multiple regression analysis revealed that both these changes were predominantly due to pubertal development rather than to age. After the age of 16 IBP-1 levels remained low despite fasting insulin levels returning to prepubertal levels. A strong negative correlation was obtained between IBP-1 and insulin in children of 5-16 years (r = -0.63; n = 60; P less than 0.001), no such relationship being found after the age of 16. In the second study, IBP-1 underwent a marked circadian variation in all cases and an inverse correlation with insulin, measured at the same time, was obtained at pubertal stages 1 to 4, but not at stage 5 (pooled data stages 1-4, r = -0.69; n = 53; P less than 0.001). We have demonstrated that a potential inhibitor of IGF-activity is inversely related to insulin throughout the period of active GH-related growth and that this relationship weakens after puberty.

Adolescent↗
PubMed2001

Autoregulation of the gonadotropin-releasing hormone (GnRH) system during puberty: effects of antagonistic versus agonistic GnRH analogs in a female rat model.

To address whether gonadotropin-releasing hormone (GnRH) regulates its own expression and the expression of its receptor in the hypothalamus and ovary, we treated five groups of prepubertal/peripubertal female rats from postnatal days 25-36 with either the GnRH agonist triptorelin (TRIP) or the GnRH antagonist cetrorelix (CET), each 10 or 100 microgram/day, or a placebo. We compared their effects regarding pubertal development, serum gonadotropins and the expression of GnRH and GnRH-receptor in the hypothalamus, pituitary, ovary and uterus. Onset of puberty was determined by vaginal opening, and expression levels of GnRH and GnRH-receptor were determined using either quantitative real-time PCR or competitive RT-PCR. Onset of puberty was retarded by both analogs but CET (100 microgram/day) inhibited while TRIP (10 and 100 microgram/day) stimulated serum gonadotropins (P<0.05). The expression of GnRH in the preoptic area did not show significant differences among the treatment groups but ovarian GnRH mRNA levels were significantly stimulated by CET (100 microgram/day). GnRH mRNA could not be detected in the uterus by either real-time PCR or competetive RT-PCR. The GnRH-receptor expression in the hypothalamus (preoptic area and mediobasal hypothalamus) did not vary among any of the groups, whereas in the pituitary GnRH-receptor mRNA levels were stimulated by TRIP (10 microgram/day) but inhibited by CET (100 microgram/day). In contrast, in the ovary GnRH-receptor mRNA levels were inhibited by both TRIP (100 microgram/day) and CET (100 microgram/day). Interestingly, the GnRH-receptor was even expressed in the uterus where it was strongly stimulated by both CET and TRIP in a dose-related manner. This shows that in addition to their different pituitary effects, the GnRH analogs cetrorelix and triptorelin exert different actions at the hypothalamic, ovarian and uterine level. This study also demonstrates an organ-specific regulation of GnRH and GnRH-receptor gene expression which is likely part of a local autoregulatory system. We conclude that the ovarian and uterine effects of GnRH analogs must be considered in addition to their known pituitary effects when deciding which GnRH analog is most suitable for treating precocious puberty.

Analysis of Variance↗
PubMed1993

Histrelin. A review of its pharmacological properties and therapeutic role in central precocious puberty.

Histrelin is a synthetic gonadotrophin-releasing hormone (GnRH) agonist which, when administered over a prolonged period, suppresses the release of gonadotrophins from the anterior pituitary. Data from clinical trials undertaken in small numbers of patients with idiopathic central precocious puberty have demonstrated that histrelin 8 to 10 micrograms/kg/day administered subcutaneously desensitises the anterior pituitary to gonadotrophin secretion within 3 months, ablating the pubertal gonadotrophin response to GnRH stimulation and reducing circulating gonadal sex steroid levels. When histrelin is administered to treat central precocious puberty, the rate of secondary sexual maturation is slowed and in some cases there is a reversal of maturation which occurs before initiation of treatment. Of equal importance, histrelin therapy appears to have decelerating effects on skeletal maturation, allowing more statural growth; an increase in final adult height is predicted from available data, but will need to be confirmed in long term follow-up studies currently being undertaken. The most common adverse event reported during histrelin therapy was a skin reaction at the site of subcutaneous injection. Few patients have discontinued therapy because of any adverse event. Although experience with histrelin is limited, the absence of effective clinically available alternatives and the demonstrated efficacy of histrelin justifies its place as a first-line therapy for patients with central precocious puberty.

Amino Acid Sequence↗
PubMed1996

Effect of puberty on markers of glomerular hypertrophy and hypertension in IDDM.

Epidemiological data implicate puberty as a factor in the initiation of diabetic nephropathy. However, the mechanism remains unclear. We hypothesized that puberty would result in an increase in glomerular hypertrophy and hypertension; these two early concomitant events are seen as pivotal to the pathophysiology of diabetic nephropathy. We studied the effect of pubertal duration on three surrogate markers of glomerular hypertrophy/hypertension: kidney volume (KV), microalbuminuria (MA), and Na-Li countertransport (CT). We recruited 177 subjects (87 female and 90 male; aged 6.2-22.1 years) with IDDM of 5 to 10 years' duration (6.8 +/- 1.6 years) into three groups with different pubertal duration: prepubertal since IDDM diagnosis; prepubertal at diagnosis, now pubertal; or early puberty at diagnosis, now postpubertal. KV was measured by ultrasound and corrected for body surface area; MA was defined as urinary albumin excretion of 15-200 micrograms/min in two of three 24-h samples, and Na-Li CT was measured in erythrocytes. As pubertal duration increased, there was a disproportionate increase in mean KV (prepubertal, 247 +/- 6 [SE] ml/1.73 m2; pubertal, 282 +/- 7/1.73 m2; postpubertal, 295 +/- 7/1.73 m2, P = 0.001), prevalence of nephromegaly (KV > 300 ml/1.73 m2) (14, 31, and 45%, respectively, P = 0.001), and prevalence of MA (0, 9.7, and 20.5%, respectively, P = 0.003). Subjects with KV > 300 ml/1.73 m2 were eight times more likely to have MA than those with KV < 300 (odds ratio 8.1, 95% confidence interval 2.4-27.4, P = 0.0001). There was no effect of pubertal duration on Na-Li CT. Multiple regression with KV as the dependent variable found an association with pubertal duration, MA, Na-Li CT, and current HbA1c (P < 0.0001). Our findings indicate that pubertal duration is an important determinant of both KV and MA and suggest that nephromegaly precedes microalbuminuria. We postulate that these effects are attributable to the influence of the pubertal milieu on glomerular hypertrophy/hypertension.

Adolescent↗
PubMedDate not supplied

Contribution of diabetes duration before puberty to development of microvascular complications in IDDM subjects.

The contribution of diabetes duration, both pre- and postpuberty, to the development of microvascular complications and mortality in diabetic subjects was investigated in three study populations from the Children's Hospital of Pittsburgh Insulin-Dependent Diabetes Mellitus (IDDM) Registry. Life-table analyses by total and postpubertal IDDM duration were used to evaluate differences in the prevalence of microvascular complications and diabetes-related mortality in subjects diagnosed before and during puberty, as defined by an age at IDDM onset marker of 11 yr for girls and 12 yr for boys. The prevalence of retinopathy and overt nephropathy in 552 White adult diabetic subjects (population 1, mean IDDM duration 20.8 yr was significantly greater in subjects diagnosed during puberty compared with those diagnosed before puberty. However, similar analyses by postpubertal duration showed no difference in microvascular complication prevalence between the two groups. These findings did not appear to be due to a confounding effect of age. Additional analyses of 239 adolescent diabetic subjects (population 2, mean duration 8.3 yr) revealed the same trend for the prevalence of retinopathy. Finally, results concerning the risk of diabetes-related mortality in a cohort of 1582 subjects (population 3, mean duration 12.9 yr) indicated that postpubertal duration of IDDM may be a more accurate determinant of the development of microvascular complications and diabetes-related mortality than total duration, and it is suggested that the contribution of the prepubertal years of diabetes to long-term prognosis may be minimal.

Adolescent↗
PubMed1993

Association of lipoprotein(a) with puberty in IDDM.

OBJECTIVE: To determine serum lipoprotein(a) in a large sample of IDDM and control children and to examine a possible association with puberty. RESEARCH DESIGN AND METHODS: Serum lipoprotein(a), apoB-100, and apoA-I were measured under identical conditions in 170 Caucasian children with IDDM aged 12.3 +/- 3.59 yr and 233 Caucasian control children aged 13.6 +/- 1.12 yr. Patients with persistent microalbuminuria were excluded. Lipoprotein(a), apoB-100, and apoA-I were measured by nephelometry using a specific monoclonal antibody. Pubertal assessment was performed using Tanner staging and testicular volume measurement. RESULTS: Lipoprotein(a) was higher in the IDDM than control group (geometric mean 237 mg/L, 25-75th percentile 134-465 vs. 172 [99-316] mg/L, P = 0.0008). When analyzed according to pubertal stage, only pubertal and postpubertal patients had higher levels than control subjects (265 [148-560] vs. 174 [101-320] mg/L, P = 0.0001), with prepubertal patients showing no difference. Pubertal and postpubertal patients showed both higher lipoprotein(a) (P = 0.01) levels and higher albumin excretion rates (P = 0.02) than prepubertal patients, correcting for the other variable. Lipoprotein(a) was not related to HbA1c, albumin excretion rate, duration, age, sex, mean arterial pressure, or a family history of premature coronary artery disease in the IDDM group. Lipoprotein(a) was not higher in patients with overnight albumin excretion rate above the 95th percentile but below the microalbuminuric range. ApoB-100 did not differ between IDDM and control children. ApoA-I was significantly lower in the IDDM group (1.04 [0.94-1.17] vs. 1.21 [1.10-1.31] g/L; P < 0.0001). CONCLUSIONS: Pubertal and postpubertal IDDM patients have higher serum lipoprotein(a) than Caucasian control subjects. Our findings suggest a rise in lipoprotein(a) may occur during puberty in IDDM. Longitudinal studies are required to clarify the relationship between lipoprotein(a), albumin excretion rate, and puberty.

Adolescent↗
PubMed1999

Microalbuminuria prevalence varies with age, sex, and puberty in children with type 1 diabetes followed from diagnosis in a longitudinal study. Oxford Regional Prospective Study Group.

OBJECTIVE: The predictive value of microalbuminuria (MA) in children with type 1 diabetes has not been defined. We describe the natural history of MA in a large cohort of children recruited at diagnosis of type 1 diabetes. RESEARCH DESIGN AND METHODS: Between 1985 and 1996, 514 children (279 male) who developed type 1 diabetes before the age of 16 years (91% of those eligible from a region where ascertainment of new cases is 95%) were recruited for a longitudinal study with central annual assessment of HbAlc and albumin excretion (three urine samples). Dropout rates have been < 1% per year, and 287 children have been followed for > 4.5 years. RESULTS: MA (defined as albumin-to-creatinine ratio > or = 3.5 and > or = 4.0 mg/mmol in boys and girls, respectively) developed in 63 (12.8%) and was persistent in 22 (4.8%) of the subjects. The cumulative probability (based on the Kaplan-Meier method) for developing MA was 40% after 11 years. HbAlc was worse in those who developed MA than in others (mean difference +/- SEM: 1.1% +/- 0.2, P < 0.001). In subjects who had been 5-11 years of age when their diabetes was diagnosed, the appearance of MA was delayed until puberty, whereas of those whose age was < 5 years at diagnosis of diabetes, 5 of 11 (45%) developed MA before puberty. The adjusted proportional probability (Cox model) of MA was greater for female subjects (200%), after pubertal onset (310%), and with greater HbAlc (36% increase for every 1% increase in HbAlc). Despite earlier differences based on age at diagnosis of diabetes (< 5, 5-11, and > 11 years), the overall cumulative risks in these groups were similar (38 vs. 29 vs. 39%, respectively) after 10 years' duration of diabetes. CONCLUSIONS: Prepubertal duration of diabetes and prepubertal hyperglycemia contribute to the risk of postpubertal MA. The differences in rates of development of MA relating to HbAlc, sex, and age at diagnosis relative to puberty may have long-term consequences for the risk of subsequent nephropathy and for cardiovascular risk.

Adolescent↗
PubMed2006

Can bone age determination provide criteria for growth hormone treatment in adopted girls with early puberty?

In treatment of idiopathic central precocious puberty, GnRH analogues (GnRHa) have been accepted as the treatment of choice. Since growth velocity may be impaired with GnRHa treatment growth hormone (GH) treatment has been added in clinical trials. Recently, a study followed adopted girls with early or precocious puberty on GnRHa or combined GnRHa and GH treatment to final height. It was found that final height was significantly higher in the combined treatment group, although the difference was small. It was seen that patients that were extremely short at arrival and short at start of treatment seemed to be candidates for combined treatment. We have now analysed the data in order to define criteria for the sub-group in need of combined GnRHa-GH treatment in order to achieve normal final height, i.e. above -2 SDS. Bone ages of 46 patients at start of treatment, randomized to either GnRHa treatment or GnRHa treatment combined with GH, were examined blindly by the same radiologist and the PAH calculated. The methods according to Greulich-Pyle / Bayley-Pinneau (GP/BP) and Tanner-Whitehouse (TW2) were used. Predictions versus final height data were analysed. The accuracy of FH prediction was greatest for GnRHa treated group using the GP/BP method. The GP/BP method gave useful cut off limits for when combined treatment was necessary to possibly achieve normal height. If pre-treatment GP/PAH was > 157cm, the patients attained normal height with GnRHa treatment only. Ten out of 13 (77%) such girls could be correctly identified. Using TW2 with a cut off of 164 cm, 9 out of 13 could be selected. Using a multi regression equation of best fit the number of correctly selected cases for GnRHa treatment only, could not be further increased in this group. We conclude that bone age determination and adult height prediction with the Greulich-Pyle/Bayley-Pinneau method, provides useful criteria for selecting the subgroup of adopted girls with early puberty where combined treatment with GnRHa and GH is not necessary to reach normal final height.

Adoption↗
PubMed2004

[Simplified gonadorelin stimulation test in diagnosis of precocious puberty].

OBJECTIVE: To assess the diagnostic value of the simplified gonadorelin stimulation test for precocious puberty. METHODS: Two hundred and ninety-two girls with signs of advanced breast development received the gonadorelin stimulation test. According to the result of gonadorelin stimulation test, the girls were divided into 3 groups: 151 with central precocious puberty (CPP),119 with premature thelarche (PT) and 22 with peripheral precocious puberty (PPP). RESULTS: LH or FSH levels at 15 min, 30 min, 60 min in PPP group were not significantly different (P>0.05). Those were significantly different in PT group (P<0.01). The highest levels of LH were at 30 min and the highest levels of FSH were at 60 min. LH or FSH levels at 15 min, 30 min, 60 min in CPP group were significantly different (P<0.01) with the highest levels at 30 min. The ratio of basal LH and FSH >0.2 had a diagnostic sensitivity of 48.3 % and specificity of 69.7%. Taking the LH/FSH ratio >0.9 at 15 min, 30 min, 60 min as cut-off value, the diagnostic sensitivity was 80.1%, 68.9% and 38.4%, and the specificity was 90.8%, 96.6% and 69.7%, respectively. CONCLUSION: The LH/FSH ratio>0.9 at 15 min after gonadorelin stimulation test can be used as a cut-off value to differentiate CPP from PT and blood sample at 60 min were not necessary.

Child↗