Biomedical subjects
Publications and source records attributed to G L Spadoni.
This paper describes the main clinical features of growth hormone deficiency (GHD). Some aspects of the classic GHD and particular clinical conditions characterized by GHD and normal growth are considered.
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The response to growth hormone (GH) of cultured lymphocytes from three patients with Laron dwarfism (LD), one subject with growth hormone deficiency and a normal adult volunteer was examined by employing the cytochemical method of selective silver staining that evidentiates the chromosomal sites of those gene clusters (Nucleolus Organizers, NOs) which are actively involved in rRNA transcription. Lymphocytes from the normal donor responded to GH administration with a significant increase of the mean number of silver positive NOs per cell as well as lymphocytes from the growth hormone deficient patient (P less than 0.001). No response to GH administration was observed in lymphocytes from any of the three subjects with LD. These results suggest that the technique of selective silver staining of NOs can be usefully applied to the study of those growth disorders in which a peripheral unresponsiveness to GH is suspected, as demonstrated by data obtained on lymphocytes from patients with LD. This method seems to offer considerable potentialities for studying the cellular response also to other hormones and environmental stimuli.
Differential activity of rRNA gene clusters following growth-hormone administration has been demonstrated in cultured lymphocytes from subjects with different genetic backgrounds, i.e., with or without in vivo peripheral responsiveness to the hormone. The influence of different culture conditions on ribosomal gene responsiveness was also tested. Ribosomal gene activity was evaluated by selective silver staining of nucleolus organizing regions. The results show that hormone-induced enhancement of transcriptional activity requires both genetically determined cell responsiveness and environmentally determined permissive factors.
Twelve-hour nocturnal GH secretion was studied in 30 children with familial short stature (FSS), constitutional growth delay (CGD), total growth hormone deficiency (TGHD), partial growth hormone deficiency (PGHD), or idiopathic short stature (ISS). No difference was observed between subjects with FSS and children with CGD. The mean 12-hour serum GH concentration was significantly lower in patients with TGHD (p less than 0.001), children with PGHD (p less than 0.01), and subjects with ISS (p less than 0.01) than in subjects with FSS and CGD. No overlap was observed between the range of mean concentration values of children with TGHD and that of subjects with FSS. A significant correlation was found between growth velocity expressed as SD from the mean for bone age and GH concentration (p less than 0.001). All patients with a growth velocity less than 3rd percentile for bone age showed a mean nocturnal concentration less than 4 ng/ml. These data suggest that evaluation of 12-hour spontaneous nocturnal GH secretion with GH sampling every 30 minutes can be usefully employed in the diagnosis of GH deficiency.
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The role of Growth Hormone and Dexamethasone in the regulation of rRNA gene activity was evaluated on cultured human fibroblasts by the cyto-chemical method of selective silver staining. By this method the transcriptionally active r-gene clusters can be specifically visualized in individual cells. Statistically significant increases in the rate of rRNA transcriptional activity were demonstrated after hormone administration.
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Oxygen consumption in blood platelets of 14 pituitary dwarfs aged from 2 to 8 years was investigated before and after a 2 months' treatment with growth hormone (GH). No significant difference was found between dwarfs and control subjects in respect of basal platelet oxygen uptake (4.0 +/- 3.8 mmol O2/10(9) platelets/min in dwarfs as against 6.4 +/- 4.1 in controls), but the abrupt increase in oxygen consumption induced by thrombin was significantly reduced in dwarfs (4.3 +/- 4.1) as compared with controls (12.3 +/- 7.6; p less than 0.01). During GH treatment, however, the dwarfs' response to thrombin stimulation was similar to that of controls. Since dwarfs had normal platelet malonyldialdehyde production, it is likely that the mitochondrial component of thrombin-induced high oxygen consumption was deficient. These results suggest that blood platelets may contribute to the protective effect of GH deficiency against atherosclerosis.
The authors observed different clinical forms of Albright's hereditary osteodystrophy in 4 members of a family (two sisters, their mother and the maternal grandfather). The sisters were affected by pseudohypoparathyroidism type I, the older manifested the hypocalcemic variety, the younger the normocalcemic variety; the mother and the grandfather presented only with short stature and subcutaneous calcifications. The variety of clinical and biochemical alterations observed in these 3 generations supports evidence that Albright's hereditary osteodystrophy has a broad spectrum and that distinctions between the various forms of pseudohypoparathyroidsim should not be rigidly considered.
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A total of 21 patients with somatotropic deficiency have been enrolled in a clinical trial of biosynthetic growth hormone (bio-GH) and pituitary growth hormone (pit-GH). Five of them not previously treated (naïve) and 7 previously treated with pit-GH, received bio-GH; 9 received only pit-GH. Biosynthetic-GH was given 12 UI/m2/week. Height velocities during treatment rose, for naïve patients, from 3.6 +/- 0.3 cm/year (before treatment) to 8.7 +/- 1.3 cm/year (after 12 months treatment). For previously treated patients, after a period at least 6 months without any GH therapy, the increase in height was from 2.5 +/- 0.9 cm/year to 6.8 cm/year; and for the patients who received only pit-GH was from 3.4 +/- 1.2 cm/year to 8.0 +/- 1.1 cm/year. No significant difference was observed between the growth velocities obtained with the two preparations. No specific side-effects were noted.