[Liver damage and obesity in pediatric age]. / Alterazioni epatiche e obesità in età pediatrica.

In adult obese patients both an increase of aminotranspherase values and hepatic steatosis have been frequently showed. Conversely in childhood the existence of a liver's damage is often not investigated. To assess the prevalence of hepatic alterations in obese children, we studied 135 subjects, all affected by simple obesity, showing in a 20% of them the presence of ultrasonographic evidence of hepatic steatosis and/or hyperaminotransferasemia. Our study demonstrates the existence of silent hepatic alterations also in obese children and suggests to improve the treatment of obesity in childhood to prevent the progression of liver's damage.

[Non-specific pituitary responses in insulin-dependent diabetes mellitus in children and adolescents]. / Réponses hypophysaires aspécifiques dans le diabète insulinodépendant des enfants et des adolescents.

OBJECTIVES: Several reports indicate a number of changes in the control of the release of PRL, LH, FSH, GH and beta-endorphin (B-EP) as a result of insulin-dependent diabetes mellitus (IDDM). In this study we evaluate the presence of non-specific pituitary responses to releasing hormones in IDDM children and adolescents. METHODS: The non-specific effects of TRH on plasma GH, LH and B-EP levels and of GnRH on plasma GH, PRL, TSH and B-EP levels were measured in 16 IDDM children and in 16 healthy children matched by age and sex. All subjects were tested with injection of TRH (200 micrograms i.v. bolus) and GnRH (50 micrograms i.v. bolus). GH, TSH, PRL, LH and B-EP levels were evaluated with radioimmunological methods on blood samples collected before and after stimulation by releasing hormones. RESULTS: GH and B-EP non-specific responses to TRH and GnRH were significantly more pronounced in IDDM patients than in controls. All patients showed at least one non-specific response to one of the two releasing hormones. No significant correlations were found between non-specific pituitary responses and the patient's age, the duration and onset of disease or the degree of metabolic control. CONCLUSIONS: These observations may indicate that: in IDDM hypothalamus-pituitary regulating mechanism is altered; the hormones whose levels are most often found to be abnormal in IDDM (other than insulin) are also hormones which respond non specifically to the neuropeptides TRH and GnRH.

Growth hormone response to growth hormone-releasing hormone (GHRH), insulin, clonidine and arginine after GHRH pretreatment in obese children: evidence of somatostatin increase?

To clarify the possible neuroendocrine mechanisms underlying the impairment in growth hormone (GH) secretion present in obesity, the GH response to GH-releasing hormone (GHRH, N = 6), insulin hypoglycemia (N = 6), clonidine (N = 7) and arginine (N = 8) after GHRH pretreatment (1 microgram/kg iv 2 h before the tests) was evaluated in 27 obese peripubertal children and in a group of normal-weight short-normal children (N = 26). Growth hormone-releasing hormone pretreatment and all further stimuli elicited a statistically significant GH response in both obese and short-normal children; in the latter group arginine did not induce a significant GH response. No differences were found among the GH responses after the second stimuli in obese children, while in short-normal children the arginine peak and area values were lower than after GHRH and clonidine. Comparison between the two groups showed similar baseline but higher stimulated GH levels in normal-weight children after all tests except arginine, after which no difference was present. In conclusion, the neuroregulation of GH release seems to be similar qualitatively in normal-weight and obese youngsters; the different behavior observed after arginine, which is supposed to act through somatostatin inhibition, might be due to a chronic increase in somatostatinergic tone responsible for the lower stimulated GH levels in obesity.

GH response to GHRH, insulin, clonidine and arginine after GHRH pretreatment in children.

To determine whether differences in the neuroendocrine control of GH are present between children and adult subjects, the GH response to GHRH (1 microgram/kg) (group 1), insulin-induced hypoglycemia (0.1 U/kg iv) (group 2), clonidine (150 micrograms/m2 po) (group 3) and iv arginine (0.5 g/kg in 30 min) (group 4) after GHRH pretreatment (1 microgram/kg) was studied in 26 short-stature normal children (mean age 10.2 years). The results were compared with historical data in adults. No differences were present among mean peak GH levels after the first and second stimuli in groups 1, 2 and 3, while in group 4 the GH response to arginine administration was lower than that obtained after the initial GHRH (0.43 +/- 0.04 vs 0.9 +/- 0.13 nmol/l). Moreover, comparing the GH peak values following the second stimulus, it appears that the greatest GH responses were elicited by GHRH (1.31 +/- 0.23 nmol/l) and clonidine (1.11 +/- 0.22 nmol/l), while the lowest was elicited by arginine (0.43 +/- 0.04 nmol/l). In adults, sequential GHRH administration leads to inhibition of the response of the somatotropes, probably mediated by an increase in hypothalamic somatostatin. Our results confirm that after GHRH prestimulation GHRH elicits a significant GH response suggesting that activation of the somatostatinergic tone is less effective in children. This hypothesis also explains the low GH response to arginine which acts selectively through somatostatin inhibition.