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Biomedical subjects

F Mantero

Publications and source records attributed to F Mantero.

At least 235 records · Page 13Linked to original sources
PubMedDate not supplied

TGF beta 1 immunostaining patterns and locations in adenoma which later recurred.

To investigate whether the immunohistochemical pattern of TGF beta 1 may be a marker of relapse for adenomatous pathology, 18 follicular adenomas, surgically removed by hemithyroidectomy between 1977 and 1982, were studied. The adenomas were divided into two groups according to the presence (group 1, N = 9) or absence (group 2, N = 9) of nodules recurring in the residual thyroid tissue. The presence and location of TGF beta 1 were evaluated a posteriori by immunohistochemistry in the removed adenoma. Fifty randomly selected subcapsular follicles were studied in each adenoma in order to evaluate the percentage of positive follicles and TGF beta 1 intra-thyrocyte location. In adenoma of group 1, the percentage of positive follicles for TGF beta 1 was lower (80%) than in adenoma of group 2 (84%); this was, however, not statistically significant. The location of TGF beta 1 was mainly at the cell base of the epithelial cells in the microfollicles of group 1, but was dominant at the cell apex in group 2 (p < 0.01). In conclusion, adenoma recurrence is independent of TGF beta 1 production; it may be due to an abnormal TGF beta 1 regulation in response to hyperplasiogenic stimuli.

Adenoma↗
PubMedDate not supplied

HLA and hormonal data for identification of heterozygotes in 11 beta- and 17 alpha-hydroxylase deficiency syndromes.

1. In previous studies, baseline and ACTH-stimulated hormone levels, plus HLA genotyping, have been used to detect heterozygous carriers in congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency (21-OHDS). 2. In the present study similar parameters were determined in a family of four including two children with CAH due to 11 beta-hydroxylase deficiency (11-OHDS), and a family of twelve including three sibs (two females, one genotypically male) with CAH due to 17 alpha-hydroxylase deficiency (17-OHDS). 3. HLA typing showed affected sibs with 11-OHDS to differ in one of their haplotypes. No significant differences in basal and ACTH-stimulated steroid levels were seen between the parents (obligate heterozygotes) and the general population. 4. In 17-OHDS, affected members differed from one another in one to two haplotypes; one patient had identical HLA profiles with two of the normal siblings, as did the genotypically male patient with two others; each of the other healthy siblings had one haplotype found in two of the affected subjects. The genes responsible for 11-OHDS and 17-OHDS--in contrast with 21-OHDS--do not appear to be HLA-linked. However, the measurement of ACTH-stimulated corticosterone levels may be useful, since the gene responsible for 17-OHDS seems to be expressed hormonally in the heterozygous state.

Adolescent↗
PubMedDate not supplied

Expression of type 1 angiotensin II receptors in human aldosteronomas.

Type 1 angiotensin II (AII) receptors (AT1 receptors), besides stimulation of aldosterone secretion, seem to transduce the growth factor-like activity of AII on glomerulosa cells. Although a local renin-angiotensin system and AII synthesis have been found in human adrenals and aldosteronomas, it is unclear whether aldosteronomas express AT1 receptors. Utilizing polymerase chain reaction (PCR) and reverse transcription-PCR (RT-PCR) with primers complementary to both genomic and cDNA sequences of human AT1 receptor, we have amplified and cloned a 734 bp fragment of the AT1 coding region. This DNA, after cloning and sequencing, was used for Northern analysis. Total RNA was extracted from 5 non-tumorous adrenals and 5 aldosteronomas. AT1 mRNA (approximately 2.4 kb) was expressed in all the aldosteronomas tested. Densitometric analysis of AT1 signals, corrected by beta actin expression, when compared to non-tumorous adrenals, did not show significant differences. AT1 receptor density and affinity in cell membrane obtained from 9 non-tumorous adrenal cortex and 8 aldosteronomas were also studied. 125I-AII was used as ligand and Dup 753 as AT1 antagonist: AT1 receptor density and affinity were not significantly different in aldosteronomas vs non-tumorous adrenal cortex. In conclusion, the expression of AT1 gene and the formation of an apparently normal receptor suggest that AT1 receptor should have a role in aldosteronoma cell biology.

Adrenal Cortex Neoplasms↗
PubMedDate not supplied

ACTH receptor mRNA in human adrenocortical tumors: overexpression in aldosteronomas.

We previously reported that ACTH receptor (ACTH-R) mRNA is expressed in cortisol-secreting adrenal tumors, with significant differences between adenomas and carcinomas. In order to complete the study we have now evaluated 11 aldosteronomas (APA), 14 non-hypersecreting adenomas, 2 androgen-secreting adenomas and 8 normal adrenal glands. The level of ACTH-R mRNA was evaluated by competitive RT-PCR using a non-homologous competitor. ACTH-R gene was expressed in all tissues. All APA showed highest ACTH-R mRNA levels. Despite signs of individual heterogeneity, the level of ACTH-R transcripts was reduced in carcinomas. Furthermore, no significant differences were observed among cortisol-secreting adenomas, non hypersecreting adenomas and controls. The results show that ACTH-R mRNA is expressed in all adrenocortical tumors. The overexpression of ACTH-R in APA supports the role of ACTH on aldosterone secretion in these tumors, as also suggested by the presence of a diurnal rhythm, the lack of response to Angiotensin II, upright posture and captopril administration. The low abundance of ACTH-R in carcinomas might be a useful molecular marker of malignancy even if some overlap between carcinomas and adenomas does exist.

Adenoma↗
PubMedDate not supplied

[Plasma renin activity in renal veins in different types of arterial hypertension (author's transl)].

Peripheral plasma renin activity (PRA), vena cava and renal veins PRA were measured in 85 patients; arterial PRA was also measured in several cases. 25 patients had essential hypertension or primary aldosteronism; whereas in 60 patients renal or renovascular abnormalities were present. Peripheral PRA was elevated in 17/30 patients with parenchimal or excretory tract diseases. The following ratios came from the results of vena cava, and renal veins PRA were calculated: Ra/Rc and Rc/P according to Stockigt et al. and V-A/A according to Vaughan et al. The ratios were calculated only when v. cava PRA was greater than 4 ng/ml/3 hrs. A good correlation was found between v. cava can arterial PRA. Among the 60 cases with renal hypertension, 26 underwent either revascularization or nephrectomy surgery. Eleven of the 15 patients operated on for renovascular diseases showed a significant reduction of blood pressure (greater than 30 mmHg); all had high peripheral PRA and 6 had significant Ra/Rc and Rc/P (respectively greater than or equal to 1,5 and less than or equal to 1,3). The same patients also had V-A/A of the affected kidney greater than or equal to 0,48 and 5 also V-A/A of the controlateral kidney less than or equal to 0,23, both values being significant for a unilateral renin secretion and controlateral suppression. Among the 4 patients who were unsuccessfully operated on, only 2 had elevated peripheral PRA and 1 had Ra/Rc and Va-A/A greater than normal, but not significant values of Rc/P and Vc-A/A. 11 patients with small kidney or other forms underwent surgery; among the 6 cases with satisfactory results, 5 had high peripheral PRA, 2 showed significant ratios Ra/Rc and 3 a significant V-A/A for both kidneys. Only 1 of the patients not cured by surgery had supernormal peripheral PRA and none had any significant ratio. Therefore both methods for elaborating data obtained from the measurement of PRA in renal veins seem to offer similar prognostic indications. The finding of significant ratios is an almost sure criterium for predicting a surgical cure of renal hypertension, whereas the cases where we may expect a failure present ratios which are not significant. However, patients of the latter group may sometimes have successful results at surgery too, which demonstrates that other mechanisms may also be involved in the pathogenesis of this form of hypertension.

Adolescent↗
PubMedDate not supplied

Prediction and consistency of blood pressure salt-sensitivity as assessed by a rapid volume expansion and contraction protocol. Salt-Sensitivity Study Group of the Italian Society of Hypertension.

BACKGROUND: This multicenter trial in essential hypertensive patients (n=94) is aimed i) to evaluate the distribution of blood pressure salt-sensitivity by a rapid volume expansion/contraction protocol over three days; ii) to investigate the within-patient reproducibility and to identify predictors of the response to the test; iii) to compare this response with the response to dietary NaCl restriction. METHODS: The study design included: 1) screening for salt-sensitivity by the rapid test; 2) a controlled trial of dietary salt restriction; 3) repetition of the rapid test in a subgroup of patients. RESULTS: The mean BP response to the rapid test fitted a Gaussian curve. In multivariate regression analysis, controlling for the effect of potential confounders, the blood pressure increment during the intravenous saline infusion was the best independent predictor of the response to the test (r=0.713) with minor contributions by the 24-h urinary sodium excretion before the test and by baseline fasting serum insulin. These three variables together explained 61% of the overall variability of the response. The Spearman rank correlation coefficient between the BP response to the rapid test and the response to the dietary protocol was 0.21, p=0.05. Upon repetition of the rapid test, the correlation coefficient between the responses observed on the two occasions was 0.60 (n=19, p<0.01); there were no patients misclassified across the extreme tertiles of the distribution of salt-sensitivity. CONCLUSION: We conclude that the rapid test reproducibly identified patients in the upper and lower parts of the distribution of salt sensitivity. The analysis of possible predictors of the response to the test suggested that the evaluation of the blood pressure response to saline infusion, upon careful standardization of dietary NaCl intake, may represent an alternative to the completion of the whole test for the screening of the salt-sensitivity.

Adult↗
PubMedDate not supplied

[Clinical evaluation of desmopressin (DDAVP) in diabetes insipidus: solution vs tablets].

Efficacy and tolerability of perorally administered desmopressin were evaluated in 12 adult patients suffering from central diabetes insipidus. According to the results of the study desmopressin should be administered at a higher dosage than 300 micrograms/die to obtain the same antidiuretic effect as with the intranasal administration. No significant changes in body weight, arterial pressure and blood chemistry parameters have been detected over the whole administration period and only some slight side-effects occurred. Oral desmopressin may be considered as an effective alternative to traditional intranasal administration and it may significantly improve patients' compliance.

Administration, Intranasal↗
PubMedDate not supplied

[Role of ketanserin in the treatment of primary hyperaldosteronism].

Ketanserin (Ket), a 5HT-2 serotoninergic receptor antagonist, is currently used as an antihypertensive agent. In our previous studies, both in vitro and in vivo when administered as bolus i.v. in subjects with primary aldosteronism (IAP), Ket exhibited an inhibitory action on aldosterone secretion. Therefore in the present study we investigated, in IAP patients, the effects of chronic treatment with Ket on blood pressure and mineralocorticoid secretion. Ket was administered at increased doses of 20 and 40 mg twice daily per os for 30 days and the following parameters were evaluated: blood pressure, heart rate, ur. aldosterone, pl. aldosterone both basal and after ACTH and angiotensin II (AII) stimulation, PRA, and atrial natriuretic factor (ANF). Our study demonstrated that Ket is a powerful blood pressure lowering agent with no relevant side effects and no variations of heart rate. Ur and pl aldosterone levels did not change during therapy; correspondingly, Ket did not modify ACTH or AII-induced stimulation. ANF levels, basally elevated in this syndrome, increased during Ket treatment. This new and interesting aspect deserves further evaluation. In conclusion Ket showed an effective antihypertensive effect in this syndrome, even if steroidogenesis inhibition does not seem to be a relevant component of its antihypertensive effect.

Administration, Oral↗
PubMedDate not supplied

[Medical treatment of Cushing syndrome].

Cushing's syndrome is a serious endocrine condition for which no treatment has been proven fully satisfactory at least for its pituitary dependent form (Cushing's disease). Indeed, despite some advances in pharmacology (cyproheptadine, bromocriptine, lisuride) and in surgical and radiation procedures at pituitary level, a definitive cure is often delayed. The inhibitors of steroids synthesis (ketoconazole, aminoglutethimide, metyrapone, mitotane) are still very valuable tools in its management as a palliative treatment.

Cushing Syndrome↗
PubMedDate not supplied

[Addison's disease: principal clinical associations and description of natural history of the disease].

From 1967 to 1988 we studied 75 cases of Addison's disease (AD). An autoimmune etiology was found in 68%, while previous tubercular infection was demonstrated in 21% of the cases; minor causes were involved in 3%, and in 8% of the cases the disease remained of unknown origin. Autoimmune adrenalitis has become the most frequent cause of AD as a consequence of decreased tubercular infection. Autoimmune AD prevailed in children or in young people, and tubercular AD in adults. The finding of calcifications in adrenals and/or other organs was the specific diagnostic sign for the identification of tubercular forms. On the other hand, the finding of circulating adrenal autoantibodies (AA) and/or other organ specific autoantibodies was the fundamental diagnostic marker of autoimmune forms. In 72% of the cases autoimmune AD is associated with other organ-specific autoimmune diseases. Subjects with AA but without clinical signs of hypoadrenalism were considered to have "potential AD", because they showed a high risk of developing clinical hypoadrenalism. This condition develops over a long period characterized by different stages of subclinical adrenal hypofunction. Steroid cell autoantibodies (StCA) are frequently detectable in patients with autoimmune AD, in whom they are markers of autoimmune premature ovarian failure. The study of StCA-positive cases without hypogonadism will be important to clarify whether or not these autoantibodies could be markers of potential autoimmune hypogonadism.

Addison Disease↗