Thyroid function in systemic sclerosis.
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Biomedical subjects
Publications and source records attributed to A Bellastella.
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HLA haplotypes, complement C4 factor and factor B immunochemical concentrations and autoantibodies titer have been studied in six patients with mild congenital adrenal hyperplasia (MC-AH), in two patients with classical congenital adrenal hyperplasia (CCAH) and in their parents. A high frequency of DR5 and C4BQO alleles have been found in MCAH patients. Moreover, C4BQO allele is carried out in three out of four cases associated with DR5. In the two CCAH patients we found a B51 and a B14 allele, the last one usually described in the non classical form of the disease in population of different ethnic origin. Signs of autoimmunity in some patients and parents have been found. C4 null alleles were several-fold more frequent among our patients with respect to the same ethnic control group and the autoantibody positivity could be the result of an altered immune regulation. The presence of a positive correlation between cortisol basal levels and C4 and Bf concentrations in the six MC-AH patients suggests an interrelationship between hormonal factors and immunological findings in this disease. Our finding about HLA antigens not previously described in this syndrome may stimulate more profound studies by genomic and cDNA probes.
In some acromegalics, GH release can be induced by TRH and/or LHRH administration. The pathogenesis of these GH paradoxical responses was supposed to be a somatotroph-reduced sensitivity to somatostatin, somatotrophin release-inhibiting factor (SRIF), or an hypothalamic derangement of the SRIF release. In this study, this hypothesis was investigated by means of GH suppression during chronic therapy with octreotide [Somatostatin analogue (SMS)] in order to evaluate the possible correlation between GH and insulin-like growth factor 1 (IGF-1) normalization and the disappearance of these paradoxical responses in 15 acromegalic patients: 15/15 with a paradoxical GH rise after TRH and 7/15 with a paradoxical GH rise after LHRH. SMS therapy was administered subcutaneously at the dose of 150-450 micrograms/day. During the treatment, GH and IGF-1 levels normalized in 12 patients and were reduced in the remaining 3 others. The GH response to TRH disappeared in 7 patients, while the GH response to LHRH disappeared in 4 patients. chi 2 analysis failed to show any significant correlation between GH and IGF-1 normalization and the disappearance of GH response to TRH and LHRH (chi 2 = 0.00686). No linear correlation existed between GH/IGF-1 decrease and GH peak or area under the curve at any time ('r' values: TRH test, GH -0.47, IGF-1 -0.48; LHRH test, GH -0.50, IGF-1 -0.49). The absence of any significant correlation between GH/IGF-1 normalization and the disappearance of GH paradoxical responses during chronic octreotide administration suggests that other factors apart from SRIF sensitivity are involved in the genesis of these responses.
The role of thyroid hormones in a short loop feedback in the thyroid is controversial. This process was studied in dog thyroid slices stimulated by TSH, carbachol and phorbol esters. Incubation of thyroid slices with T3 and T4 for 1 hour inhibited the subsequent stimulation of glucose oxidation induced by carbachol and phorbol esters but not by TSH. T3 also inhibited the stimulation of 32P incorporation into phospholipids stimulated by these two agonists. Glucose oxidation stimulated by TSH, carbachol and 12-0-tetradecanoyl-phorbol-13-acetate (TPA) was inhibited by rT3 and the inhibition was not reversed by methimazole, which did abolish the inhibition induced by iodide, MIT and DIT. TSH stimulation of cAMP was not blocked by T3 or T4 but was by rT3 and MIT- and DIT. The mechanism of such inhibition appears to be complex, possibly involving formation of iodide from rT3, MIT and DIT but also dependent on the intact iodothyronine. Moreover, our data suggest that T3 and T4 exert their inhibition on the thyroid through the phospholipids cascade and this mechanism is probably independent on the release of iodide from these iodocompounds.
Height and weight were measured in 7902, 3.5-11-year-old children from Torre del Greco nursery and primary school and arranged in centiles by cumulative frequencies calculation after sorting into ascending order measurements and counting up from the bottom. Our population height and weight measurements were compared to Tanner's by chi-square test. Our population seems to be taller and fatter with respect to Tanner's. Two possible explanation can be suggested: 1) British data are findings published several years ago; 2) Modified conditions of life in South-Italy in the last 30 yr, especially increased feeding availability can explain both increased height and frequent weight excess observed. These data suggest that for a correct auxological evaluation it seems useful to compare children not only to Tanner's standards but to centiles derived from the same population.
To investigate how blindness influences GH secretion, we studied the GH response to L-dopa and arginine in 8 blind adult males and 10 normal age-matched control males. Arginine and L-dopa tests were performed in random order at least 1 week apart at 0800 h, and plasma GH was measured by RIA. The blind subjects showed GH responses to arginine similar to those in normal subjects [peak, 22.1 +/- 1.3 vs. 20.5 +/- 1.3 micrograms/L (+/- SE)], but their GH response to L-dopa was significantly reduced [peak, 5.4 +/- 1.3 vs. 20.3 +/- 2.4 micrograms/L (+/- SE); P less than 0.01]. Because L-dopa is believed to release GH by stimulating endogenous GHRH, whereas arginine may act by suppressing endogenous somatostatin secretion, we propose that blindness may impair GH release by inhibiting GHRH secretion.
We investigated the plasma and urinary growth hormone (GH) levels, and plasma insulin-like growth factor (IGF-I) in 15 (8 prepubertal and 7 pubertal) subjects with chronic renal insufficiency. Four of our 7 pubertal patients had a short stature (standard deviation score from -2.7 to -4.0). Significantly increased plasma GH and IGF-I levels were found in pubertal subjects alone (p less than 0.05). The urinary GH levels was significantly increased in prepubertal and pubertal subjects (p less than 0.001 and 0.05, respectively). A significantly inverse correlation between urinary GH excretion and creatinine clearance was found (r = -0.55; p less than 0.05). Increased plasma GH, IGF-I and urinary GH levels seem to suggest a complex alteration of GH and somatomedin metabolism in central and peripheral (receptor) cells.
To investigate if blindness influences the growth rate of young subjects we measured height and weight of 71 prepubertal blind subjects (33 females and 38 males) aged 7-10 yr, in Tanner stage one puberty, living at the Institute "Martuscelli" for young blind individuals in Naples, Italy. They were divided into two groups: group 1 consisting of 27 subjects (14 females and 13 males) with total blindness; group 2 consisting of 44 subjects (20 females and 24 males) having only a light perception. The distribution in quintiles of their height and weight was compared by X2 test for trend to that of an age-matched large population (7902 subjects: 3808 females and 4094 males) of primary school from the same district. A stature significantly lower than controls was evidenced in both group 1 (p = 0.0006) and in group 2 (p = 0.008). When the comparison is performed taking into account the sex of subjects, the girls of both group 1 (p = 0.0014) and group 2 (p = 0.0004) show a stature significantly lower than female controls, whereas the stature of boys of both groups did not differ from that of male controls. No statistically significant differences in weight distribution were found between controls and either group 1 and group 2. Our results suggest that total or partial blindness could influence negatively the growth of prepubertal subjects; in particular it can cause short stature or growth delay especially in female sex.
The effect of a combined test (insulin, TRH, LHRH) on plasma levels of GH, LH, FSH, PRL and Cortisol was studied in 5 subjects with short stature. Two test were performed at 8 a.m. and at 8 p.m. In all subjects the GH, FSH, LH, TSH, PRL and Cortisol levels showed no relevant response during the two tests.
The effect of a combined test (insulin, TRH, LHRH) on plasma concentrations of LH, FSH, PRL, Cortisol was studied in 18 normal subjects in prepubescent state and in 65 patients in prepubescent state with short stature. In 6 subjects with short stature there was no change of LH, and in 7 subjects with short stature there was no change of FSH. In conclusion the combined test for pituitary stimulation provides an useful method for localizing the lesion in disorders of hypothalamo-pituitary axis.
Two HGH (insulin and L-Dopa) stimulating tests were performed at time interval on 65 subjects with short stature (SDs between -2 and -4.5 according to Tanner) and on 18 control subjects, in order to study the influence of short stature degree on the HGH behaviour during the stimulating tests. The results obtained show that: 1. Statistically the short stature degree does not affect the response to HGH stimulating tests. 2. Two tests are necessary to avoid erroneous diagnosis of dwarfism caused by lack of HGH. 3. No response to HGH stimulating tests in subjects with normal stature may prove a discrepancy between the hormone measured radioimmunologically and its biological action.
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Following L-Dopa administration (single oral dose of 500 mg), plasma Growth hormone (GH) levels significantly rose in 7 out of 8 normal subjects (aged between 64-83) and in 4 out of 8 blind subjects (aged between 60-88). The mean peak +/- SE in the 8 normal subjects was 24.9 +/- 4.9 ng/ml and in the 8 blind subjects was 11.5 +/- 2.8 ng/ml. These findings represent an additional anomaly in pituitary hormone release in the blind and may indicate that dopamine receptors in the hypothalamus are less sensitive to L-Dopa in blind people than in normal subjects.
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