[Data on nutritional and dietetic knowledge of some food of the second and third stages of childhood].
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Biomedical subjects
Publications and source records attributed to F Morabito.
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It is well established that children with extreme short stature, secondary to GH deficiency (GHD) or achondroplasia, face a disability that may affect their adult psychosocial outcome, while contrasting data are reported for short normal children. In our hands, adults with GHD have shown an unsatisfactory psychosocial adjustment due to the low adult height and hypothetically to the persistent GHD. This study has been carried out to evaluate the influence of growth in height on the social outcome in 45 adults with constitutional growth delay (CGD). Interviews with subjects and parents were used for assessment. Data obtained were compared with those found in an age, sex and social matched control group of adults with normal height. Some issues were also compared with the data we previously found in adults with GHD. Present mean age of the patients is 24 +/- 2 yr. A high percentage (32.8%) of unemployment or underemployment (part-time work) was found. Four patients (8.8%) were married, while 84.4% lived with their parents or relatives, confirming the notion of prolonged economic dependency on the family. The patients preferred single sporting activities, avoiding team work. Surprisingly, scholastic achievement was in general similar to that observed in controls. Similar findings have been previously observed in patients with GHD. Since no defect in GH secretion has been documented in CGD, the presence of a negative psychosocial outcome more probably seems to be due to the final unsatisfactory height rather than to a GH defect.(ABSTRACT TRUNCATED AT 250 WORDS)
It has been reported that adult obese subjects present a reduced growth hormone secretion. As no data are available in the pubertal period, which is characterized in lean subjects by an increased spontaneous growth hormone secretion, the growth hormone circadian concentration was studied in a group of 18 obese male subjects in different pubertal stages, and compared to 26 age-matched control subjects. The data observed evidenced no statistically relevant differences regarding LH and FSH circadian secretion and morning testosterone concentration. On the contrary a statistically significant (p less than 0.02) difference in growth hormone 24 h integrated concentration was evident, particularly in prepubertal subjects; the sleep-related peak was evident in 28% of obese subjects and in 85% of controls. Sm-C/IGF-I concentration was similar to the concentration observed in controls in the prepubertal stage, but did not show the expected increase in the late puberty. Auxological data, performed on a sample of 80 subjects, showed both advanced height and bone age at beginning of puberty, and a trend toward a reduction of percentile for height in parallel with the pubertal maturation, suggesting that pubertal growth spurt in obese subjects is at least less pronounced than in lean subjects. It is concluded that GH and Sm-C/IGF-I secretion is impaired during puberty in obese subjects, leading to a reduced growth rate, while in the prepubertal period factors other than GH may replace or even potentiate its action.
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.
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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.