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S. BERNASCONI, F. PETRAGLIA, L. IUGHETTI, F. FACCHINETTI, C. MARCELLINI, G. GIOVANNELLI, and A.R. GENAZZANI

Abstract

To further evaluate the role exerted by endogenous opioids on LH secretion a naloxone challenge (0.08 mg/Kg b.w. i.v.) was performed in 23 healthy children at different stages of puberty, in 5 adolescents in different period of menstrual cycle, in 3 case of idiopathic precocious puberty (PP), in 7 cases of delayed puberty (DP), in 4 females affected by hypogonadotropic hypogonadism (HH) and in 6 patients affected by polycystic ovary disease (PCOD). Naloxone does not induce any significant change on LH plasma levels in prepubertal helathy children and in all the cases of PP and DP. Similarly there was no LH response in healthy adolescents neither in HH nor in PCOD, the response to naloxone appears only in preovulary and luteal phases. These data indicate that the central opioid system regulating LH secretion in humans is active only at more advanced stages of puberty and it does not seem to play a role in the beginning of sexual maturation. Moreover gonadal steroids seem to play a fundamental modulatory role on opioid-controlled LH secretion.

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Tohru Uozumi, Hisao Manabe, Hideyuki Tanaka, Yuji Hamanaka, Kiyoshi Kotoh, Keiichiro Suzuki, and Keishi Matsumoto

ABSTRACT

Urinary 17-hydroxycorticosteroids, 17-ketosteroids and 16α-hydroxydehydroepiandrosterone from eighty-six healthy subjects from the ages of 2 to 79 of both sexes were determined quantitatively by elution chromatography on cation exchange resin. Daily urinary excretions of 17-hydroxycorticosteroids and 17-ketosteroids increased from childhood to the ages of 15 to 40 and then decreased gradually with advancing ages over 60 to 79. The ratio of tetrahydrocortisone to tetrahydrocortisol decreased gradually from adolescence to old age. The ratios of 17-ketosteroids to 17-hydroxycorticosteroids and C19O2- 17-ketosteroids to total 17-ketosteroids were much higher between the ages of 20 and 40 than at other ages particularly in males. The ratios of aetiocholanolone to androsterone and tetrahydrocortisol to allo-tetrahydrocortisol seemed to be lower between the ages of 15 and 40 than at other ages. It was possible to determine the daily urinary excretions of 16α-hydroxydehydroepiandrosterone only in subjects over the age of 15, particularly between the ages of 20 and 40.

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M. Karp, A. Pertzelan, M. Doron, A. Kowadlo-Silbergeld, and Z. Laron

ABSTRACT

Lysine-8-vasopressin (LVP) was administered intramuscularly in a dose of 5–10 units to 20 children and adolescents, divided into the following 3 groups: I – normal controls; II – patients with isolated growth hormone deficiency; III – patients with pituitary insufficiency involving several hormones. In all the patients studied, LVP induced a rise in plasma 11-hydroxycorticosteroids. In the normal controls LVP induced a moderate rise in blood glucose. Patients with isolated growth hormone deficiency showed no rise, and those with pituitary insufficiency involving several hormones showed a great variability in response. In all 3 groups there was a sharp decrease in plasma free fatty acids, most marked in the patients with isolated growth hormone deficiency, and a slower return to base line levels. There was no change in the plasma concentration of growth hormone in any of the patients. Plasma insulin rose moderately in the normal controls; there was little or no change in any of the patients with pituitary insufficiency. The above finding that LVP induced a reduction in plasma free fatty acids in the patients with pituitary insufficiency without any concomitant elevation of plasma insulin and blood glucose, is in agreement with the assumption that LVP acts directly on adipose tissue.

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Klaus Kruse and Ute Kracht

Abstract.

The effect of iv calcium on the urinary excretion of total adenosine-3',5',-monophosphate (cAMP) and total hydroxyproline (OH-P) was investigated in 5 children with parathyroid hormone (PTH)-deficient and PTH-resistant hypoparathyroidism, two of them being normocalcaemic during the study, in comparison to 4 healthy and 8 epileptic children and adolescents. Eighteen mg/kg body weight calcium, infused over 3 h, induced a decrease of cAMP to (mean ± sd) 82.1 ± 2.5% of the baseline value in controls and to 69.8 ± 9.7% in epileptic patients with an inverse correlation to the relative increase of serum calcium after the infusion in both groups (r = −0.75, P < 0.01). In contrast, the cAMP excretion increased after calcium load in the 5 hypoparathyroid children to 118.7 ± 14.9% of baseline despite a comparable serum calcium increase. OH-P decreased to (mean ± SD) 48.0 ± 6.8% of baseline in controls, 48.2 ± 12.7% in the epileptic patients and 39.4 ± 9.8% in the children with hypoparathyroidism, the differences between the three groups being statistically not significant.

It is concluded that the simple measurement of urinary cAMP before and after calcium infusion may provide a diagnostic tool to identify hypoparathyroid patients even in the normocalcaemic state. In contrast, the measurement of the calcium-induced suppressibility of OH-P does not discriminate these patients from subjects with normal parathyroid function.

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R. Rosskamp, R. Mallmann, N. Liappis, and S. Soetadjii

Abstract. According to desired phenylalanine (Phe) levels of 50–80 mg/l during treatment, three groups of patients with classical phenylketonuria (PKU) (5.3–17.1 years) were formed. They were investigated for their growth hormone (GH) and insulin response to arginine infusion: Group I (N = 5) had Phe levels below (22 ± 4 mg/l), group II (N = 3) within (61 ± 6 mg/l), and group III (N = 3) above therapeutic limits (156 ± 3 mg/l). Nine children (5.2–14.5 years) with short stature served as controls. Whereas group I and II PKU children showed normal GH response to arginine infusion, group III children exhibited impaired GH response expressed as integrated GH response (218 ± 38.6 μg · 1−1 · 2 h vs 911 ± 145 μg · 1−1· 2 h; P <0.01) or peak GH response (6.6 ± 1.2 μg/l vs 18.7 ± 2.3 μg/l; P < 0.05). Integrated insulin responses did not differ between the three PKU groups but were significantly higher in all PKU patients compared with controls (4903 ± 421 mU/l vs 2750 ± 378 mU/l; P < 0.01). However, this reflects impaired insulin secretion in children with constitutional delay of growth and adolescence rather than hyperinsulinism in PKU patients.

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S. Bernasconi, F. Petraglia, L. Iughetti, C. Marcellini, A. Lamborghini, F. Facchinetti, and A. R. Genazzani

Abstract. In order to evaluate the secretion of betaendorphin in obese children and adolescents, we measured plasma beta-endorphin, ACTH and cortisol levels before and following administration of CRH (1 μg/kg). Fourteen normal weight and 22 obese subjects (weight excess ranging from 30 to 98%) were studied. Plasma hormone levels were measured by radioimmunoassay directly in plasma (cortisol, ACTH) and after silicic acid extraction and Sephadex G-75 column chromatography (beta-endorphin). Basal beta-endorphin levels in obese children were significantly higher than in controls (14.7 ± 1.8 vs 6.0 ± 0.6 pmol/l; mean ± sem). No differences were found in basal ACTH and cortisol levels. CRH administration significantly increased beta-endorphin, ACTH and cortisol levels in normal subjects and ACTH and cortisol levels in obese subjects. Plasma beta-endorphin levels in obese children and adolescents did not show any significant increment. These data confirm the higher than normal beta-endorphin plasma levels in obese subjects in childhood and demonstrate that CRH is unable to increase beta-endorphin levels, suggesting an impairment of the hypothalamo-pituitary control mechanisms or an extra-anterior pituitary source.

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Robert L Rosenfield

Generations of pediatric endocrinologists have reassured families that idiopathic complete precocious puberty (CPP) is a normal process happening early and that affected children are "capable of leading normal, well-adjusted lives and producing children" (1). The same has been said of the common incomplete forms of sexual precocity, idiopathic premature thelarche and premature pubarche. However, data are beginning to accumulate to suggest that this is not entirely true (2).

Some patients with premature thelarche develop CPP (3) and some with CPP have been reported to go on to develop polycystic ovary syndrome (PCOS) (4, 5). In addition, those patients whose premature pubarche is due to increased production of adrenal androgens (premature or exaggerated adrenarche) appear to be at high risk of developing a PCOS-like state of persistent functional ovarian hyperandrogenism with oligomenorrhea and hirsutism or acne at adolescence (6). In this issue evidence is now presented that exaggerated adrenarche is associated

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J. Ludvigsson and L. G. Heding

ABSTRACT

Fasting serum C-peptide and total immunoreactive insulin (IRI) were determined in 38 non-diabetic children and adolescents 6–22 years old. C-peptide varied between 0.22–0.73 pmol/ml (mean ± sd, 0.45 ± 0.11). There was a tendency to higher values during puberty. No difference was found between subjects with or without a family history for diabetes. IRI varied between 0–31 μU/ml (mean ± sd, 11.3 ± 6.5).

The C-peptide response to glucagon was studied in 10 insulin dependent juvenile diabetics 11–19 years old, who had had measurable amounts of fasting C-peptide on some occasions during the previous years. Duration of diabetes varied between 4–12 years. A slight but significant rise in C-peptide level occurred in 3 patients. Their metabolic control estimated on the basis of daily urinalysis was "excellent" or "good". The results support the hypothesis that even trace remnants of the beta cell function may be of importance for the metabolic control in juvenile diabetes.

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Christian J Strasburger and Wieland Kiess

In the 1960s pharmacotherapy with pituitary-derived human growth hormone (GH) preparations was introduced into clinics for the treatment of children with severely impaired longitudinal bone growth (1). Initially, the generally accepted route of GH administration was deep intramuscular injections. It was not until the advent of recombinant growth hormone preparations in the 1980s that subcutaneous injection of GH proved to be at least equally effective and was propagated widely (2). The less traumatic subcutaneous injection then facilitated investigation of effectiveness as a function of number of injections per week. With respect to the promotion of longitudinal bone growth in children and adolescents, daily subcutaneous injection was shown to be more effective than administration of the same weekly dose by injection thrice weekly. Extrapolation of these findings promoted further studies in animals and humans that unanimously demonstrated the superior effectivity of continuous GH infusion as compared to administration of the same

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Liora Lazar, Rivka Kauli, Celia Bruchis, Jardena Nordenberg, Avinoam Galatzer, and Athalia Pertzelan

Lazar L, Kauli R, Bruchis C, Nordenberg J. Galatzer A, Pertzelan A. High prevalence of abnormal adrenal response in girls with central precocious puberty at early pubertal stages. Eur J Endocrinol 1995;133:407–11. ISSN 0804–4643

Abnormal adrenal response is often observed in girls with precocious adrenarche (1). We studied the adrenal response in 112 girls with idiopathic true central precocious puberty (CPP) at early stages of puberty compared to that in 21 girls with normal puberty (controls). The aims of this study were to determine the prevalence of abnormal adrenal response at early stages of puberty, the possible correlation of abnormal adrenal response with pubertal signs at onset of puberty and with plasma androgen levels, and a possible association with the activity of the hypothalamic-pituitary-gonadal (HPG) axis. All participants underwent a combined iv adrenocorticotropic hormone (ACTH)gonadrotropin-releasing hormone (GnRH) test at Tanner stage 2-3: 62 of the CPP girls before and 50 during treatment with GnRH analog. The stimulated levels of 17-hydroxypregnenolone (17OHPreg) and the stimulated 17OHPreg/17-hydroxyprogesterone ratio were analyzed and compared to previously reported norms. The result revealed three patterns of adrenal response: normal (17OHPreg ⩽24 nmol/l and 17OHPreg/17OHP ratio ⩽7) in 50/112 (44.6%) CPP patients and 17/21 (80.9%) controls; exaggerated (17OHPreg> 24 nmol/l, 17OHPreg/17OHP ratio ⩽ 7) in 50/112 (44.6%) CPP patients and 3/21 (14.3%) controls; and non-classical 3β-hydroxysteroid dehydrogenase deficiency (17OHPreg> 24 nmol/l and 17OHPreg/17OHP ratio > 7) in 12/112 (10.8%) CPP patients and 1/21 (4.8%) controls. The clinical features at onset of puberty were comparable in all girls with the CPP in spite of the different adrenal response patterns. The levels of androstenedione and testosterone were within normal range in all cases. Dehydroepiandrosterone sulfate was significantly elevated only in 3β-hydroxysteroid dehydrogenase deficiency, 4.8 ± 2.7 (p < 0.03) as expected. The adrenal response was not affected by GnRH analog therapy. In conclusion, an abnormal adrenal response was found in 55.4% of girls with CPP in early puberty. This response did not cause clinical signs and laboratory findings of a hyperandrogenic state at early stages of puberty and was not affected by the activity of the HPG axis. Its role in evoking precocious puberty remains to be explored further.

A Pertzelan, Institute of Adolescent Endocrinology, Children's Medical Center of Israel, Beilinson Medical Campus, Petah Tiqva 49202, Israel