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Biomedical subjects

N Potau

Publications and source records attributed to N Potau.

At least 37 records · Page 2Linked to original sources

Leptin values in placental cord blood of human newborns with normal intrauterine growth after 30-42 weeks of gestation.

OBJECTIVE: To evaluate leptin values in placental cord blood of newborns with normal intrauterine growth after 30-42 weeks of gestation. DESIGN: Leptin, a protein encoded by the ob gene, plays an important role in the regulation of feeding behaviour and energy balance in rodents, primates and humans. The presence of leptin in human amniotic fluid and cord blood has recently been reported in human gestations at term and the possible role of leptin in human fetal growth suggested. However, little is known of leptin synthesis during human foetal development. Thus, the aim of our work was to measure leptin (RIA, Linco Research, Inc.) in placental cord blood of human newborns at different fetal ages. PATIENTS: One hundred and twenty-six healthy newborns with normal intrauterine growth were studied. Twenty-nine were preterm (15 males and 14 females; gestational age: 30-36 weeks) and 99 were at term (49 males and 48 females; gestational age: 37-42 weeks). RESULTS: Leptin values increase progressively throughout gestation from 1.30 +/- 0.53 ng/ml at 30 weeks of gestation to 7.98 +/- 4.96 ng/ml (mean +/- SD) at term, and correlate positively with birth weight (r = 0.56, p < 0. 005, n = 126), length (r = 0.37, p < 0.005, n = 126), BMI (r = 0.57, p < 0.005, n = 126), head circumference (r = 0.37, p < 0.005, n = 126), gestational age (r = 0.48, p < 0.005, n = 126) and placental weight (r = 0.38, p < 0.003, n = 59). Leptin values are statistically significantly lower (p < 0.005) preterm (median: 2.05 ng/ml; range: 0.7-8.3 ng/ml) than at term (median: 7.0 ng/ml; range: 1.1-28.1 ng/ml). Leptin values are also significantly (p < 0.005) higher in females (median: 7.2 ng/ml; range: 0.9-23.6 ng/ml, n = 62) than in males (median: 4.8 ng/ml; range: 0.7-28.1 ng/ml, n = 64), although there are no differences in weight (2,864 +/- 536 g in females vs. 2,937 +/- 744 g in males). Multiple regression analysis shows weight to be a positive sex-independent predictor of serum leptin values (p < 0.0005). Sex also proves to be a predictor of leptin, independently of weight and is higher in females than in males (p < 0.003). CONCLUSION: Leptin is present in placental human cord blood after 30-42 weeks of gestation. Newborn weight and sex are independent predictors of leptin values.

Birth Weight↗

Pronounced adrenarche and precocious pubarche in boys.

In girls, pronounced adrenarche with precocious pubarche (PP) has been related to reduced fetal growth and to a cluster of endocrine-metabolic abnormalities. We examined whether these associations are also evident in boys with PP. The study population consisted of matched groups of boys (n = 58; age range 5-15 years) without or with a history of PP. After stratification for pubertal development, non-PP and PP boys displayed comparable results for the studied variables, including serum insulin-like growth factor I, sex hormone binding globulin, insulin-like growth factor binding proteins 1 and 3, indices of circulating glucose and insulin responsiveness to an oral glucose load, and birth weight SD score. In conclusion, the present results indicate that adrenarche-driven PP in boys is, in contrast to PP in girls, not associated with a cluster of endocrine-metabolic abnormalities and is not related to reduced fetal growth. These observations support the view that adrenarche-driven PP in boys may be regarded as a variant of normal development. Copyrightz1999S.KargerAG,Basel

Adolescent↗

Precocious pubarche, dyslipidemia, and low IGF binding protein-1 in girls: relation to reduced prenatal growth.

An increasing series of pediatric endocrinopathies and metabolic anomalies has been recognized as related to reduced prenatal growth. We have tested whether the association of precocious pubarche (PP), dyslipidemia, and low serum IGF binding protein-1 in girls is also related to reduced prenatal growth. Fasting serum lipids, lipoproteins, and IGFBP-1 concentrations were measured in 187 girls (83 without PP and 104 with PP; mean age, 11.8 y; range, 5-18 y) with known birthweight and gestational age, the latter being transformed into birthweight SD scores. Birthweight SD scores of girls with PP were lower than those of girls without PP. Within the group of PP girls, those with dyslipidemia and low IGFBP-1 had lower (p < 0.0001) birth-weight SD scores (-2.02+/-0.23; mean +/- SEM) than those with normal lipids, lipoproteins, and IGFBP-1 (-0.37+/-0.15), whereas girls with an intermediate number of abnormalities had intermediate birthweight SD scores (-0.80+/-0.18). In conclusion, dyslipidemia and low serum IGFBP-1 in girls with PP were found to be related to reduced prenatal growth, an observation pointing to the prenatal origin of these metabolic abnormalities.

Adolescent↗

Corticotropin-releasing hormone as adrenal androgen secretagogue.

The regulation of adrenarche is one of the enigmas of pediatric endocrinology. Adrenarche is thought to be governed by a dual control mechanism in which an adrenal androgen secretagogue acts upon a zona reticularis primed by ACTH. We hypothesized that corticotropin-releasing hormone (CRH) may serve as adrenal androgen secretagogue. We tested the concept by infusing either saline or human (h) CRH (1 microg/kg/h in saline) over 3 h, after overnight dexamethasone pretreatment, into eight young men within a randomized, cross-over study design. Serum ACTH and dehydroepiandrosterone-sulfate were measured once hourly; DHEA, androstenedione and 17-hydroxy-progesterone were determined at baseline and after 3 h of saline/hCRH infusion. ACTH levels remained unaltered during saline infusion and average ACTH responses amounted to 13 pg/mL (3.3 pmol/L) during hCRH infusion. Neither saline nor hCRH infusion altered 17-hydroxy-progesterone levels. Serum dehydroepiandrosterone-sulfate rose swiftly within 3 h of hCRH infusion and remained unchanged after saline (mean increase 37 versus 1%; p < 0.01). On average, serum DHEA doubled and androstenedione tripled during hCRH infusion, although no changes were observed during saline infusion (p < 0.01). In conclusion, CRH appears to have the capacity to act as adrenal androgen secretagogue. We suggest that the enigma of adrenarche may have an elegant solution, with CRH and ACTH coupled in sequence at the hypothalamic-pituitary level, and in parallel within the zona reticularis, just as they presumably are within the fetal adrenal, which is exposed to CRH of placental origin.

Adolescent↗

Corticotropin-releasing hormone: a potent androgen secretagogue in girls with hyperandrogenism after precocious pubarche.

CRH is an adrenal androgen secretagogue in men and has been proposed as a candidate regulator of adrenarche. CRH also affects androgen production by theca cells and may be involved in the pathogenesis of ovarian hyperandrogenism (OH). Precocious pubarche (PP) in girls can precede adolescent OH, a condition characterized by a high ovarian 17-hydroxyprogesterone (17-OHP) response 24 h after GnRH agonist challenge. In adolescent girls with a history of PP, we assessed the early androgen response to CRH, as well as the CRH effect on the late ovarian response to GnRH agonist. Within a randomized cross-over design, saline or CRH (human CRH 1 microg/kg x h in saline) was infused over 3-h (1100-1400 h) into 12 adolescent girls (age 17+/-2 yr; body mass index 21.4+/-0.9 Kg/m2) who had been pretreated with dexamethasone (1 mg at 0 h) and GnRH agonist (leuprolide acetate 500 microg sc at 0800 h = time 0). All adolescents had hirsutism, irregular menses, hyperandrogenemia, and hyperinsulinemia after PP. Serum LH, FSH, androstenedione, dehydroepiandrosterone (DHEA), and DHEA-sulfate (DHEAS) were measured at time 0, 3, 6, and 24 h, and ACTH and 17-OHP were measured at time 0, 6, and 24 h. ACTH concentrations at the end of saline or CRH infusions were less than 45 pg/mL; neither saline nor CRH infusions evoked early changes in 17-OHP levels. Within 3 h of CRH infusion, DHEAS increased by 46%, on average; androstenedione increased 2.5-fold and DHEA increased 5-fold duringCRH infusion (all P < 0.0001 compared with saline). There was no detectable CRH effect on the responses of LH, FSH, DHEA, DHEAS, 17-OHP, androstenedione, testosterone, and estradiol 24 h after GnRH agonist administration; five of 12 girls had elevated 17-OHP responses suggestive of OH. In conclusion, CRH was found to be a potent adrenal androgen secretagogue in adolescent girls with hyperandrogenism after PP. In this study, CRH failed to detectably affect the ovarian androgen response to gonadotropins.

Adolescent↗

Exaggerated adrenarche and hyperinsulinism in adolescent girls born small for gestational age.

Serum dehydroepiandrosterone-sulfate (DHEAS) is a classic marker for adrenarche and, subsequently, for the individual hormonal milieu. We have tested the hypothesis that prenatal growth reduction is followed by exaggerated adrenarche. Serum DHEAS, androstenedione and insulin concentrations were determined together with fasting glycemia in matched populations of asymptomatic, non-obese, post-menarcheal girls (mean age 14 yr) who were born either with a strictly appropriate weight for gestational age (AGA) or small for gestational age (SGA). When compared to AGA girls, the SGA girls had identical glucose levels, higher values for insulin and androstenedione (p<0.01), and a two-fold rise of DHEAS concentrations (p<0.0001). In conclusion, girls with prenatal growth reduction were found to be prone to develop, besides hyperinsulinism, a variant of exaggerated adrenarche. It remains to be verified whether the exaggerated adrenarche in adolescence is followed by adrenal hyperandrogenism throughout adulthood and senescence.

Adolescent↗

A limited repertoire of mutations of the luteinizing hormone (LH) receptor gene in familial and sporadic patients with male LH-independent precocious puberty.

Herein, we report mutation analysis of the LH receptor gene in 17 males with LH-independent precocious puberty, of which 8 were familial and 9 had a negative family history. A total of 7 different mutations (all previously reported) were detected in 12 patients. Among 10 European familial male-limited precocious puberty (FMPP) patients who had a LH receptor gene mutation, none had the Asp578Gly mutation, which is responsible for the vast majority of cases in the U.S. The restricted number of activating mutations of the LH receptor observed in this and other studies of FMPP strongly suggests that an activating phenotype is associated with very specific sites in the receptor protein. Clinical follow-up of the 5 patients who did not have LH receptor mutations shows that such cases most likely do not have true FMPP. LH receptor mutation analysis provides a sensitive tool for distinguishing true FMPP from other causes of early-onset LH-independent puberty in males.

Amino Acid Sequence↗

Anovulation after precocious pubarche: early markers and time course in adolescence.

Adolescent girls with a history of precocious pubarche (PP) are known to be at increased risk for ovarian hyperandrogenism, an endocrinopathy related to reduced fetal growth, but the characteristics of their ovulatory function have not been fully documented. We assessed ovulatory function by weekly urinary LH and salivary progesterone measurements over 3 consecutive months in 85 adolescent girls with known weight and gestational age at birth: 49 girls had no history of PP (age, 14.7+/-1.7 yr), and 36 had a history of PP (age, 14.4+/-2.0 yr); 55 girls were in the early postmenarcheal phase (0-3 yr after menarche), and 30 were in the late postmenarcheal phase (> 3 yr after menarche). In girls with PP, the 17-hydroxyprogesterone (17-OHP) response to ACTH was determined at prepubertal diagnosis of PP, and serum androgen and gonadotropin concentrations were measured in adolescence together with insulin responses to an oral glucose load. Early postmenarche, the fraction of girls with ovulations was similar in the non-PP and PP subgroups (61% vs. 62%), as was the fraction of ovulatory cycles (25% vs. 22%). Late postmenarche, however, the fractions of ovulating girls and ovulatory cycles were strikingly higher (P < or = 0.001) in the non-PP than in the PP subgroup (91% vs. 20% and 47% vs. 12%). Within the PP subgroup, anovulatory girls were found to have a lower weight SD score at birth (mean+/-SEM) than ovulatory girls (-1.22+/-0.3 vs. -0.36+/-0.3; P = 0.03), a higher 17-OHP response to ACTH before puberty (333.1+/-31 vs. 203.8+/-26 ng/dL; P < 0.002), and, in adolescence, lower serum sex hormone-binding globulin levels and higher circulating LH, free androgen indexes, and insulin responses. In conclusion, these findings indicate that girls with PP are at increased risk for anovulation from late (not early) adolescence onward, particularly those girls with a low weight at birth and/or a high 17-OHP response to ACTH at prepubertal diagnosis of PP.

17-alpha-Hydroxyprogesterone↗

Sexual dimorphism in the maturation of the pituitary-gonadal axis, assessed by GnRH agonist challenge.

OBJECTIVE: To assess whether the maturational changes of the pituitary--gonadal axis in a healthy population show gender-specific changes and to establish normative data for the different Tanner stages. DESIGN: Prospective, cross-sectional study. METHODS: The GnRH agonist leuprolide acetate (500 microgram) was administered s.c. to 60 boys and 81 girls (age range, 5--17 years). Serum steroids and gonadotropins were determined at 0 and 24 h and at 0, 3 and 24 h after GnRH agonist challenge respectively, whereas IGF-I, IGF-binding protein-1 (IGFBP-1), IGFBP-3 and sex hormone-binding globulin were measured at baseline. RESULTS: Baseline and peak LH responses to the agonist in late puberty, and basal and peak FSH levels at all Tanner stages, were higher in girls than in boys. Girls showed higher IGF-I levels than boys throughout puberty, sharper decreases in IGFBP-1 and earlier and greater increases in 17-hydroxypregnenolone, dehydroepiandrosterone (DHEA) and DHEA-sulfate. Testosterone responses to the agonist increased during puberty in males, and showed no changes in females. Conversely, estradiol responses rose throughout puberty in females and remained unchanged until late puberty in males. CONCLUSION: Leuprolide acetate stimulates gonadotropin and gonadal steroid secretion during puberty in both sexes and increases FSH levels in prepubertal girls. Pubertal maturation of gonadotrope function is gender specific, as it appears to involve increases in both the releasable and reserve pools of LH in males, and of LH and FSH in females. The earlier increase in Delta(5)-steroids in girls may suggest a sharper rise in ovarian cytochrome P450c17 activity along the Delta(5)-steroid pathway, while the failure of estradiol to increase in response to leuprolide acetate in early pubertal males suggests a late maturation of aromatase activity.

Adolescent↗

Premature pubarche, ovarian hyperandrogenism, hyperinsulinism and the polycystic ovary syndrome: from a complex constellation to a simple sequence of prenatal onset.

Adolescent girls with a history of premature pubarche have an increased incidence of functional ovarian hyperandrogenism [a form of polycystic ovary syndrome (PCOS)] at adolescence, which is usually associated with hyperinsulinemia and dyslipemia. The hyperinsulinemia and lipid disturbances can often be detected in the prepubertal period and throughout puberty, and are associated with an exaggerated ovarian androgen synthesis. Birthweight SD scores are lower in premature pubarche girls than in control girls, and particularly so in those girls who show hyperinsulinemia and subsequently develop ovarian hyperandrogenism. Therefore, although the mechanisms interlinking the triad of premature pubarche, hyperinsulinism and ovarian hyperandrogenism remain enigmatic, these data indicate that the triad may result, at least in part, from a common early origin, rather than from a direct interrelationship later in life.

Adolescent↗

Hyperinsulinaemia, dyslipaemia and cardiovascular risk in girls with a history of premature pubarche.

Girls with a history of premature pubarche, i.e. appearance of pubic hair before 8 years of age, show hyperinsulinism in response to an oral glucose tolerance test. As hyperinsulinaemia has a major role in dyslipaemia, and is considered an independent risk factor for cardiovascular disease, we assessed the patterns of plasma insulin concentration after a standard oral glucose tolerance test as well as fasting serum lipid, lipoprotein, and sex hormone-binding globulin concentrations in girls (n = 81) with premature pubarche compared with girls (n = 55) matched with them for stage and bone age to ascertain their metabolic states to identify those potentially at risk for the development of premature cardiovascular disease. Mean serum insulin concentrations were higher in patients at all pubertal stages, and associated with elevated serum triglyceride, very low density cholesterol and very low density triglyceride concentrations (p value range 0.04 to < 0.0001) but reduced sex hormone-binding globulin. Premature pubarche patients also displayed higher low density to high density lipoprotein cholesterol ratios compared with control subjects (p = 0.004 to 0.008). In conclusion, hyperinsulinaemia, decreased sex hormone-binding globulin concentrations and an unfavourable lipid pattern are common features in premature pubarche girls supporting the contention that atherogenic abnormalities composing the metabolic syndrome could start in childhood. To determine the clinical sequelae of such clustering of metabolic deviations, girls who were identified need to be followed up for the potential development of premature cardiovascular disease.

Adolescent↗

Changes in growth, growth hormone, and insulin-like growth factor-I (IGF-I) after orthotopic liver transplantation.

Growth failure is an important consequence of chronic liver disease in childhood. Insulin-like growth factor-I (IGF-I), which is synthesized and released by the liver, plays an important role as a growth regulator in humans. We examined the growth hormone (GH)/IGF-I axis before and after orthotopic liver transplantation (LT) in 14 children aged between 2 and 11 years (mean 5.6 +/- 1.1 years). Pre-transplantation serum GH levels (7.5 +/- 1.2 ng/ml) were significantly higher (P < 0.001) compared with controls (5 +/- 0.5 ng/ml). However, post-transplantation levels (1.8 +/- 0.8 ng/ml) did not differ from those in the control group. Serum IGF-I levels showed a statistically significant increase after LT (20.1 +/- 9.4 vs 190 +/- 66.2 ng/ml; P < 0.001) and became indistinguishable from the levels in the control group (180 +/- 96 ng/ml). In comparison with pre-transplantation data (z - 2.70), there was an increase in height 4 years postoperatively (z - 1.68). Catch-up growth was highly significant, in particular during the 1st year after LT (z -1. 58 +/- 1.63 vs 2.59 +/- 5.29; P < 0.01). We conclude that a GH resistance state found in patients with severe chronic liver disease reverted following LT. Given that IGF-1 depends upon liver function, this could be one of the main factors in the significant catch-up growth in pediatric LT recipients.

Child↗

Diagnosis and treatment in utero of goiter with hypothyroidism caused by iodide overload.

A fetal goiter was detected by ultrasonography in a woman receiving potassium iodide. After this medication was discontinued at 29 weeks, a fetal hypothyroidism was confirmed by cordocentesis, and two doses of levothyroxine were administered by amniocentesis. At 34 weeks repeated cordocentesis showed fetal euthyroidism and ultrasonography shrinkage of the goiter. Growth and development normal at 1 year.

Adult↗

Protein in infant formulas. Future aspects of development.

Cow's milk protein intolerant infants (CMPI), shifted to a cow's milk protein hydrolysate based formula, often experience an improvement in signs of malabsorption; on the other hand, they also present a pattern of watery stools. In an attempt to find high levels of some gastrointestinal hormones that might induce hypermotility, motilin and neurotensin levels were studied in infants on starting formula and in cow's milk protein intolerant infants, on a cow's milk protein hydrolysate based formula. In 12 infants on unmodified cow's milk based formula (starting formula), motilin levels were: mean 71.66 pmol/L (s: 17); neurotensin 26.53 (s: 10.9). In 19 cow's milk protein intolerant infants on a cow's milk protein hydrolysate based formula, motilin levels were: mean 163.65 pmol/L (s: 70.06) (p<0.05); neurotensin: 31.76 pmol/L (s: 15.03) (p>0.05). Motilin (but not neurotensin) is higher in cow's milk protein intolerant infants on a cow's milk protein hydrolysate based formula. We conclude that high motilin levels can induce a different pattern of motility, and can be a pathogenetic factor in the persistence of loose and watery stools in infants with CMPI on a protein hydrolysate based formula.

Body Height↗

Precocious pubarche, hyperinsulinism, and ovarian hyperandrogenism in girls: relation to reduced fetal growth.

Pronounced adrenarche with precocious pubarche (PP) in girls has been associated with hyperinsulinism and subsequent functional ovarian hyperandrogenism (FOH). Recently, pronounced adrenarche and insulin resistance have each been related to low birth weight. We have now tested the hypothesis that the frequent concurrence of PP with pronounced adrenarche, FOH, and hyperinsulinemia in girls may be secondary to separate relationships between these conditions and low birth weight. A total of 185 girls (aged 5-18 yr) without endocrinopathy or with PP and pronounced adrenarche with or without FOH were studied; mean serum insulin (MSI) concentrations were determined after a standardized oral glucose tolerance test. Birth weight SD scores [mean (SEM)] of control girls (0.38+/-0.08; n = 83) were higher (P < 0.0001) than those of PP girls (-0.81+/-0.13; n = 102). Among postmenarcheal PP girls, birth weight SD scores of girls without FOH (-0.25+/-0.19; n = 25) were higher (P < 0.0001) than those in girls with FOH (-1.51+/-0.28; n = 23). In pubertal girls (n = 145), MSI levels correlated negatively with birth weight SD scores (r = -0.48; P < 0.05), independently of PP. MSI levels in girls with birth weight below 1 SD (93+/-9 mU/L; n = 33) were higher (P < 0.0001) than those in girls with birth weight between -1 and +1 SD (52+/-2 mU/L; n = 94), whereas glycemia profiles were comparable. Integration of the aforementioned data suggests that there may be a sequence in the associations between reduced fetal growth and components of the postnatal endocrine system; minor fetal growth reduction appears to be associated with amplified adrenarche, whereas more pronounced prenatal growth restriction seem to precede FOH and hyperinsulinemia during adolescence. In conclusion, these findings corroborate the hypothesis that the frequent concurrence of PP (with pronounced adrenarche), FOH, and hyperinsulinemia in girls may result from a common early origin (low birth weight serving as a marker), rather than from a direct interrelationship later in life.

Adolescent↗

[Adult height, pattern of growth and pubertal development in patients with congenital adrenal hyperplasia, salt losing form].

BACKGROUND: The height growth pattern in 24 patients with the salt-wasting from of congenital adrenal hyperplasia was retrospectively evaluated from the neonatal period to attainment of adult height. PATIENTS AND METHODS: All patients were on mineralcorticoid therapy and received hydrocortisone (mg/m2 body surface and day. Mean +/- SD): 34.53 +/- 8.2 during the first year of life, 22.83 +/- 4.1 from then to the puberty onset and 21.83 +/- 3.6 during puberty. Height was measured every 3-4 months and compared with that of the normal age- and sex-matched controls. RESULTS: Height differences with respect to reference population (M +/- SD) were: +0.38 +/- 0.82 in the neonatal period; -2.21 +/- 1.1 at one year of age; -0.76 +/- 1.25 at three years of age; -0.45 +/- 0.99 at the onset of puberty and -1.34 +/- 0.79 at attainment of adult height. Adult height differed significantly (p < 0.01) from control values and in girls from those of their mothers (p < 0.05). Hyperandrogenism, evaluated through urinary 17-ketosteroids, testosterone, delta 4 androstenedione and DA-S, was not documented during prepuberty and puberty. CONCLUSIONS: Our patients showed a lower growth rate than those of the control population during the two periods of higher growth potentiality: the first year of life and puberty, and this results in adult height impairment.

Adrenal Hyperplasia, Congenital↗

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↗