Sagittal abdominal diameter is more predictive of cardiovascular risk than abdominal fat compartments in severe obesity.

OBJECTIVE: To compare the predictive role of abdominal fat distribution by computed tomography (CT) with that of total abdominal fat by sagittal abdominal diameter (SAD) on cardiovascular risk in severe obesity. DESIGN: A cross-sectional, clinical study. SUBJECTS: 64 males and 64 females, aged 42+/-15 years (mean+/-s.d.; range 18-75 years), BMI (kg/m(2)) 41.7+/-5.3 (30.2-57.6). MEASUREMENTS: Blood glucose, total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, triglycerides (TGLs), insulin (IRI), insulin resistance (HOMA-IR), slice areas (cm(2)) of total (tSAT), superficial (sSAT) and deep subcutaneous adipose tissue (dSAT), visceral adipose tissue (VAT) and SAD (mm) by CT. RESULTS: The sSAT depot was negatively associated with blood glucose, HOMA-IR, LDL cholesterol and TGLs, whereas dSAT was negatively associated with HDL cholesterol. VAT was associated with blood glucose and HOMA-IR, whereas SAD was associated with all variables evaluated. In males, VAT was associated with blood glucose (r(2)=0.12, P<0.01), SAD was associated with blood glucose (r(2)=0.67, P<0.01), IRI (r(2)=0.65, P<0.05), and HOMA-IR (r(2)=0.67, P<0.01). In females, sSAT was negatively associated with blood glucose (r(2)=0.63, P<0.05), whereas VAT was associated positively with blood glucose (r(2)=0.21, P< 0.001), total cholesterol (r(2)=0.16, P<0.01), LDL cholesterol (r(2)=0.20, P<0.001) and TGLs (r(2)=0.12, P<0.01). SAD was associated positively with IRI (r(2)=0.52, P<0.05), HOMA-IR (r(2)=0.53, P<0.05), total cholesterol (r(2)=0.52, P<0.05), LDL cholesterol (r(2)=0.54, P<0.01), TGLs (r(2)=0.52, P<0.05) and negatively to HDL cholesterol (r(2)=0.51, P<0.001). CONCLUSION: When compared with CT-based measures of abdominal fat compartments, SAD is a more predictive indicator of cardiovascular risk in severe obesity.

Abdominal fat index by ultrasound does not estimate the metabolic risk factors of cardiovascular disease better than waist circumference in severe obesity.

OBJECTIVE: To evaluate by ultrasound the ratio between preperitoneal (P) and subcutaneous (S) fat (AFI), in quantifying the cardiovascular risk in 258 obese patients (BMI 41.2+/-6.3 kg/m2; age 45.1 +/- 13.6 years). RESEARCH METHODS AND PROCEDURES: Glucose, insulin, lipid profile, uric acid and fibrinogen were measured. HOMA-IR, waist girth, AFI and quartiles of BMI were calculated. RESULTS: AFI lowered with increasing BMI and showed a positive correlation with TGL (r=0.37, P<0.01) and uric acid (r=0.40, P<0.001) in the 1st quartile of BMI (30.2-36.4) and a negative correlation with HDL (r=- 0.32, P<0.001) in the 3rd quartile (40.6-45.1). When BMI exceeded the value of 45.2 kg/m2 these correlations were no longer significant. In all subjects S correlated positively with uric acid (r=0.64, P<0.001), and negatively with HOMA-IR (r=- 0.41, P<0.001) and TGL (r=- 0.35, P=0.02); P correlated positively with CHOL (r=0.48, P=0.04) and TGL (r=0.33, P=0.03), and negatively with HDL (r=- 0.46, P=0.03). Waist girth showed more significant correlations than AFI in the lower quartiles of BMI, but not at the highest one. DISCUSSION: AFI, P and S, as waist girth do not seem to quantify the metabolic risk factors of cardiovascular disease in severe obese subjects, but AFI is probably useful in obese populations with BMI<45 kg/m2, even though not as strong as waist girth.

Failure of biliopancreatic diversion in Prader-Willi syndrome.

BACKGROUND: Prader-Willi syndrome (PWS) is the most common genetic obesity. Excessive weight gain follows failure-to-thrive in early infancy; in adolescents and young adults, excess body weight can exceed 100%. The hyperphagia associated with PWS is responsible for the early mortality. Dietary restriction, alone or combined with anorexic drugs, are ineffective to induce a permanent weight loss. Thus, surgical treatment of morbid obesity in PWS has been attempted, but gastric restrictive operations are unable to produce stable weight loss. In a small number of patients, favorable results have been reported with biliopancreatic diversion (BPD). CASE REPORT: A 24-year-old woman with PWS, Pickwickian, at age 21 weighed 80 kg (BMI= 50) and underwent BPD. RESULTS: 3 years after the BPD she regained 21 of the 26 kg lost; somnolence and respiratory difficulties were the same as before surgery. The patient now presents severe reduction of bone mass density, hypochromic anemia, hypoproteinemia, and diarrhea associated with eating. CONCLUSION: The regain of weight following BPD suggests that this procedure alone is not adequate for long-term control of obesity in PWS.

Growth hormone response to hexarelin, growth hormone-releasing hormone plus pyridostigmine and arginine plus estrogen in prepubertal and early pubertal short children.

BACKGROUND: Hexarelin (HEX), a synthetic hexapeptide with a strong GH-stimulating activity, has been suggested as a stimulus for evaluating GH secretion. However, in childhood it has never been compared with other stimuli capable to reduce the effect of the somatostatinergic tone and of the low production of gonadal steroids. METHODS: We evaluated GH response (expressed as the maximum value after stimulus [Cmax] and as area under the curve [AUC], mean +/- SD) to HEX at a dose of 2 micrograms/kg i.v., in comparison with those obtained after GHRH (1 microgram/kg i.v.) + pyridostigmine (PD, 60 mg p.o.) and arginine + ethynylestradiol (E2, 1 mg/day p.o. for 3 days before the test), in 5 subjects with familial short stature (FSS), 11 with constitutional growth delay (CGD), prepubertal (Tanner's stage I) and early pubertal (stage II), and in 8 healthy children age-matched as controls. RESULTS: HEX induced a Cmax of 31.9 +/- 18.4 micrograms/l and an AUC of 1511 +/- 923 micrograms/min x l in stage I, of 36.7 +/- 12.3 micrograms/l and 1938 +/- 903 micrograms/min x l in stage II (ns). GHRH + PD induced a Cmax of 33.8 +/- 14.6 micrograms/l and an AUC of 2072 +/- 1233 micrograms/min x l in stage I, of 29.6 +/- 15.6 micrograms/l and 1901 +/- 1252 micrograms/min x l in stage II (ns). ARG + E2 induced a Cmax of 17.8 +/- 7 micrograms/l and an AUC of 1157 +/- 505 micrograms/min x l in stage I, of 15.6 +/- 11.6 micrograms/l and 649 +/- 452 micrograms/min x l in stage II (ns). The Cmax of HEX was higher than that of ARG + E2 in both stages I and II (p < 0.05); AUC of HEX, was higher than that of ARG + E2 only in stage II (p < 0.01); the Cmax and the AUC of GHRH + PD were higher than those of ARG + E2 both in stage I (p < 0.01 and p < 0.05, respectively) and in stage II (p < 0.05). No difference, neither in the extent of GH response to HEX and GHRH + PD nor in that to stimuli between subjects and controls, was found. HEX has given 32% false positives in stage I and 17% in stage II, GHRH + PD 12% and 15%, while ARG + E2 provided 20% in stage I and 32% in stage II. On the whole, specificity was 76% for HEX and ARG + E2 and 89% for GHRH + PD. CONCLUSIONS: HEX induced greater GH response than that of ARG + E2 but similar to that of GHRH + PD and its specificity was not different to that of ARG + E2 and lower than that of GHRH + PD: then its use does not show a diagnostic advantage in respect to the other two stimuli in peripubertal age.

[The effect of GH on erythropoiesis in vivo]. / Effetto, in vivo, del GH sull'eritropoiesi.

It has been demonstrated that the direct and/or indirect stimulation of hematopoiesis is one of the effects of the growth hormone (GH) in vitro. In order to study the effect of GH on erythropoiesis in vivo, the variation of hemochrome in a group of 8 subjects with GH deficiency (GHD) were monitored during a substitutive therapy with biosynthetic GH (rhGH) at dose of 0.4 U/kg/week. Hemoglobin (Hb), hematocrit (Ht), mean corpuscular volume (MCV), number of red blood cells (RBC) were analysed in all subjects at the beginning and after 9 months of treatment. The effectiveness of therapy was demonstrated by statistically significant variations in height, height SDS, growth velocity, serum levels of IGF-I. After 9 months of rhGH therapy, a significant increase was observed in all values considered with exception of MCV. In conclusion Gh would appear to stimulate erythropoiesis, directly or indirectly, and these results would appear to indicate an in vivo confirmation.

[The TRH test in Turner syndrome]. / TRH-test nella sindrome di Turner.

In order to evaluate the functionality of the hypothalamic-hypophyseal-thyroid axis in Turner's syndrome (TS), 27 subjects, aged between 5.1 and 16.1 years old, were studied, 14 of whom were karyotype 45,XO and 13 affected by mosaicism. The TRH test (200 mcg i.v.) was performed in all subjects using a single bolus. TRH titers were assayed in serum samples collected at 0, 15, 30, 60 and 90 minutes, and anti-microsome and anti-thyroglobulin, T4 and T3, were assayed in the basal sample; the latter were also assayed in the blood sample collected at 120 minutes. These results were compared with those obtained using the same test in a group of age- and sex-matched controls. Anti-thyroid antibodies and basal levels of T3 and T4 were within the norm in 26 subjects; a high basal value of TSH was only found in one patient with chromosomic mosaicism with an elevated response to TRH and a high titer of anti-microsomic antibodies. Apart from this no statistically significant differences were found in patients compared to control subjects in relation to TSH values at all stages of the test and between the two groups of TS; no significant results were found in the comparison between the areas below the curves (AUC). On the basis of these results the Authors conclude that it is not possible to reveal alterations in thyroid function attributable to hypothalamic and hypophyseal anomalies in this group of patients either with karyotype 45,XO and mosaicism.

[Leptin and neuropeptide Y serum levls in young obese during weight loss]. / Valori serici di leptina e neuropeptide Y in giovani obesi durante la riduzione ponderale.

BACKGROUND AND AIM: Correlations between serum leptin (LEP) and BMI and the percentage of fat mass (FM), as well as differences between male and female serum levels and their behaviour during weight loss have already been extensively described in adult obesity, whereas few cases have been examined in child and adolescent obesity. There are also few studies of the alterations in NPY in peripheral blood in obese subjects during weight loss. METHODS: This study aimed to evaluate the correlations between LEP and BMI, FM% and NPY in 72 obese subjects, with BMI > 35 (29 males and 43 females) aged between 9.6 and 19.8 years old, during weight loss together with any differences between the sexes. RESULTS: LEP was positively correlated in both sexes with BMI and FM%, whereas no correlation emerged with NPY; LEP levels decreased gradually during weight loss, whereas no changes were observed in NPY except during the first phases of weight loss in males when the decrease was significant. LEP concentrations were significantly higher in females, who also showed a higher FM% with equal BMI. No difference was observed between NPY levels in both sexes. CONCLUSIONS: The authors conclude that: 1) the behaviour of LEP in child-adolescent obesity is broadly comparable to that described in adult obesity; 2) the highest LEP concentrations with equal BMI in females appear to reflect the different body composition of the two sexes given that females have a higher FM%; 3) the control exerted by LEP on hypothalamic NPY cannot be seen in peripheral blood and no differences emerged between the two sexes.

[Effect of sex on the increase of GH induced by galanin, alone or in combination with GHRH with or without pyridostigmine in pubescent subjects]. / Influenza del sesso sull'increzione di GH indotta dalla galanina, da sola ed in associazione con GHRH e/o piridosstigmina, in soggetti puberi.

Growth hormone response to galanin (GAL) and growth hormone releasing hormone have been demonstrated to be higher in females than in males, and moreover the cholinergic system appears to be able to enhance them. On the basis of this presumption, we evaluated the GH response (expressed as area under the curve: AUC-GH) to galanin (GAL, 10 mg/kg i.v.) or GHRH (1 mg/kg i.v.) either alone or associated together and with pyridostigmine (PD, 60 mg p.o.), and to saline infusion as a control, in 5 males and 5 females, in puberty, aged 16 +/- 0.4 years old (mean +/- SD). In females tests were performed during the follicular phase of the menstrual cycle. GAL alone cannot provoke a response from GH unless associated with GHRH. The contemporary administration of PD does not increase the extent of the response. The latter did not differ between sexes. The GHRH-GAL association induced a higher response in GH compared to GAL alone and GAL-PD, without any differences between the sexes. Lastly, the combination GHRH-GAL-PD induced responses that were comparable to GHRH and GAL alone. Therefore GAL does not act alone but enhances the effect of GHRH and the cholinergic system appears to be involved as a modulator. Moreover, the effect of GAL is comparable in both sexes.

[Beta-pancreatic function in adult patients with GH deficiency]. / Studio della funzionalità beta-pancreatica in pazienti adulti con deficit di GH.

We investigated the beta-pancreatic function in response to a standard oral glucose tolerance test (OGTT) and a tolbutamide test in a group of GH-deficient adult subjects and in a group of control subjects. Fasting plasma glucose levels were normal in all subjects; the insulin levels, basal (0.19 +/- 0.02 vs 0.99 +/- 0.08) and, as n-AUC, after OGTT (195.2 +/- 23 vs 520.5 +/- 69) and tolbutamide test (33.6 +/- 4.4 vs 177.7 +/- 12.1) (means +/- ES), were significantly lower (p less than 0.001) in the GH-deficient subjects compared to controls. These data indicate a reduced beta-cell activity, secondary to absence of trophic effect of GH on pancreatic beta-cells, in GH-deficient adults.

[No correlation between insulinemic levels and arterial hypertension in obese females]. / Assenza di correlazione tra livelli insulinemici ed ipertensione arteriosa in donne obese.

High blood pressure and impaired glucose tolerance are frequently associated with obesity: it has been suggested that hyperinsulinemia could represent one of the possible pathogenetic connections between obesity and systodiastolic hypertension. In order to verify this hypothesis we examined fasting and post-load insulin and glucose levels in a group of 102 obese females, 58 hypertensive and 44 normotensive. All of the subjects underwent standard OGTT in order to measure their glycemic and insulinemic levels. No differences were found between two groups, as regard age and degree of obesity; blood pressure values were significantly different (p less than 0.01). No significative differences were detected for glycemic and insulinemic levels between hypertensive and normotensive subjects. These results indicate that hyperinsulinemia is not the prominent link between obesity and arterial hypertension; the relationship between these two conditions may be indirect.

Differences of hexarelin-induced prolactin and cortisol responses between prepubertal and early pubertal short children and lack of correlation with gonadotropin-releasing hormone-induced gonadotropin response.

Hexarelin (HEX), a synthetic hexapeptide with strong GH-stimulating activity, is known to induce the release of prolactin (PRL) and cortisol (F). The responses of GH and F vary according to age and pubertal development, correlating with serum levels of sex steroids, while the release of PRL does not. We evaluated GH, PRL and F responses to HEX (2 microg/kg i.v.) in 19 children with short stature, 12 prepubertal (Tanner stage I) and 7 early pubertal (stage II), and their correlation with those of FSH and LH to GnRH and with the serum levels of testosterone (T) or estradiol (E2). At baseline, the GH, PRL, F and sex steroid serum levels did not vary in the two groups of patients. HEX induced a strong GH and a slight PRL increase in prepubertal and early pubertal children, with no differences in the extent of the response, while F secretion was not affected in either group; these responses did not correlate with those of the gonadotropins to GnRH nor with basal T or E2.

[Relationship between blood insulin and arterial hypertension in obese adults]. / Studio dei rapporti tra insulinemia ed ipertensione arteriosa in adulti obesi.

The well know fact that high blood pressure and impaired glucose tolerance are frequently associated with obesity has suggested that hyperinsulinemia could represent one of the possible pathogenetic connections between obesity and systodiastolic hypertension. With the aim of verifying this hypothesis 67 obese subjects (36 hypertensive and 31 normotensive), males, were admitted to our study. All of the subjects underwent standard OGTT in order to measure their glycemic and insulinemic levels. No differences were found between two groups, as regard age and the degree of obesity; blood pressure values were significantly different (p less than 0.01). No significative differences were detected for glycemic and insulinemic levels between normotensive and hypertensive subjects; basal hyperinsulinemia was detected in a similar percentage (16.6 vs 19.3%) in the two groups. Under these circumstances it is not possible to confirm that hyperinsulinemia is the prominent link between obesity and high blood pressure, as previously observed by others.

[Correlation between lipid pattern and body mass index in obesity]. / Correlazione fra quadro lipidico ed indice di massa corporea nell'obesità.

Lipid plasma levels were measured in a group of 519 obese subjects, aged 7-66 years, divided according to age, sex and BMI. Lipidemia and total cholesterolemia increased both with age and BMI, irrespective of sex; LDL and VLDL increased in relation to age and, with less evident differences, to BMI. Triglycerides increased in the age bracket from adolescent to adult, especially in males, whereas their increase in relation to BMI showed no difference between the sexes. Chylomicron plasma levels remained steady both in relation to age and BMI.

[Impaired glucose tolerance in obesity in children and adolescents]. / Ridotta tolleranza glucidica nell'obesità infanto-giovanile.

The incidence of impaired glucose tolerance (IGT) in obese juvenile has not yet been well defined. Glycemic and insulin responses to OGTT were evaluated in 398 obese juveniles (and 70 healthy control subjects) to investigate possible correlations with age, body mass index (BMI) and obesity duration. Subjects were subdivided into two groups according to OGTT results: obese with normal glucose tolerance (OB-NGT) and obese with impaired glucose tolerance (OB-IGT). IGT was found in 11% of subjects but no correlations were observed in relation to age, BMI and obesity duration. There was no difference in the glycemic response to OGTT in terms of the biological parameters examined. Insulin plasma levels were twice as high in OB-NGT in comparison to control subjects and OB-NGT. Basal insulinemia increased with BMI in OB-IGT but not in OB-NGT.

[Melatonin secretion in Klinefelter's syndrome]. / Studio della secrezione di melatonina nella sindrome di Klinefelter.

It has been observed that the pineal gland seems to modulate diencephalic neuroendocrine activity through its principal hormone, melatonin. In animals, melatonin inhibits the secretion and release of hypophyseal gonadotropins, probably by inhibiting hypothalamic releasing factors; in man, on the contrary, the administration of LHRH seems to have a stimulating effect on melatonin serum levels. In the light of this, in pathologies characterised by an imbalance in the hypothalamus-hypophyseal-gonad axis, it is possible to hypothesise variations in the secretion of melatonin and/or in its circadian fluctuations. In order to clarify further the relationship between the epiphysis and the hypothalamus-hypophyseal axis, the present study evaluated the pattern of melatonin secretion in a group of 16 patients with Klinefelter's syndrome. The circadian rhythm of melatonin secretion was determined from venous blood samples taken at 9 am, 1 pm, 5 pm, 9 pm, 1 am and 5 am; the same protocol was also followed in two control groups of respectively prepuberal and puberal healthy subjects. During the night samples were taken as rapidly as possible, using a red light source in order to not interfere with melatonin secretion. All of the examinations were performed during the winter period. Serum levels of melatonin were determined, after extractions with diethylether, by means of a double antibody RIA using commercially available kits (Bioscience Product--The Netherlands). Intra- and inter-assay coefficients of variation were respectively 3% and 8%. The data are reported as mean values +/- SD; the results were analysed by means of Student's test for unpaired data and analysis of variance.(ABSTRACT TRUNCATED AT 250 WORDS)

Impairment of GH responsiveness to GH-releasing hexapeptide (GHRP-6) in Prader-Willi syndrome.

The aim of this study was to evaluate the GH-releasing activity of a synthetic hexapeptide, GHRP-6, in the Prader-Willi syndrome (PWS). Sixteen PWS patients (7 males and 9 females, aged 12.7-38.3 yr), 15 with essential obesity (OB) (7 males and 8 females, aged 12.9-42.9 yr), and 8 short normal children (SN; 3 males and 5 females, aged 10.2-14.3 yr) underwent 2 tests on separate occasions, being challenged with GHRP-6 (1 microg/kg, iv) or GHRH (1 microg/kg, iv)+PD (60 or 120 mg for children or adults, po). Moreover, in 11 patients with PWS and in the group of SN, the GH response to at least 2 stimulation tests had been previously determined. GH was analyzed either as mean peak values (GHp, mcg/l), or as the area under the curve (AUC, mcg/l/h) and the net incremental area under the curve (nAUC, mcg/l/h). In the group of PWS subjects, GH responses to both GHRP-6 (GHp: 11.4+/-2.0; AUC: 588+/-113; nAUC: 483+/-108) and GHRH+PD (GHp: 7.3+/-1.8; AUC: 486+/-122; nAUC: 371+/-250) were significantly lower than those observed either in OB (GHRP-6: GHp: 25.7+/-3.2, p<0.003; AUC: 1833+/-305, p<0.005; nAUC: 1640+/-263, p<0.0001. GHRH+PD: GHp: 15.1+/-2.4, p<0.009; AUC: 1249+/-248, p<0.003; nAUC: 918+/-230, p<0.006) or in SN patients (GHRP-6: GHp: 39.1+/-3.1, p<0.0001; AUC: 2792+/-158, p<0.0001; nAUC: 2705+/-165, p<0.00005. GHRH+PD: GHp: 27.5+/-3.7, p<0.0001; AUC: 1873+/-251, p<0.0001; nAUC: 1692+/-219, p<0.0005). Unlike control groups, in PWS patients GH levels after GHRP-6 did not differ from those obtained after GHRH+PD. Interestingly, low IGF-I values were present in all PWS subjects. Furthermore, no patient with PWS showed normal GH response to the previously performed GH stimulation tests. As already reported, GH release after GHRP-6 or GHRH+PD was significantly lower in OB than in SN subjects. In conclusion, our data indicate that: 1) GH response to GHRP-6 is clearly impaired in PWS; 2) the blunted GH responses to the provocative stimuli in PWS are not an artifact of obesity; 3) short stature in PWS is caused by a complex dysfunction of the hypothalamo-pituitary structures.

Hexarelin-induced growth hormone response in short stature. Comparison with growth hormone-releasing hormone plus pyridostigmine and arginine plus estrogen.

UNLABELLED: Hexarelin (HEX) is a synthetic hexapeptide with strong GH-stimulating activity. We evaluated GH response (expressed as maximum value after stimulus [Cmax] and as area under the curve [AUC]) to HEX at the doses of 1 microg/kg i.v. (HEX 1) and 2 microg/kg i.v. (HEX 2), in comparison with the responses to GHRH (1 microg/kg i.v.) + pyridostigmine (PD, 60 mg po) and to arginine (ARG, 0.5 mg/kg i.v.) + ethinylestradiol (EE, 1 mg/day po for 3 days before the stimulation), in 5 subjects with familial short stature (FSS), 11 with constitutional growth delay (CGD), 6 with GH neurosecretory dysfunction (NSD), and 5 with isolated growth hormone deficiency (GHD). Cmax and AUC after HEX 1 were 26.8+/-10.5 ng/ml and 1448+/-514 ng/min x ml in FSS, 23.6+/-14.4 ng/ml and 1146+/-750 ng/min x ml in CGD, 36.9+/-21.5 ng/ml and 2048+/-1288 ng/min x ml in NSD, 9.4+/-5.8 ng/ml and 498+/-200 ng/min x ml in GHD (Cmax and AUC in FSS and CGD, p<0.05 vs GHD). Cmax and AUC after HEX 2 were 37.7+/-16 ng/ml and 1979+/-888 ng/min x ml in FSS, 32.5+/-16.2 ng/ml and 1613+/-237 ng/min x ml in CGD, 39.7+/-20.7 ng/ml and 2366+/-1569 ng/min xml in NSD, 13.4+/-4.2 ng/ml and 645+/-293 ng/min x ml in GHD (Cmax in FSS, CGD and NSD p<0.01 vs GHD; AUC in NSD, p<05 vs GHD). Cmax and AUC after GHRH+/-PD were 46.6+/-8.8 ng/ml and 3294+/-1031 ng/min x ml in FSS, 25.9+/-11.2 ng/ml and 1464+/-735 ng/min x ml in CGD, 38.8+/-21.7 ng/ml and 2428+/-1399 ng/min x ml in NSD, 8.4+/-6.2 ng/ml and 685+/-572 ng/min x ml in GHD (Cmax and AUC in FSS, p<0.001 vs CGD and GHD; Cmax in CGD and NSD, p<0.001 vs GHD). Cmax and AUC after ARG+EE were 21.3+/-4.2 ng/ml and 1432+/-514 ng/min x ml in FSS, 14.8+/-10 ng/ml and 805+/-489 ng/min x ml in CGD, 22.2+/-12.8 ng/ml and 1199+/-309 ng/min x ml in NSD, 4.6+/-2.5 ng/ml and 247+/-191 ng/min x ml in GHD (Cmax and AUC in FSS, CGD and NSD, p<0.01 vs GHD). Specificity was 62% for HEX 1 and 75% for HEX 2, GHRH+PD and ARG+EE. From a diagnostic point of view, HEX 1 + HEX 2 was the association with the largest percentage of false positives (20% in FSS, 27% in CGD and 33% in NSD), HEX 1 +GHRH+PD resulted in 9% in CGD, while the combined use of HEX 1 or HEX 2 with GHRH+PD or ARG+EE and of GHRH+PD with ARG+EE did not show false positive responses. IN CONCLUSION: I) the most effective dose of HEX was 2 microg/kg i.v.; 2) HEX did not show more specificity than GHRH+PD and ARG+EE; 3) the association of GHRH+PD with ARG+EE could yield the best results at lower costs, confirming these tests as first-line tools in evaluating GH secretion.

[Lipid profile in adiposity in children and adolescents]. / Osservazioni sul profilo lipidemico nell'adipostà infanto-giovanile.

Lipid plasma levels were measured in a group of 251 adipose juveniles. Triglycerides were elevated in relation to age but not to weight excess. Cholesterol and LDL levels had a same behaviour, through childhood toward adolescence, with significantly higher values in males than in females. VLDL levels prove a significative increase in reference to BML rise, but not so much increasing age. In short, the juvenile adiposity doesn't seem to produce considerable alterations of lipidaemia incides, even if we can foresee a possible evolution toward an acclaimed dislipidaemic pattern in adulthood.

[Growth in stature in infantile-juvenile obesity]. / La crescita staturale nell'adiposità infanto-giovanile.

The study aimed to assess the effect of juvenile simple adiposity on growth. The height (measured using a Hapenden stadiometer) of 1443 subjects (799 boys and 644 girls) aged from 6 to 16 was measured. The Quetelet index (QI) of adiposity was used; all subjects examined exceeded the 95th centile of the standard Cronk and Roche scale. Heights are expressed as standard deviation scores (SDS) and are compared to the British Standard. Adipose boys are taller than British boys up to the age of 12, then the difference lessens and the average heights of 15-year-old adipose boys are below the 50th centile of British growth charts. Female subjects showed a higher SDS from 6 to 8 years, after which the difference lessens gradually, and after 13 years the average height is below the 50th centile of British standards. Adipose boys are taller than normal boys during childhood; in prepuberty and puberty this difference lessens and during puberty they are shorter than British boys. This growth model is probably due to advanced skeletal maturity in adipose subjects with the result that at puberty growth lessens because it is exhausted. The wide epidemiological cross-sectional study confirms that growth is favourable in juvenile adiposity but does not alter adult height.

Thyroid-stimulating hormone and prolactin responses to thyrotropin-releasing hormone in juvenile obesity before and after hypocaloric diet.

This study was performed on 36 obese subjects aged 8.5-17.4 yr, 14 boys and 22 girls (prepubertal: 5 boys and 5 girls [stage I, according to Tanner]; BMI: 35.5 +/- 1.4 [mean +/- SEM] and 35 +/- 1.3 respectively; pubertal: 9 boys and 17 girls [stage IV-V]; BMI: 36.2 +/- 1.8 and 36 +/- 1.5 respectively) before and after 8 weeks of a 1000 kCal/day diet. The responses of serum TSH and PRL to TRH (200 micrograms iv as a bolus) were evaluated as Area Under the Curve (AUC) and net increase in respect to basal values (delta TSH and delta PRL). Serum T4, fT4 and rT3 were assayed at the baseline and T3 and fT3 at the baseline and 120' after TRH injection. A similar analysis was performed on 14 age- and sex-matched lean subjects as controls. In females at baseline fT4 serum levels were greater than controls and were significantly reduced after weight loss; rT3 increased after weight loss in the whole study group. In patients of both sexes the PRL peak after TRH injection was earlier but not greater (15') than in controls (30'). After weight loss PRL peak after TRH was found at 30' (as controls) in females only. Taking into consideration the stage of pubertal development, the results were the following: a) in puberal girls, after weight loss, TSH and PRL peaks after TRH were delayed with respect to baseline and to the other considered subgroups; b) in prepubertal girls TSH and PRL peaks, delta TSH, delta PRL, AUC-TSH and AUC-PRL were blunted with respect to pubertal ones; c) the other considered variables were unchanged after the period of caloric deprivation. No correlation between BMI and the AUC of TSH and PRL was found. These data suggest that thyroid function is substantially normal in adolescent obese subjects and not influenced by a prolonged period of caloric restriction, even though a reduced hypothalamic dopaminergic tone on pituitary thyreotrophs and lactotrophs could cause subtle alterations on TSH and PRL release, partially influenced by gender and sexual development.