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N Potau

Publications and source records attributed to N Potau.

At least 55 records · Page 3Linked to original sources
PubMed1997

Pubertal changes in insulin secretion and peripheral insulin sensitivity.

Using a simple and standardized method we estimated both insulin secretion and insulin sensitivity in peripheral tissues in relation to Tanner pubertal stages. Early insulin response, mean blood glucose (MBG), mean serum insulin (MSI), glucose uptake rate in peripheral tissues and insulin sensitivity index (SI) in response to the standard oral glucose tolerance test were evaluated in 73 normal girls. Study subjects were divided into 4 groups: group 1 (Tanner stage I, n = 20); group 2 (Tanner stage II, n = 14); group 3 (Tanner stages III and IV, n = 15), and group 4 (Tanner stage V, n = 24). Steroid levels and insulin-like growth factors were determined to characterize clinical pubertal development. MBG was similar in all groups but MSI increased at stage II and retained similar values throughout puberty, with those of group I being statistically lower than in the other groups (p < 0.001). When MSI values were adjusted per kilogram of body weight, a significant increase was observed in group II (p < 0.05). The MSI adjusted values were: group 1, 1.0 +/- 0.4; group 2, 1.4 +/- 0.4; group 3, 1.0 +/- 0.3, and group 4, 1.0 +/- 0.4 mU/l/kg. SI values were similar in groups 1 and 2 and significantly lower than in groups 3 and 4 (p < 0.001). Our results confirm both that insulin secretion is related to age and that an insulin-resistant state occurs during puberty. Thus, the insulin-resistant state coincides with Tanner stage II. In conclusion, this mathematical approach is considered to be a simple and reliable method for analyzing the possible alterations in insulin secretion and action in children and adolescents in whom more sophisticated procedures must be limited in this early period of life for ethical reasons.

Adolescent↗
PubMed1997

Hyperinsulinemia and decreased insulin-like growth factor-binding protein-1 are common features in prepubertal and pubertal girls with a history of premature pubarche.

The fasting insulin resistance index, mean blood glucose, mean serum insulin (MSI), early insulin response to glucose, glucose uptake rate in peripheral tissues, and insulin sensitivity indexes in response to a standard oral glucose tolerance test; serum insulin-like growth factor I (IGF-I), IGF-binding protein-1 (IGFBP-1), IGFBP-3, and sex hormone binding-globulin (SHBG) levels; and the free androgen indexes were evaluated in 98 girls with premature pubarche [PP; prepubertal (B1; n = 32), early pubertal (B2; n = 27), midpubertal (B3; n = 23), and postmenarcheal (B5; n = 16)] and in 86 Tanner stage- and bone age-matched controls. We ascertained whether hyperinsulinemia is already present in PP girls before or during pubertal development and whether these patients show a similar pattern of growth factor secretion as normal girls. Body mass indexes did not differ significantly between patients and controls within the same pubertal stage. MSI levels showed a significant increase with pubertal onset in all subjects, as expected. Patients showed significantly higher MSI values than controls at all Tanner stages (P < 0.03, P = 0.03, P = 0.03, and P < 0.05 for B1, B2, B3, and B5, respectively); higher insulin response to glucose at B1, B2, and B3 (P < 0.03, P = 0.03, and P < 0.05, respectively); higher glucose uptake rate in peripheral tissues at B1 and B2 (P < 0.04 and P = 0.02, respectively); and a later rise in insulin sensitivity compared to controls. PP girls also showed lower IGFBP-1 levels at B1 and B5 (P < 0.01 and P = 0.02, respectively), lower SHBG concentrations at B5 (P < 0.0005), and higher free androgen indexes at B1, B3, and B5 (P < 0.01, P < 0.05, and P < 0.001, respectively) compared to controls. Among others, significant correlations between SHBG and MSI levels (r = -0.49; P < 0.0001) and between SHBG and IGFBP-1 levels (r = 0.41; P < 0.0001) were found in all subjects. Hyperinsulinemia, increased early insulin responses to glucose, increased glucose uptake rate in peripheral tissues, elevated free androgen indexes, and decreased SHBG and IGFBP-1 levels are present in most girls with PP from childhood. These findings lend strong support to the concept that PP is not a benign condition, and long term follow-up of these patients into adulthood is recommended. The possible causal role of hyperinsulinemia in adrenal and/or ovarian androgen hypersecretion remains to be established.

Adolescent↗
PubMed1997

Ovarian 17 alpha-hydroxyprogesterone responses to GnRH analog testing in oligomenorrheic insulin-dependent diabetic adolescents.

OBJECTIVE: To investigate the pituitary-ovarian function in adolescent girls with insulin-dependent diabetes mellitus (IDDM). DESIGN: Clinical case-control study. METHODS: The GnRH analog leuprolide acetate was administered subcutaneously to 16 adolescents with IDDM (seven eumenorrheic and nine oligomenorrheic) and 13 controls between 0800 and 0900 h. Blood samples were collected at baseline and 0.5, 3, 6 and 24 h after leuprolide to measure levels of gonadotropins, 17 alpha-hydroxyprogesterone (17-OHP), androgens and estradiol. RESULTS: Mean baseline serum LH levels were significantly higher in eumenorrheic compared with oligomenorrheic IDDM patients, while peak LH responses to GnRH analog testing were similar in all subjects. Oligomenorrheic IDDM girls showed, as a group, a distinct 17-OHP response to GnRH analog stimulation, which in five out of nine girls was in the range of functional ovarian hyperandrogenism (> or = 8.6 nmol/l). Androgen and estradiol levels were not significantly altered in any group. No correlation was found between steroid levels and HbA1c levels, although the latter were significantly higher in oligomenorrheic than in eumenorrheic patients. CONCLUSION: About 50% of the oligomenorrheic IDDM adolescents had an increased ovarian 17-OHP response to GnRH analog stimulation in the range of functional ovarian hyperandrogenism. Factors other than metabolic control, such as stress, may play an etiologic role in IDDM ovarian dysfunction.

17-alpha-Hydroxyprogesterone↗
PubMed1997

Bone mineral density in prepubertal and in adolescent and young adult patients with the salt-wasting form of congenital adrenal hyperplasia.

OBJECTIVE: To evaluate bone mineral density (BMD) in prepubertal and in adolescent and young adult patients with the salt-wasting form of congenital adrenal hyperplasia (CAH). DESIGN: A relationship between bone mineral content and risk for osteoporotic fractures has been observed in adulthood. Infancy, childhood, and adolescence are critical periods for skeletal mineralization; thus, chronic diseases may impair bone mass peaking, particularly if children and adolescents are overexposed to glucocorticoids, as may occur in patients with CAH. Lumbar L2-L4 BMD values were measured by dual x-ray absorptiometry and compared with those of 471 age- and sex-matched controls. PATIENTS: Thirty-three patients with the salt-wasting form of CAH were studied. Sixteen (10 girls and 6 boys; age range, 1.5 to 8.3 years) were prepubertal and 17 (13 women and 4 men; age range, 17.1 to 28.2 years) were adolescent and young adults who had reached final height and had presented normal pubertal development and normal gonadal function thereafter. The average doses of hydrocortisone (mg/m body surface/day) received from diagnosis in the neonatal period to BMD evaluation were 21.2 +/- 2.2 and 22.3 +/- 2.6, respectively. RESULTS: Mean BMD Z score values were 0.16 +/- 1.01 in prepubertal patients and 0.06 +/- 1.02 in adolescent and young adult patients with no statistically significant differences with age- and sex-matched controls. Mean height Z score values were -0.03 +/- 1.13 in prepubertal patients and -1.13 +/- 0.62 in adolescent and young adult patients with significant differences between the latter and their respective age- and sex-matched controls. CONCLUSION: Long-term glucocorticoid therapy does not impair bone mass peaking in CAH patients with normal gonadal function, even though their adult height values are low.

Adolescent↗
PubMed1996

Ovarian 17-hydroxyprogesterone hyperresponsiveness to gonadotropin-releasing hormone (GnRH) agonist challenge in women with polycystic ovary syndrome is not mediated by luteinizing hormone hypersecretion: evidence from GnRH agonist and human chorionic gonadotropin stimulation testing.

Women with polycystic ovary syndrome (PCOS: hyperandrogenism and oligomenorrhea) have been shown to have exaggerated ovarian 17-hydroxyprogesterone (17-OHP) responses after GnRH agonist stimulation, suggestive of disordered ovarian cytochrome P450c17 alpha activity. However, most hyperandrogenic women also have an exaggerated LH response to both native GnRH and GnRH agonists. To assess whether the known LH hyperresponsiveness in PCOS patients mediates their exaggerated 17-OHP response to GnRH agonist challenge or whether the 17-OHP response can be duplicated by direct stimulation of the ovary with a fixed amount of hCG, 25 PCOS women [age, 20.6 +/- 1.1 yr; body mass index (BMI), 24.9 +/- 1.3 kg/m2] and 5 controls (age, 29.4 +/- 2.3 yr; BMI, 29.2 +/- 3.0) underwent both GnRH agonist (leuprolide acetate) and hCG testing. In addition, 23 normal women (age, 26.5 +/- 1.5 yr; BMI, 27.2 +/- 1.7 kg/m2) underwent hCG testing, and 21 other normal women (age, 19.3 +/- 0.5 yr; BMI, 23.0 +/- 0.8 kg/m2) underwent leuprolide acetate challenge. Blood was sampled before and 24 h after (the previously determined time of the peak response) leuprolide acetate (500 micrograms, sc) and hCG (5000 IU, im) stimulation tests. The tests were administered during the early follicular phase in women who were ovulatory and in randomized order in the subjects receiving both stimuli. Peak serum 17-OHP levels did not differ between leuprolide acetate or hCG stimulation in PCOS patients or controls when measured at 24 h (324.9 +/- 41.9 vs. 360.4 +/- 54.0 in PCOS; 183.2 +/- 19.6 vs. 141.2 +/- 11 ng/dL in controls). Peak 17-OHP levels after hCG challenge and GnRH agonist stimulation were highly correlated (r = 0.82; P < 0.001) in the subjects receiving both stimuli. Although leuprolide acetate elicited a higher estradiol (E2) response than hCG in all subjects, serum E2 levels increased significantly after hCG treatment in both patients and controls (P < 0.001 and P < 0.0001). The small, but significant, increase in serum E2 after hCG stimulation suggests that a rigid two-cell model of ovarian steroidogenesis may be an oversimplification of in vivo physiology. Our results suggest that exaggerated 17-OHP responses to GnRH agonist stimulation in hyperandrogenic women are not mediated by the known hyperresponsiveness of LH in these patients, but are due to increased ovarian androgen sensitivity to LH stimulation.

17-alpha-Hydroxyprogesterone↗
PubMed1996

Hyperinsulinemia in postpubertal girls with a history of premature pubarche and functional ovarian hyperandrogenism.

Previous studies have documented the association of insulin resistance and hyperandrogenism in adult women with functional ovarian hyperandrogenism (FOH) or polycystic ovary syndrome (a form of FOH). However, the possible impact of adrenal hyperandrogenism development during childhood in premature pubarche (PP) patients on postpubertal insulin secretion patterns remains unclear. The fasting insulin to glucose ratio, C peptide, early insulin response to glucose (IRG), mean blood glucose, mean serum insulin (MSI), glucose uptake rate in peripheral tissues (M), and insulin sensitivity indexes (SI) in response to a standard oral glucose tolerance test were evaluated in 13 PP girls with FOH (group A; age, 17.2 +/- 0.5 yr), 11 eumenorrheic nonhirsute PP girls (group B; age, 16.6 +/- 0.5 yr), and 21 age-matched controls (group C). Body mass indexes (BMI) were similar in the 3 groups (group A, 23.3 +/- 0.8; group B, 22.5 +/- 0.6; group C, 20.6 +/- 0.5 kg/m2). MSI values were significantly higher in FOH patients than in controls (74.7 +/- 17.6 vs. 45.7 +/- 4.1 mU/L; P < 0.01), but were not different from those in group B (63.3 +/- 11.1 mU/L). Thirty-eight percent of FOH patients (group A) and 27% of non-FOH patients (group B), all of whom had normal BMI, showed MSI levels well above the upper normal limit for controls (> 83.3 mU/L). MSI correlated with the degree of ovarian hyperandrogenism [defined by an abnormal 17-hydroxyprogesterone response to challenge with the GnRH analog leuprolide acetate; group A] and with the free androgen index [testosterone (nanomoles per L)/sex hormone-binding globulin (nanomoles per L) x 100; groups A and B)]. Although IRG, glucose uptake rate in peripheral tissues, mean blood glucose, and SI values were not significantly different in the 3 groups, 3 patients in group A and 1 patient in group B showed decreased insulin sensitivity and/or an enhanced early IRG. Among others, significant correlations between MSI and free androgen index values (r = 0.6; P < 0.002; groups A and B) and between BMI and SI (r = -0.53; P < 0.05; groups A and B) were found. Peak 17-hydroxyprogesterone responses to ACTH at PP diagnosis correlated positively with SI in both groups of patients (r = 0.53; P < 0.007). Hyperinsulinemia is a common feature in adolescent PP patients with FOH and appears to be directly related to the degree of androgen excess. Long term follow-up of PP patients into adulthood is warranted to ascertain whether hyperinsulinemia actually precedes FOH development and whether overt insulin resistance ensues.

Adolescent↗
PubMed1995

Growth hormone, insulin-like growth factor-I axis, and insulin secretion in hyperandrogenic adolescents.

OBJECTIVE: To assess GH and insulin-like growth factor I (IGF-I) axis variability in hyperandrogenic adolescents with different sources of androgen excess and their relationship with insulin resistance. DESIGN: Baseline IGF-I, insulin-like growth factor binding protein-1 (IGFBP-1), IGFBP-3, GH response to the exercise-propranolol test, and insulin responses to a standard oral glucose tolerance test were compared among patients with functional ovarian hyperandrogenism, hyperandrogenic nonfunctional ovarian hyperandrogenism patients, and age-matched controls. SETTING: Outpatient clinic in a medical center. PATIENTS: Twenty-one adolescents with ovarian (group A) and 17 with nonovarian (group B) hyperandrogenism, and 20 controls. RESULTS: Serum IGF-I and poststimulated GH levels were similar among groups, whereas serum IGFBP-3 levels were significantly lower in group A than in controls. Mean serum insulin levels were significantly higher in patients than in controls, whereas 24% of patients had abnormal insulin responses to glucose and/or insulin sensitivity indexes. Serum IGFBP-3 levels correlated negatively with the free androgen index (free androgen index = T/sex hormone-binding globulin [SHBG] x 100), whereas mean serum insulin levels correlated positively with the free androgen index and negatively with SHBG levels in all subjects. CONCLUSIONS: Hyperinsulinemia is common in hyperandrogenic adolescents and correlates with the degree of hyperandrogenism and not with the androgen source. Hyperinsulinemia and decreased IGFBP-3 levels may enhance IGF-I bioavailability, which in turn may both decrease SHBG levels and increase androgen production.

Adolescent↗
PubMed1994

Ovarian suppression with triptorelin and adrenal stimulation with adrenocorticotropin in functional hyperadrogenism: role of adrenal and ovarian cytochrome P450c17 alpha.

OBJECTIVES: To validate combined ovarian suppression with triptorelin and adrenal stimulation with ACTH in the diagnosis of female hyperandrogenism and to provide new insights into the adrenal-ovarian relationship present in this disorder. DESIGN: Comparison of sexual steroids and basal and ACTH-stimulated steroid levels before and after ovarian suppression induced by triptorelin. SETTING: Department of Endocrinology, Hospital Ramón y Cajal, Madrid, Spain. PARTICIPANTS: Thirty-nine nonselected women with hyperandrogenism. MAIN OUTCOME MEASURES: Serum levels of T, 17-hydroxyprogesterone (17-OHP), 17-hydroxy-pregnenolone, DHEA and DHEAS, androstenedione (delta 4-A), 11-deoxycortisol, and cortisol. RESULTS: Elevated T independent of ovarian suppression pointed to an adrenal disorder in six patients (one with an androgen-producing adenoma, two with late-onset 21-hydroxylase deficiency, three with functional adrenal hyperandrogenism). Nineteen patients had functional ovarian hyperandrogenism as elevated T normalized after ovarian suppression and were subdivided into ovDHEAS+ (n = 7) and ovDHEAS = (n = 12) subgroups depending on the presence of DHEAS hypersecretion. Finally, 14 patients had idiopathic hirsutism according to normal T before and after ovarian suppression. Comparisons of initial hormonal values between groups and with reference values obtained from normal women (n = 11) disclosed in functional adrenal hyperandrogenism an elevation of T and basal and stimulated DHEAS, delta 4-A, and 17-OHP with respect to normal women. These abnormalities were also present in ovDHEAS+ except for basal delta 4-A, which was normal, whereas only T and stimulated 17-OHP were elevated in ovDHEAS =. In the idiopathic group all steroids were normal with the exception of a mild elevation in stimulated DHEAS. CONCLUSIONS: These results show a continuum of abnormalities in hyperandrogenic women, suggesting an enhanced cytochrome P450c17 alpha activity in the adrenal and the ovary as the shared mechanism between functional adrenal hyperandrogenism and functional ovarian hyperandrogenism.

Adenoma↗
PubMed1994

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

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

Child↗
PubMed1994

Source localization of androgen excess in adolescent girls.

Functional ovarian hyperandrogenism (FOH) is characterized by an abnormal ovarian response to challenge with the GnRH analogs nafarelin and leuprolide acetate, similar to that observed in women with well defined polycystic ovary syndrome, regardless of whether elevated LH levels or polycystic ovaries are present. We studied an unselected group of 42 hyperandrogenic adolescents (age range, 14-22 yr; mean, 18.1 +/- 2.5 yr) 1) to determine FOH incidence through the assessment of ovarian-steroidogenic response to a single dose of leuprolide acetate, 2) to assess the clinical characteristics of patients according to their responses to GnRH analog stimulation, and 3) to evaluate adrenal steroidogenic function and its relation to ovarian hyperandrogenism in patients with either normal or abnormal responses to leuprolide acetate challenge. All patients underwent leuprolide acetate and ACTH testing, dexamethasone and ovarian suppression tests, and pelvic ultrasonography. Twenty-four (58%) patients had supranormal plasma 17-hydroxyprogesterone (17-OHP) responses to leuprolide acetate characteristic of FOH, and in 18, the 17-OHP response was similar to that of controls (n = 24; age, 17.1 +/- 2.3 yr). Seven patients (5 with FOH and 2 with normal responses to leuprolide acetate) had an abnormal response to ACTH, but only 1 had conclusive evidence of 21-hydroxylase deficiency. In 16 patients, the response to both stimulation tests was normal. Only 13 (54%) of the 24 FOH patients had polycystic ovaries on ultrasonography, and in 11 (46%), basal plasma LH levels were elevated. In FOH patients, reduction in testosterone and androstenedione plasma levels was significantly greater after ovarian suppression than after dexamethasone challenge (P < 0.0005 and P < 0.02, respectively). Peak plasma 17-OHP levels postleoprolide acetate simulation correlated with dexamethasone-suppressed plasma testosterone concentrations, dexamethasone-suppressed plasma androstenedione levels, and the free androgen index postdexamethasone treatment (r = 0.4, P = 0.01; r+ 0.4, P < 0.05; and r = 0.41, P = 0.007, respectively), Plasma sex hormone-binding globulin levels after dexamethasone administration correlated negatively with the baseline free androgen index (r = -.0.67; P < 0.0001). Considering our diagnostic criteria, 26 (62%) of our collective of 42 patients had abnormal responses to one or both stimulation tests, whereas 16 (37%) had normal response. FOH is the most common cause in (58%) of androgen excess in adolescence. Short term leuprolide acetate stimulation is a reliable tool fro identification of the ovary as the source of their hyperandrogenism.

17-alpha-Hydroxyprogesterone↗
PubMed1993

Postpubertal outcome in girls diagnosed of premature pubarche during childhood: increased frequency of functional ovarian hyperandrogenism.

The postpubertal outcome of a group of girls diagnosed of premature pubarche during childhood was assessed 1) to determine the incidence of functional ovarian hyperandrogenism (FOH) through the ovarian-steroidogenic response to the GnRH agonist leuprolide acetate, 2) to validate leuprolide acetate stimulation in FOH diagnosis, and 3) to ascertain whether FOH-predictive biochemical markers exist at the diagnosis of premature pubarche. Of 35 patients (age, 15.4 +/- 1.5 yr), 16 showed hirsutism, oligomenorrhea, and elevated baseline testosterone and/or androstenedione (delta 4-A) levels. Subcutaneous administration of leuprolide acetate (500 micrograms) produced similar increases in gonadotropin levels in oligomenorrheic patients, regularly menstruating patients (n = 19), and controls (n = 12; age, 15.3 +/- 1.3 yr) when tested at 6 h. Of all of the steroids measured, 17-hydroxyprogesterone (17-OHP) and delta 4-A levels 24 h postleuprolide acetate stimulation were significantly higher in oligomenorrheic patients than in the other two groups (P < 0.0001). No overlapping in 17-OHP responses occurred between oligomenorrheic patients and the other groups. Baseline dehydroepiandrosterone sulfate and delta 4-A levels at the diagnosis of premature pubarche correlated with 17-OHP values postleuprolide acetate challenge (r = 0.47; P < 0.005 and r = 0.67; P < 0.0001, respectively). These results show a distinct leuprolide acetate challenge response in 45% of the postpubertal premature pubarche girls studied, suggestive of an increased incidence of FOH, and support the need for continued routine postmenarcheal evaluation of this group of patients. Responses of 17-OHP to leuprolide acetate challenge facilitate the identification of FOH patients, establish this test as a reliable diagnostic tool in FOH diagnosis, and confirm the ovaries as the source of hyperandrogenemia in most patients with androgen excess. Although increased 17-OHP responses after leuprolide acetate stimulation seem to occur more frequently in girls with elevated dehydroepiandrosterone sulfate and/or delta 4-A levels at the diagnosis of premature pubarche, specific biochemical markers predictive of FOH in this group of patients are still lacking.

Androgens↗
PubMed1992

Natural history of premature pubarche: an auxological study.

The natural history of girls with premature pubarche is reported to be normal, but the effects on puberty and on final height are not well documented. We assessed the outcome of a group of girls with premature pubarche from two Latin populations in whom 21-hydroxylase deficiency had been ruled out by an ACTH test. Patients comprised 127 girls (70 Northern-Italian and 57 Northern-Spanish), of whom 69 had entered puberty and 38 had attained adult height. Height, bone age, onset and progression of puberty, height prognosis, adult height, and baseline plasma androgen levels were evaluated. Advanced skeletal maturation and tall stature were constant features during the first years of follow-up and subsequently declined. Puberty began at 9.7 +/- 0.9 yr, and age at menarche (12.0 +/- 1.0 yr) was comparable to maternal and population menarcheal ages. The appearance and chronology of pubertal milestones in both populations were very similar. Adult heights correlated with the height prognosis at diagnosis and at onset of puberty, and were above midparental heights. Premature pubarche produces a transient acceleration in growth and bone maturation with no negative effects on the onset and progression of puberty and final height.

Adolescent↗
PubMed1991

Ontogenesis of insulin receptors in human cerebral cortex.

This study examines the ontogenesis of insulin receptors in human cerebral cortex. Synaptosomal membrane fraction was obtained after subcellular fractionation of human brain tissue. The 24 cases studied were classified according to the statistical differences found in: Group I, pre-term, up to 30 weeks of gestation; group II, full-term and newborns; group III from one year to adulthood. Scatchard plots of insulin binding to brain membranes were curvilinear and showed a decrease in insulin receptor number as a function of age with slight differences in affinity. Receptor number were 3.0 +/- 0.8 pmol/mg in Group I, 0.6 +/- 0.14 pmol/mg and 0.2 +/- 0.024 pmol/mg in Groups II and III respectively. Values of 5'nucleotidase and Na+ K+ ATPase activities, were similar in all groups, which indicates that the purity of the fraction used for binding was similar in each group. According to the ontogenic profile in insulin binding described in this work, it may be assumed that the higher concentration of insulin receptors in human brain during the fetal period can determine some insulin action in this early stage of maturation, even though the functionality of these receptors remains to be elucidated.

5'-Nucleotidase↗
PubMed1989

Insulin treatment in adolescence.

Treatment of the adolescent diabetic continues to be a challenge for the physician. Ninety-five diabetic patients aged from 12-18 years were treated according to several therapeutic regimens. Principally the Spanish school time-table and, in some cases, life-style or brittle diabetes, determined the adoption of one of five proposed routines. The degree of control achieved assessed by the mean levels of HbA1 (10.6-10.3%), and the frequency and severity of hypoglycaemic accidents ("mild" variety in 25-30% of patients) were similar in all groups with total pancreatic insufficiency. The switch to a four-daily injection regimen (routine 5) with a pen-injector failed to improve metabolic control but patients had more flexibility in meal size and timing. These results suggest that even in teenagers diabetes can be acceptably treated.

Adolescent↗
PubMed1987

Chronic growth retardation with normal growth hormone response to provocative stimuli and low somatomedin activity. Long-term therapy with human growth hormone.

Four prepubertal children with chronic growth retardation (growth velocities less than or equal to 4 cm/yr), normal growth hormone (GH) response to provocative stimuli and low basal but increased somatomedin activity values after GH administration, received continuous GH-therapy (4 IU/three times a week) for an 18-24-month period. Growth velocity doubled during the first 12 months of therapy and remained 4-6 cm/yr until the end. Bone age progressed according to chronological age and adult height predictions improved. No thyroid function or carbohydrate and lipid metabolism anomalies were observed. After completion of this GH-therapy period, patients remained off treatment during the following six months. Growth velocities were similar to pre-GH-treatment values in two patients, lower in the third and higher in the fourth, who was by then pubertal. Thus, in these patients, long-term GH-therapy promoted growth and improved adult height prediction.

Child↗
PubMed1986

Clinical experience with somatrem in growth hormone deficiency.

Three studies of human growth hormone (hGH) in hGH deficiency were initiated. In the first of these, adolescent patients were switched from pituitary hGH to somatrem (SI preparation) for 1 month. No significant differences were noted in any of the clinical parameters measured during treatment with either preparation. In the second study, nine patients (six of them naïve) were treated with somatrem (SII preparation) for 9-12 months. The naïve patients exhibited catch-up growth, and bone age developed in parallel to chronological age during the study period. Somatomedin activity increased and correlated positively with growth. Antibodies to hGH and Escherichia coli polypeptide (ECP) developed in some patients, but titres and binding capacities were low. In the third study, 21 patients are currently being treated with Somatonorm; the first 3-6 months are evaluable. Growth velocities increased to normal values. Antibodies to hGH and ECP were present in several patients, but again the titres and binding capacities were low, and Somatonorm was less antigenic than the SI and SII preparations.

Adolescent↗
PubMed1986

[Chronic delay of growth with normal response of growth hormone secretion to provocation stimuli for its liberation and decreased somatomedin activity: treatment with growth hormone over 6 months].

Four prepuberal children, two girls and two boys, aged 7 years 3 months to 11 years 6 months with chronic growth retardation were studied. Informed parental consent was obtained. Growth was followed for two years or more and was always less than P 3. Growth velocity during observation period was 4 cm/y or less. Gastrointestinal, hepatic, renal and thyroid functions were normal. Skeletal X-ray examination revealed no anomalies. karyotype in the two girls was 44XX. Growth hormone (GH) secretion was evaluated in all cases by two different test: exercise-propranolol and insulin-induced hypoglycemia. Peaks of GH secretion were 10 ng/ml or more. In three patients, GH secretion was also evaluated during first two hours of deep-sleep. GH peaks were 10, 4 and 13.4 ng/ml, respectively. Somatomedin activity (SA) measured in basal condition on two different days with six month interval was low (0.28-0.70 U/ml) and increased after seven daily doses of 2 mg of GH, in all patients (0.80-1.12 U/ml). All patients were treated with GH (2 mg/3 times/week), and growth velocity increased from 4 to 8.7, from 3.9 to 8.8, from 3 to 6.5 and from 3.2 to 6 cm/y, respectively. In conclusion, SA is of value in selection of patients with chronic growth retardation, who may benefit from long-term GH therapy.

Child↗