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Growth retardation is a considerable clinical problem in children with chronic kidney disease (CKD). Optimization of metabolic and nutritional parameters does not always lead to improved growth. Recombinant human growth hormone (rhGH) treatment has been used to improve height. Several studies in the literature have shown increased growth velocity, although data on the final height (FH) reached are scarce. We assessed the effect of rhGH on FH standard deviation score (SDS) in children with CKD following renal transplantation (RTx), comparing it with patients who did not receive rhGH (control group) but were treated with the same protocol and followed up in a single Center. Thirty-three patients received rhGH treatment until FH. Fourteen who refused rhGH therapy were included in the controls. Prognostic factors for FH and changes in glomerular filtration rate (GFR) during follow-up were also analyzed FH SDS in rhGH-treated patients was significantly higher than in controls (−1.88 ± 1.14 vs −3.48 ± 1.19 SDS, respectively, p

Adrenarche is a process of postnatal sexual maturation occurring in higher primates, in which there is an increase in the secretion of adrenal androgens. It is the consequence of a process of postnatal organogenesis characterized by the development of a new zone in the adrenal cortex, the zona reticularis (ZR). The mechanism of this phenomenon remains poorly understood, suggesting that it might be a multifactorial event. A relationship between circulating IGF-I, insulin sensitivity, and adrenal androgens has been postulated. Boys and girls have different patterns of changes in insulin sensitivity at puberty, perhaps secondary to differences in the estrogen milieu. Estrogen effects may also play a role in premature adrenarche. Peripheral or local IGF-1 actions could regulate adrenal progenitor cell proliferation and migration. Since adrenal progenitor cells as well as IGF-I and the IGF-R1 are located in the outer zone of the adrenal cortex during childhood and adolescence, this peripheral cell layer, below the capsule, may contain undifferentiated progenitor cells. Therefore, the IGF-R1 signaling pathway might positively modulate the proliferation and migration of adrenal progenitor cell to stimulate the development of adrenal zones, including ZR. However, no evidence of a direct action of IGF-I on ZR was found. In addition, a role for estrogens in the ontogenesis of ZR is suggested by the presence of aromatase (CYP19) in the subcapsular zona glomerulosa and in the adrenal medulla. Estrogens produced locally could act on ZR by interacting with estrogen receptor beta (ERbeta), but not alpha, and membrane estrogen receptor GPR-30. An estradiol-induced increase in DHEA/cortisol ratio was indeed seen in cultures of adrenocortical cells from post-adrenarche adrenals. In summary, several lines of evidence point to the action of multiple factors, such as local adrenal maturational changes and peripheral metabolic signals, on postnatal human adrenal gland ZR formation.

Immunoexpression of IGF-I, IGF-II, type 1 IGF receptor (IGFR), insulin receptor (IR), and GH receptor (GHR) was analyzed in human testis, in three age groups (Gr): Gr1 (neonates), Gr2 (postnatal testicular activation), and Gr3 (early prepuberty). In interstitial cells, low IGF-I and GHR, but moderate IR immunoexpression was observed in all Grs. However, high expression of IGF-II in Gr1, and moderate expression of IGFR in Gr1 and Gr2 were found. In Leydig cell (LC), high expression of IGF-II, moderate expression of IGFR and GHR, and undetectable IGF-I was found. Moreover, IR was highly expressed in Gr2. The effect of IGF-I on cell proliferation (PI) and apoptosis (AI), induction of cytochrome P450 side chain cleavage (cP450scc) immunoexpression, 3beta-hydroxysteroid dehydrogenase mRNA and testosterone (T) secretion was evaluated in human testis cell cultures. IGF-I increased P450scc immunoexpression, 3beta-hydroxysteroid dehydrogenase mRNA, T secretion, and PI, but decreased AI. We propose that IGF-II, mainly through IR, is involved in functional LC differentiation. In some interstitial cells, probably in LC precursors, IGF-II/IR could be involved, among other factors, in the stimulation of PI and/or inhibition of AI, and in LC differentiation.

The expression of aromatase, estrogen receptor alpha (ERalpha) and beta (ERbeta), androgen receptor (AR), and cytochrome P-450 side chain cleavage enzyme (cP450scc) was studied in prepubertal testis. Samples were divided in three age groups (GRs): GR1, newborns (1- to 21-d-old neonates, n = 5); GR2, postnatal activation stage (1- to 7-mo-old infants, n = 6); GR3, childhood (12- to 60-mo-old boys, n = 4). Absent or very poor detection of ERalpha by immunohistochemistry in all cells and by mRNA expression was observed. Leydig cells (LCs) of GR1 and GR2 showed strong immunostaining of aromatase and cP450scc but weak staining of ERbeta and AR. Interstitial cells (ICs) and Sertoli cells (SCs) expressed ERbeta, particularly in GR1 and GR2. Strong expression of AR was found in peritubular cells (PCs). For all markers, expression in GR3 was the weakest. In germ cells (GCs), i.e. gonocytes and spermatogonia, aromatase and ERbeta were immunoexpressed strongly whereas no expression of ERalpha, AR, or cP450scc was detected. It is proposed that in newborn and infantile testis, testosterone acting on PCs might modulate infant LC differentiation, whereas the absence of AR in SCs prevents development of spermatogenesis. The role of estrogen is less clear, but it could modulate the preservation of an adequate pool of precursor LCs and GCs.

IGF-1, IGF-2, and type 1 IGF receptor (IGF-R1) mRNA expression and immunolocalization and cell proliferation index were studied in human adrenals from early infancy to late puberty. Adrenals were obtained from transplantation donors or from necropsies of endocrinologically normal subjects. Subjects were divided into three age groups: group 1

Little is known on the hormonal regulation of the early postnatal phase of Leydig cell activation in the human. Testosterone secretion by prepubertal testicular cells in culture was studied in two different age groups, 0-7-no-old (group 1) and 16-36-no-old (group 2) boys. A mixed cell preparation was isolated from testes collected at necropsy and maintained in culture for 6 d. Cells were cultured in serum-free medium in basal conditions and under the stimulation of human (h)LH, hFSH, or recombinant hGH, and the secretion of testosterone was determined on d 6 by RIA. In basal conditions, cells of group 1 secreted more testosterone (median 5.83 pmol/10 6 cells.d, n = 7) than cells of group 2 (median 1.73, n = 5), p < 0.05, reflecting the steroidogenic potential of the testes in vivo. Under hLH stimulation, cells of group 1 responded by increasing testosterone secretion significantly. Surprisingly, hFSH stimulation elicited a similar response in cells of group 1. Because FSH receptors are presumably located in Sertoli cells, it is concluded that these cells secreted a paracrine factor that stimulated testosterone secretion by Leydig cells. On the other hand, recombinant hGH also stimulated the secretion of testosterone by cells of group 1. Recombinant hGH could have interacted with either GH or prolactin receptors of testicular cells. Cells of group 2 did not respond to any stimulus. Because serum levels of LH, FSH, GH, and prolactin are higher during the first months of life than later in childhood, it is possible that the early postnatal activation of the testis is under multiple pituitary hormone influence.

Madurative Changes of 3β Hydroxysteroid Dehydrogenase (3βHSD) mRNA Expression in Human Prepubertal Adrenal Tissue Implications in the Physiology of Adrenarche

Lack of Expression of the Aromatese (Cyp19) Gene in Human Prepubertal Testis. Transient Stimulation of Estradiol Secretion in Vitro At the Onset of Steroidogenesis

Evaluation of Hypothalamo-Pituitary-Gonadal (HPG) Function in Prepubertal Males (PPM) with Hepatic Insufficiency (HI) before H Transplantation (Tx)

Influence of Growth Hormone (GH) Treatment in the Regulation of Gonadotropin Secretion in Patients with Turner Syndrome (TS)

Intracranial Tumors (It) of the Midline in Pediatrics. Incidence of Cellular Types and of Precocious Puberty

In humans. Leydig cells are present during the first 6 months of postnatal life and they regress thereafter. We have described that basal (B) secretion of testosterone (T) in human testicular cells in culture is higher between 1 and 7 months (M) of age than between 8 and 36 M. Furthermore. T was stimulated by LH, FSH and GH only in the younger group (Ped Res 1995, in press). In the present study of primary cultures of human testicular cells obtained at necropsy, we have evaluated the activity of 3 enzymes of testicular steroidogenesis, 17,20 -DES, 3βHSD and 17β HSD, by correlating the production of T (the final product of steroidogenesis) with that of 17OH-progesterone (17OHP) (for 17,20-DES and 17βHSD), dehydroepiandrosterone (DHEA) (for 3βHSD and 17βHSD) and androstenedione (A) (for 17βHSD). Activities were estimated from the slopes (SL) of regression lines. Levels of T, 17OHP, DHEA and A were determined by RIA in conditioned media of day 6 of culture. The following groups (G) were defined, G1B, aged 1 to 7 months (n=8), G1 ST same age but under chronic stimulation (ST) with LH (10 ng/ml), FSH (2 ng/ml) or GH (50 ng/ml) and G2B, aged 8 to 36 M (n=7). Between 17OHP and T, SL was 1.95(r=0.73, p=0.0001) in G1B and 6.99 (r=0.97, p=0.0001) in G2B These two SL were significatively different (p

Short(St) and Long Term (Lt) Thyroid (T) Dysfunction After Treatment in Patients With Hodgkin's Disease (H) With Different Agressive Scores

We have previously described that a GnRH test (100 ug of SC Buserelin acetate administered twice at a 24 hs interval) can be used to evaluate the HPG axis in normal prepubertal girls (J Pediat 122:46,1993). In order to evaluate ovarian steroidogenic capacity and the role of sex steroids (SS) in the regulation of pituitary gonadotropins LH and FSH at late prepuberty (Pre), a GnRHa test was carried on in 14 girls with TS and bone ages (BA) between 6.16 and 12 years (y). Serum LH, FSH and E2 was evaluated in basal (B) conditions. 24 hs after the first and 4, 6 and 24 hs after the second injection of Buserelin. A positive response of serum E2 (E2≥55 pmol/L) was only detected in 4 patients. To evaluate LH and FSH responses, patients were divided into 2 groups (Gr) as a function of E2 response: Gr1(E2 ≥55pmol/L), mean±SD chronological age (CA) 9.94±1.84 y and BA 7.41±1.33 y and Gr2 (E2

3βHSD is an essential enzyme in the biosynthesis of steroid hormones. Little information is available on the regulation of the 3βHSD gene in the human testis. We have studied the role of IGF-I and of insulin in the expression of 3βHSD in mRNA in primary culture of mixed testicular cells collected at necropsy from a 15.5-year-old boy with sexual development and no endocrinological disorder. On day 6 of culture, the levels of testosterone(T). Δ4 androstenedione (A) dehydroepiandrosterone (DHEA) and 17OH progesterone (17OHP4) in conditioned medium were determined by RIA in basal conditions and under chronic stimulation with IGF-I (500 ng/ml) or insulin (50 ng/ml). On the same day, 3βHSD mRNA was analyzed by Northern Blot in the cells. A complete fragment of hp3βHSD 63 cDNA. labelled with P32, was used as a probe. The same membrane was washed and rehybridized with a 244 bpβ-active cDNA probe as an internal control. Mean ±SD (n=3 basal levels of T, A, DHEA and 17OHP4 were respectively: 34.3±0.66, 75.2±10.4, 119±29.5 and 119±14.8 pmol/106 cells.24 hs. Only under IGF-I stimulation the 3 steroids were significantly increased: T 159±2.5, A 216±10.5 and 17OHP4 237±6.2 (p< 0.05, ANOVA). The 1.7 Kb characteristic band of 3βHSD mRNA was only detected in the presence of IGF-I. It is concluded that during pubertal development of the human testis IGF-I stimulates steroidogenesis regulating the expression of the 3βHSD gene. The fact that insulin did not stimulate steroidogenesis neither it induced expression of 3βHSD mRNA suggests that the effect of IGF-I was mediated through the IGF-I receptor and not through the insulin receptor.

Growth retardation is frequently observed in patients with CRI after renal Tx. However, the causes of stunted growth and long-term evolution are not clearly established. We have followed the growth of 26 prepubertal children with CRI after renal Tx and we have correlated it with creatinine clearance rate (CrCl) and the dose of corticoids (Cort) in equivalents of hydrocortisone. Before Tx (6-12 months follow-up), mean ±SD chronological age (CA) was 6.93±2.35 years (y), bone age (BA) 4.86±1.96 y, height SDS - 2.27±1.30. After Tx between 1-2y(n=26), >2-3y(n=22) and >3-5.7y (n=15) follow-up periods: no change in height SDS, in CA-BA difference, in CrCl nor in Cort dose was observed. Changes in height were studied by evaluating ΔSDS. The following groups(Gr) were defined: Gr1 ≥-0.5. Gr2 between -0.5 and 0, Gr3>0 and the distribution of these Δ SDS Gr among the 3 follow-up periods after Tx was evaluated. Between 1-2y, Gr1 was 17.4%, Gr2 43.5% and Gr3 39.1%; between>2-3y, Gr1 was 21.4%, Gr2 52.6% and Gr3 26.3%; and between >3-5.7y, Gr1 was 28.6%, Gr2 42.9% and Gr3 28.6%. These% did not change significantly during follow-up. CrCl was significantly lower and dose of Cort significantly higher in Gr1 as compared to Gr2 and 3 (Cr cl:62.0±16.6, 95.1±35.8 and 108±24.2, Cort: 26.7±6.23, 22.8±4.73 and 21.3±4.44, respectively p

5 PRIMARY CULTURE OF TESTICULAR CELIS FROM A LARGE CELL CALCIFYING SERTOLI TUMOR OF A PREPUBERTAL BOY WITH GYNECOMASTIA

It has been described that only 25% of lesions in the active CYP 21B gene can be detected by Southern blotting, i.e.. 30 KPB deletions and large gene conversions (D-C). The remaining 75% are probably PM. The 8 most frequent PM are present in the pseudogene, suggesting that they are the consequence of gene microconversions. D-C, as well as several PM or microconversions (codon 318, C → T; codon 234-238, T-T-T → A-A-A; exon 3, -8BP and codon 172, T → A. but in only 4 patients (p) were studied in 20 p with CAH (12 salt losers, SL, 2 simple virilizing form, SV, and 2 late onset non-classical, NC, CAH). By POR technique, D-C were found in 3 p (6 alleles, a) while the alteration in codon 234-238 was detected in 1 p (2a). PM in codon 318 was detected in 4 p (4 a) after digestion with restriction endonuclease (RE) PST 1 followed by fragment analysis, and in exon 3 in 2 p (2 a) with RE ALU-1. Codon 172 PM was discarded by the SSCP technique in the 4 p studied. Alterations were detected in 50% of SL, 50% if them being D-C, 33% codon 318 PM and 17% exon 3-8BP deletions. One p with SV was homozygous for codon 234-238 M. It is concluded that by combining PCR and RE fragment analysis several of the most frequent PM can be studied in a simple and rapid way when a change in a normal restriction site has taken place.

It has been reported that the half life (HL) and MCR of endogenous GH is similar in normal male and female adults and in normal children and that children with short stature without GH deficiency (ST) show no differences. To reevaluate these studies, HL and MCR of GH were studied after a GH-RH bolus in 8 prepubertal children with idiopathic ST, chronological age (X±SD) 11.3±2.75 years (y), bone age 8.75 ± 2.76 y and height SDS -3.14 ± 0.77, and in 14 normal adults (c). After overnight fasting, GH secretion was stimulated with a single dose of 3 ug/Kg(iv) of GH-RH followed by 250 ug of somatostatin(S) 30 min later. Three basal samples, were obtained at 15 minutes intervals and, after GH-RH, samples were collected every 5 min for 90 min. GH HL was calculated monoexponentially after S injection from at least 3 descending values. Basal GH levels were similar in ST and C (2.66 ± 1.66 and 3.62 ± 5.35 ug/ml) HL in ST (24.0 ± 8.12 min) was significantly longer than in C (16.6 ± 4.41, p < 0.02) and MCR in BT (2.62 ± 0.76 ml/min.Kg) significantly lower than in C (3.73 ± 1.01. p < 0.02). The data suggest that in prepubertal children with ST, GH clearance would be slower than in normal children. According to these findings, after each secretory pulse in vivo, GH probably enters into target cells at a rate slower than in children with ST.

12 SERUM LH AND FSH DURING THE FIRST TRIMESTER OF LIFE IN NORMAL (C) CHILDREN AND IN AMBIGUOUS GENITALIA

Height and growth were evaluated in 31 children of both sexes after Tx:16 clinically prepubertal (PP) with a mean(X±SD) chronological age(CA) of 11.5±4.16 years (y) and a bone age (BA) of 6.91 ±2.17y, and 15 pubertal (P), Tanner's stages 2-4, with a CA of 16.4± 2.46 and a BA of 13.6±1.65 y. Height SD score(S) was -3.73 ±1.48 in PP and -3.54±1.66 in P. Height SDS was correlated with time of pre-Tx CRF (PP:6.06±4.19 and P: 6.99±4.05y), Post-Tx CRF (PP:2.28±1.59 and P: 2.15±1.67 y) and creatinine clearance (CrCl) (PP: 67.3±36.8 and 71.4±30.7 ml/min.1.73). An iverse significative correlation was found between height SDS and time of Pre-Tx CRF in PP(r:-0.50, p

Scarce information is available on serum FSH and LH levels, determined by highly sensitive assays. We evaluate gonadotropic age profiles in children of both sexes using an enzimoinmunoassay, in presence of two monoclonal antibodies (MEIA). 124 females (F) were studied: 55 prepubertal (Group G1) with a chronological age(CA) of 13.4±7.03 months, 51 prepubertal (G2), CA 4.66±1.93 years, and 18 pubertal F.8 of them in breast stage 2 (G3), CA 10.3±0.69 y and 10 in breast stage 3 (G4), CA 12.3± 1.71y;l85 males (M)were studied: 81 prepubertal(G1),CA 12.1±6.68 m, 75 prepubertal (G2), CA 4.81±2.07 y, and 29 pubertal M (G3) genital stage 2 CA 10.8±1.76 y. In both F and M,Gl was subdivided in 3 subG according to age: 0-3 m, 4-12 m and 12-24m. In F, serum FSH in G1 was higher than in G2 or G3 (5.12 ± 2.63, 2.76±1.9 and 2.89±2.0 U/L respectively, p

Idiopathic GH deficiency (I) is secondary to multiple ill-defined etiologies. Some children show symptoms in early prepuberty (early onset) viiile others show a decrease in their growth rate in the rate prepubertal years (late onset). We measured two GH-dependent serum parameters (SHBG and IGF-I) in 15 patients with I, either younger (Grl, n=10) or older (Gr2, n=5) than 7 years of age (y) at diagnosis, as well as in 11 patients with oceanic GH deficiency (Or), secondary to intracranial tumors, younger (Gr3, n=5) or older (Gr4, n=6) than 7 y, and in 52 control (C) subjects, younger (Gr5, n=18) or older (Gr6, n=34) than 7 y. Children younger than 7 y had not started adrenal puberty as evaluated by serum DHA sulfate. Mean±Sd ages in Gr1 (2.68±2.49y), Gr3 and Gr5 and in Gr2(10.3±1.95y), Gr4 and Gr6 were not statistically different. GH deficiency was diagnosed after 2 pharmacological tests for GH release. Serum T4 and T3 were normal in all patients. SHBG was determined by saturation analysis ana IGF-I by RIA. Serum SHBG (nmol/L) and serum IGF-I (U/L) were respectively, as follows (+SD): Grl:154±58 and 0.06±0.06; Gr3:79.6±24.4 and 0.22±0.16; Gr5:132±47 and 0.47±0.25;Gr2:108±17.4 and 0.17±0.11;Gr4:113±72 and 0.32±0.16;Gr6:68.7±31.7 and 1.04±0.36. In patients younger than 7 y, both SBEG and IGF-I were statistically different (p

It has been reported that the 24-hour integrated concentraticn of GH is higher in F than in M. These differences should be secondary to different GH production rates provided that metabolic clearances rates (MCR) were similar in the two sexes. To clarify this point, GH HL was studied in 5 F and 4 M. Serum estradiol (nmol/L) was 329±103 and 31.4±29.3 and serum testosterone (nmol/L) 1.63±1.21 and 13.5±2.29 in F and M, respectively. No food was allowed since the previous night. GH secretion was stimulated with a single IV bolus of GH-RH (3 ug/Kg) followed at 30 min of a single IV bolus of 250 ug somastotatin (S). After drawing 3 basal samples every 15 min. Sampling was continued every 5 min for 90 min after GH-RH. GH HL was calculated after S injection when a decrease was found in at least 3 consecutive GH values. Basal GH was not significantly different in the two groups (M:1.15±0.33, F:3.97±4.91 ng/ml) but the maximal increment was lower in M than in F (19.2±8.64 an 43.8±18.6, p < 0.05) HL was calculated assuming a monoexponential decay. HL and MCR were not statistically different in M and F (HL:15.2±2.35 and 13.2±2.74 min; MCR:4.77±0.45 and 5.26±0.23 ml/min. Kg, respectively). It is concluded that there are no differences in GH release rate between M and F.

Recent reports have described nan classical 21CHlasa deficiency in girls with precocious pularche (PP). In order to assess the prevalence of this deficiency, 26 girls with PP were studied, chronological age (CA) (X±SD) 6.47±2.04 a. Height, bone age (BA) and sexual development (Tanner) were evaluated and in eight cases pelvic and adrenal ultrasound examination were performed. An ACTH stimulation test was done in all patients using 25UI given as an IV bolus measuring basal and post ACTH (30 and 60 min.) 17CH progesterone (17CHP) and cortisol levels. The results were compared with the nanogram standards for serum 17CHP (Naw and col. JCEM 57:320, 1983) and with a control group of normal girls (3 prepubertal and 5 pubertal). Basal SHBG, T and SDHEA levels were measured in 10, 24 and 12 patients respectively. All patients had MI, VPII-III. The height SDS was 0.53±1.18, the ratio BA/BC was 0.85±1.08. In eight patients where ultrasound study vas performed, the results were normal. The 17CHP baseline serum levels were (X±SD) 0.65±0.66 ng/ml and the cortisol levels 12±9 ug/100 ml and the highest respense to ACTH vas 2.42±1.31 and 29.2±7.1 respectively. None of the studied patients showed 17CHP levels to ACTH higher than those of normal population of the published nanogram, nor of our normal controls (prepubertal ng/ml B:0.35±0.31, maximal response 2.88±0.53;pubertal B: 1.6±0.73, maximal response 6.48±3.26. Tne basal serum levels of SHBG, T and SDHEA were: X+SD (nmol/L) 94.50±31.04, 0.98±0.73 and 2300±2320. Only the SDHEA serum levels were significantly higher than in those previously published controls (103±8, 1.06±0.08 and 348±117) p

8 HYPOTHALMO-PITUTARY-OVRIAN FUNCTION IN PREPUBERTAL GIRIS WITH CHRONIC RENTAL FAILURE (CRF)

Pituitary function was evaluated in 25 patients with intracraneal Tumors (T). Basal thyroid function (T4, T3 and TSH) was altered in 1/22 patients before (Pre) and in 3/19 within the first month after surgery (Post). TRH-TSH was abnormal in 7/14 Pre and in 9/18 Post. Basal prolactin (PRL) was high in 4/14 Pre and in 4/15 Post (2 patients had prolactinoma) while TRH-PRL was high in 3/12 Pre and in 2/15 Post. Serum somatotropin response to a stimuli was < 10ng/ml in 8/14 patients Pre and in 13/15 Post and < 5ng/ml in 5/14 patients Pre and in 7/15 Post. In pubertal patients gonadotrophic function was deficient in 4/7 Pre and 2/3 Post. In prepubertal patients (n= 8-9), the LH-RH test was normal. Basal cortisol was low in 1/14 Pre and 2/11 Post; in another 2 patients symptoms of adrenal insufficiency were observed Post. Diabates insipidus was diagnosed in 3/25 patients Pre and in 10/25 Post being transient in 4 of the latter. B-hCG was high in 2/7 cases, both with germ cell T. A high Pre incidence of somatotrophic, thyrotrophic and pubertal gonadotrophic deficiency was found. PRL was high in prolactinomas and it was moderately increased in only 2 other patients. Surgical morbidity was low, except for the somatotrophic function.

The function of the definitive and fetal zones of the adrenal cortex were studied in 8 pre-term(PT) neonates with adequate weight for gestational age (AGA) and in 10 small for gestational age (SGA) PTs during the first 14 days of post-natal life, as well as in 9 full-term (FT)AGA newborns during the first 7 days of postnatal life. Peripheral vein serum Cortisol and 17α-hydroxyprogesterone (17-OH-P) were used as parameters of the function of the definitive zone, while serum dehydroepiandrosterone sulphate (DS) was taken as indicator of the function of the fetal zone of the adrenal cortex. Cord vein blood (CVB) serum 17-OH-P was used as a marker of the function of the fetoplacental unit. There was a significant negative correlation between 1-day-old and 5-day-old serum 17-OH-P, Cortisol or DS and gestational age in the 27 subjects studied. On the other hand, there was a significative negative correlation between serum 17-OH-P and days of postnatal life in the 3 groups of neonates, and between serum Cortisol and days of postnatal life in PT AGA neonates but not in PT SGA newborns. During the first week of life, mean ± SD serum Cortisol was 267±143 and 273±136 mol/l in PT AGA and PT SGA neonates respectively, significantly higher (p

Elevated levels of serum 17-hydroxyprogesterone (17-OH-P), either by direct assay (DRIA), which includes an interference substance, or after diethyl either extraction (E), have been described in premature babies (PT). However the nature of the interference substance remains unknown. Serum 17-OH-P by DRIA were determined in 8 full term newborns with adequate weight for gestational age. Mean values during the first 7 days of life were 24.75±15.19, 62.85±25.25 and 74.78±37.09 nmol/l respectively. These values were significantly higher than those determined after E (3.60±2.81, 8.77±6.6 and 6.14 ±4.34 nmol/L, p

At present no Laboratory test is available to predict the evolution of J H (Graves'disease). A follow ip to 2 to 14 y. was carried up in 59 patients aged 2 4/12 to 17 y. old (X ± SD: 9.4 ± 3.9). They all received antithyroid drugs as initial treatment. Thirty six patients followed for 3 to 14 y., could be reevaluated with T4, T3 and TSH and/or TRH after treatment in at least 2 ocassions: at short-term (ST: 1-2 y. post onset of treatment) and at long-term (LT:more than 3 y.; X ± 6.23 ± 3.3). Twenty three patients (64%) remained hyperthyroid (Hper) between ST and LT and 9(25%) hypo or euthyroid (Hpo/Eu) between ST and LT; only 4 (11%) changed from Hper at ST to Hpo/Eu at LT. Thus, 89% did not modify their thyroid function between ST and LT. The period of the evolution from Hper to Hpo/Eu showed two distinct populations, one with a X ± SD of 17.3 ± 3.8 months and another with X ± SD of 9.4 ± 2.5 y. It is concluded that evaluation of thyroid function at ST is useful to predict their status at LT since 90% of patients showed no variations. Since patients who changed thyroid fuction from Hper to Hpo/Eu at ST did it in X 17.3 months it is advisable to wait up to this time to select another therapeutic options. If Hper persists the possibility of I 131 administration should be considered to avoid the excessively long treatment required by the unrelenting course of this disease.

Recent evidence suggests that normal growth during male puberty depends on the combined effect of testosterone(T) and growth hormone while the role of estrogens, if any, has not been established. Correlations between growth velocity (GV) and serum totalT(Tb T), non-SHEG-b T, To E2 or non-SHEG-b E2 was made in 16 normal boys (mean ± SD chronological age, 14.1 ± 1.4, mean ± SD bone age 12.3 ± 1.64 years) in Tanner's stages II-IV of genital development. GV was evaluated in a 6-months-period but growth was followed up for at least 1 year. None of the subjects had overcome their peak height velocity as judged by 3 consecutive measurements. T and E2 non-SHEG-b fractions were calculated by a mathematical model based on the law of mass action. Mean ± SD To T and non-SHEG-b T were 222 ± 48 and 75 ± 22ng/dl respectively while To E2 and non-SHEG-b T were 222 ± 48 and 75 ± 22ng/dl respectively while To E2 and non-SHEG-b E2 were 18.1 ± 4.4 and 9.07 ± 2.88 pg/ml respectively. To T and non-SHEG-b T shoed a highly significant correlation with GV (p < 0.001) while no significant correlation was found between To E2 or non-SHEG E2 and GV. These studies suggest that serum E2 does not play a role in the pubertal growth spurt of boys.