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Biomedical subjects

S Seminara

Publications and source records attributed to S Seminara.

At least 19 recordsLinked to original sources
PubMed2005

Changes of thyroid function during long-term hGH therapy in GHD children. A possible relationship with catch-up growth?

BACKGROUND: Growth hormone (GH) treatment in patients with GH deficiency (GHD) can determine changes in the thyroid function. The clinical significance of these changes remains controversial, and all studies have so far covered rather a short period--usually no longer than one year. OBJECTIVE: To determine the effect of long-term recombinant hGH treatment in children with idiopathic GHD on the thyroid function. PATIENTS AND METHODS: Nineteen prepubertal children (12 boys and 7 girls, mean age 9.2 +/- 3.1 years) with idiopathic GHD were studied and followed for twenty-four months. None of the patients showed multiple pituitary hormone deficiencies. Nineteen healthy children matched for age and sex acted as controls. RESULTS: Patients with GHD showed a significant increase in TT (3) at twelve months and in FT (3) at six and twelve months after starting GH treatment, with a significant decrease at eighteen and twenty-four months. TT (4) level decreased significantly at twelve months and increased significantly at eighteen and twenty-four months. FT (4) also decreased, but only slightly, after twelve months of hGH treatment, and then increased significantly at twenty-four months. TSH levels did not vary significantly during the course of therapy. TT (3)/TT (4) and FT (3)/FT (4) ratios increased significantly after six and twelve months of therapy and significantly decreased later, approaching pre-therapy values. The SDS of Growth Velocity (SDS-GV) increased remarkably during the first year of therapy and then decreased significantly during the second year, although it remained significantly higher than the pre-therapy values. TT (3) and TT (3)/TT (4) ratio displayed a significant correlation with SDS-GV at twelve months of therapy. In a multiple regression analysis with age, bone age, parental height, GH dose, TT (3,) TT (3)/TT (4), and the SDS of IGF-I, only the TT (3)/TT (4) ratio at twelve months of therapy (p < 0.001) was identified as a significant predictor of SDS-GV. CONCLUSION: Our data confirm that changes in thyroid function are present in GHD children during long-term hGH therapy. These changes probably resulted from the effect of hGH on the peripheral metabolism of thyroid hormones and appear to be transitory, disappearing during the second year of hGH treatment. We speculate on the functional significance of these changes, and in particular, on their role in catch-up growth after hGH therapy.

Body Height↗
PubMed2004

A role for kisspeptins in the regulation of gonadotropin secretion in the mouse.

Kisspeptins are products of the KiSS-1 gene, which bind to a G protein-coupled receptor known as GPR54. Mutations or targeted disruptions in the GPR54 gene cause hypogonadotropic hypogonadism in humans and mice, suggesting that kisspeptin signaling may be important for the regulation of gonadotropin secretion. To examine the effects of kisspeptin-54 (metastin) and kisspeptin-10 (the biologically active C-terminal decapeptide) on gonadotropin secretion in the mouse, we administered the kisspeptins directly into the lateral cerebral ventricle of the brain and demonstrated that both peptides stimulate LH secretion. Further characterization of kisspeptin-54 demonstrated that it stimulated both LH and FSH secretion, at doses as low as 1 fmol; moreover, this effect was shown to be blocked by pretreatment with acyline, a potent GnRH antagonist. To learn more about the functional anatomy of kisspeptins, we mapped the distribution of KiSS-1 mRNA in the hypothalamus. We observed that KiSS-1 mRNA is expressed in areas of the hypothalamus implicated in the neuroendocrine regulation of gonadotropin secretion, including the anteroventral periventricular nucleus, the periventricular nucleus, and the arcuate nucleus. We conclude that kisspeptin-GPR54 signaling may be part of the hypothalamic circuitry that governs the hypothalamic secretion of GnRH.

Animals↗
PubMed2000

Catch-up growth in short-at-birth NICU graduates.

The statural catch-up growth, defined as reaching at least tenth length/height percentile (P10) for normal population standards (-1.28 SD score, SDS), was studied in 73 infants short at birth (length < P10 for gestational age) admitted to NICU. Mean gestational age at birth was 35.2 weeks (range 29-41) and mean birth length standard deviation score -2.31 (-4.52/-1.46). Infants were measured at birth, at 3, 6, 12, 18, and 24 months corrected age and then once a year until 6 years chronological age. Statural catch-up growth was studied, with reference both to normal population standards and to individual genetic target. With reference to normal population standards, 44% of infants had caught-up at 3 months of age, 51% at 3 years, 66% at 4 years and 73% at 6 years. In the case of individual genetic targets, a similar trend was present, but the absolute values were slightly higher from 4 to 6 years (73 vs. 66% and 78 vs. 73%, respectively). Statistically significant changes in mean standard deviations score for chronological age were present from birth to 3 months, 3 to 12 months, 3 to 4 years and 5 to 6 years (p<0.05). No differences were found in this trend of recovery when considering ponderal index (PI) at birth (symmetrical vs. asymmetrical), sex (male vs. female) or gestational age (p>0.05). In the majority of cases infants with short stature at birth admitted to a NICU had a statural catch-up growth within the first years of life. This is more evident when considered in relation to individual genetic target rather than to normal population standards.

Body Height↗
PubMed1999

Childhood obesity: results of a multicenter study of obesity treatment in Italy.

The prevalence of pediatric obesity is increasing and many patients are followed by specialized centers or private doctors. The aim of this study was to verify short- and medium term results of a therapeutic approach based on nutritional intervention in a large pediatric population: 1383 subjects (695 females, 688 males) aged 10.1 +/- 2.7 yr, followed in 11 pediatric departments in Italy. No difference was found between centers in age, height, weight, BMI and IBW. The drop-out rate after the first visit was 30.2% (58.1% IBW > 140%) in females and 34.2% (70.7% IBW > 140%) in males. After two years of follow-up only 9.7% of females and 6.4% of males remained on treatment. Of these patients only 7.3% of females and 6.4% of males had IBW < 120%. These data show that an approach based on nutritional intervention alone is not sufficient for long-term treatment of pediatric obesity. Only an approach started early and involving the family can produce permanent results.

Adolescent↗
PubMed1998

Effect of long-term growth hormone treatment on carbohydrate metabolism in children with growth hormone deficiency.

OBJECTIVE: Growth hormone (GH) has well known effects on carbohydrate metabolism. We have evaluated the effects of long-term growth hormone (GH) therapy on carbohydrate metabolism in children with classical GH deficiency (GHD) or GH neurosecretory dysfunction (GHND). STUDY DESIGN: Glucose, insulin and C-peptide concentrations at baseline and during oral glucose tolerance test (OGTT) were measured before and after 18 and 36 months of GH therapy (0.6-0.8 IU/Kg/week in 6 evening doses) in 13 GHD and 7 GHND children (15 boys and 5 girls, 15 prepubertal and 5 early pubertal; age at diagnosis 2.11-13.1 y). RESULTS: Mean fasting insulin and C-peptide concentrations after 18 months were similar to the pretreatment values, while after 36 months they were significantly higher than before treatment. Fasting glucose concentrations were similar to pretreatment both after 18 and 36 months. The mean areas under the curve (AUC) during OGTT for glucose, insulin, and C-peptide were significantly increased after 18 and 36 months. There were no differences between GHD and GHND patients. During the treatment period 10 of the 15 prepubertal patients entered puberty. A significant increase of insulin and C-peptide concentrations occurred after 36 months of GH treatment in the patients that remained prepubertal during treatment as well as in those who were pubertal when treatment was started. In three of our patients GH treatment caused glucose intolerance, which resolved after 6-12 months of a normal calorie low-simple carbohydrate diet without requiring discontinuation of treatment. CONCLUSION: Our data show that long-term GH treatment in GH deficient children causes hyperglycaemia and increased insulin secretion. These effects may in some patients induce glucose intolerance, which is reversible with appropriate dietary measures and does not require discontinuation of treatment.

Adolescent↗
PubMed1997

Growth hormone (GH) response to GH-releasing hormone in short children: lack of correlation with endogenous nocturnal GH secretion.

The growth hormone (GH) response to iv administration of GH-releasing hormone (GHRH, 0.3 microgram/Kg) was evaluated in 21 short children (13 boys and 8 girls, age 6.7-13.8 yr). Fourteen had familial short stature and/or constitutional growth delay, one had coeliac disease, and 6 were ultimately diagnosed as non-classical GH deficiency or neurosecretory dysfunction on the basis of subnormal integrated spontaneous GH concentrations (ICGH). The response was compared with 12-h spontaneous GH secretion measured every 30 min from 20:00 to 08:00. Mean ICGH ranged from 2.0-17.7 micrograms/l, with a maximum nocturnal GH peak ranging from 5.4-74 micrograms/l. The maximum GH peak after GHRH ranged from 9.4-50 micrograms/l, and the area under the curve (AUC) from 406-3012 micrograms.min/l. No correlation was found between the maximum GH peak and the AUC after GHRH and the maximum overnight GH peak, the ICGH and the overnight AUC. This study confirms that the GH response to GHRH is highly variable among short children with a wide range of spontaneous GH secretion, and that this response is not correlated with the spontaneous ability to secrete GH.

Adolescent↗
PubMed1996

Acute administration of recombinant human growth hormone inhibits the somatotrope responsiveness to growth hormone-releasing hormone in childhood.

In adulthood the growth hormone (GH) response to growth hormone-releasing hormone (GHRH) is inhibited by previous acute administration of either GH or GHRH and it is restored by substances that inhibit hypothalamic somatostatin release. Because in children the GH response to GHRH is not affected by previous neurohormone administration, it has been suggested that in childhood a GH increase is not able to trigger the somatostatin-mediated negative GH autofeedback mechanism. To verify this hypothesis, in 25 children (8 girls and 17 boys; 15 prepubertal and 10 in pubertal stages II-IV) with familial short stature (normal height velocity and insulin-like growth factor I levels) we studied the effect of acute i.v. administration of different recombinant human GH doses (group 1, N = 5, 0.06 U/kg; group 2, N = 6, 0.01 U/kg; group 3, N = 7, 0.005 U/kg at - 150 min) or saline on the GH response to GHRH (1 microgram/kg i.v. at 0 min). In another group (N = 7), we studied the effect of 0.005 U/kg iv recombinant human GH or saline on the GH response to GHRH combined with arginine (0.5 g/kg i.v. over 30 min), which likely inhibits hypothalamic somatostatin release. Serum GH increases after recombinant human GH were dose-dependent (GH peak, mean +/- SEM, 171.7 +/- 24.4, 33.3 +/- 3.9 and 21.8 +/- 5.1 micrograms/l, respectively). The administration of recombinant human GH strongly inhibited the GHRH-induced GH rise in all groups (group 1, 7.1 +/- 1.7 vs 23.1 +/- 7.6 micrograms/l, p < 0.05; group 2, 9.5 +/- 2.8 vs 26.9 +/- 8.5 micrograms/l, p < 0.05; group 3, 9.1 +/- 2.7 vs 34.8 +/- 7.2 micrograms/l, p < 0.02). The GH response to arginine + GHRH (56.9 +/- 13.3 micrograms/l) was higher than that to GHRH alone recorded in group 1 (p < 0.005), group 2 (p < 0.01) and group 3 (p < 0.01), while exogenous recombinant human GH failed to inhibit it (45.0 +/- 9.4 micrograms/l). Our results demonstrate that in childhood, as well as in adulthood, recombinant human GH administration inhibits the somatotrope responsiveness to GHRH. This inhibitory effect is likely to be mediated by hypothalamic somatostatin release.

Arginine↗
PubMed1991

Decrease in serum IgE associated with limited restriction in energy intake to treat toddler's diarrhea.

Toddler's diarrhea may be an allergic disease and its recurrences can be avoided with education to "internal spontaneity" in feeding, i.e., by education to a limited and reproducible decrease in eating incentives at the onset of meals. Serum IgE was thus investigated in 16 experimental children in a random comparison with 16 controls, all aged 1 to 4 years, before and after seven months' dietary treatment. Compliance was measured with a seven-day written diary, while serum IgE was measured by PRIST, before and after dietary treatment. A 21% decrease in energy intake (p less than 0.05) and about five times increase in fruit and nonstarchy vegetable intake amount was seen in treated children. A decrease in serum IgE level of 13.9 +/- 43.5 U/ml was found in the "internal spontaneity" group, as opposed to an increase of 33.2 +/- 50.5 U/ml in the control one (p less than 0.01). The differences between examinations were significantly correlated to the increase in NSV acceptance in all children plotted together (r = .51, p less than 0.005). The overall NSV effect on the changes of the 2 muscle areas, 2 symptoms, and 2 percent growth, 15 nutritional, 5 immune and 3 hepatic indices was significant with MANOVA (p less than 0.01). The education to "internal spontaneity" may be a useful tool for prevention of overeating, diarrhea recurrences and IgE increase in the second/third year of life.

Appetite↗
PubMed1990

Normal energy intake range in children with chronic nonspecific diarrhea: association of relapses with the higher level.

An increase in energy intake often occurs at weaning. The increase may be due partly to prompting by the caregiver to accelerate the child's weight gain and partly motivated by the palatability of common weaning foods. Increased food intakes initiated during weaning and continued into the second year of life may be associated with chronic, nonspecific diarrhea in selected children. An educational project was designed to reduce intakes augmented by either cause. Reductions were achieved by the regulation of energy-dense foods in the child's diet and reliance on the child's appetite control to determine meal size. The educational intervention was applied prospectively under nonblinded, controlled conditions. Children, 1 to 2 years of age, with chronic nonspecific diarrhea were assigned randomly to either a treatment or control group. Compliance, food consumption, preprandial glycemia, and outdoor activities were reported by the children's mothers in four 7-day diaries; symptoms related to the children's clinical condition and anthropometric and biochemical indices of nutritional status were noted at the beginning and end of a 7-month period. Forty-four of 53 children in the experimental group maintained compliance, and 44 of 47 children in the control group completed the follow-up. Energy intake decreased significantly by almost one-third in the experimental group. Growth, skinfold thickness measurements, and outdoor activities were similar between experimental and control groups over the 7-month period. Diarrheal episodes occurred in 6, 1, and 2 children in the experimental group at 1.5, 3, and 7 months and in 22, 18, and 15 children in the control group, respectively (p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Child, Preschool↗
PubMed1990

Effect of aflatoxins on rat peritoneal macrophages.

Phagocytosis, intracellular killing of Candida albicans, and superoxide production by rat peritoneal macrophages exposed to aflatoxins B1, B2, G1, G2, B2a, and M1 at several times and concentrations were analyzed to evaluate the intensity of a depressive effect for each mycotoxin. All aflatoxins used at very low concentrations had a depressive effect on the functions of macrophages. The biggest impairment of phagocytosis, intracellular killing, and spontaneous superoxide production was observed in macrophages exposed to aflatoxins B1 and M1.

Aflatoxins↗