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Biomedical subjects

M A Satta

Publications and source records attributed to M A Satta.

At least 37 records · Page 2Linked to original sources
PubMed1989

An unusual hormone pattern in a virilized woman affected by Sertoli-Leydig cell tumor. Report of a case.

A 24-year-old woman was admitted to hospital because of hirsutism, virilism and amenorrhea, which had appeared 6 months earlier. Endocrinological evaluation showed a slightly elevated serum level of testosterone (1.2 +/- 0.05 ng/ml), normal plasma levels of dehydroepiandrosteronesulfate (DHEA-S) (2,070 +/- 6 ng/ml), androstenedione (1.8 +/- 0.5 ng/ml) and sex hormone-binding globulin (SHBG)(42 +/- 3 nM/L); there was normal urinary 17-ketosteroid (17-KS) excretion (11.7 mg/24 h), low urinary estrogen (E) excretion (3 +/- 0.4 micrograms/24 h), suppressed basal gonadotropin concentrations (LH 0.9 microUI/ml; FSH 3.2 microUI/ml) and an exaggerated response to the LH-RH test. At laparotomy, a monolateral ovarian tumor was found, which was proved histologically to be a Sertoli-Leydig cell tumor. After tumor ablation, a regular menstrual cycle followed and progressive reduction of virilism was noted. This was followed within 4 months by complete normalization of LH, FSH, estrogen and progesterone serum levels. The responsiveness to LH-RH also became normalized. Two years after this operation, the patient had a normal pregnancy. This case of virilization in a woman affected by a benign Sertoli-Leydig cell tumor was primarily characterized by an unusual response of the hypothalamopituitary axis against an endocrinological background of notable alteration of the androgen/estrogen ratio, where the androgens were slightly increased and the estrogens greatly reduced.

Adult↗
PubMed1989

[Naloxone doesn't determine the response of growth hormone to clonidine in obese patients].

The effect of naloxone (opioid receptor blocker) on the impairment of growth hormone (GH) release after clonidine (alfa 2-adrenergic agonist) was investigated in 10 volunteer obese subjects. The patients (4 males and 6 females, 16-22 year old) with fat excess (15 +/- 2 kg) estimated by bioelectrical impedance analysis (BIA) were studied repeatedly. The patients, were perfused by a slow saline infusion. 30 min later they received a bolus dose of clonidine (150 micrograms p.o.), followed 30 min later by a bolus dose of naloxone (10 mg i.v.) or a corresponding volume of isotonic sodium cloride (I.S.) for control. No significant changes occurred in blood GH concentration after clonidine administration and naloxone did not induce GH response at clonidine. These results suggest that in obese subjects the impairment of GH release after clonidine is not mediated via receptors sensitivity to naloxone.

Adolescent↗
PubMed1989

[Partial deficiency in 21-hydroxylase in certain forms of hirsutism].

The ACTH test is important when hirsutism occurs in women with a slight 21-hydroxylase deficiency, and normal basal 17-OH Progesterone (17-OH-P/plasma levels). Extensive hormonal assays: LH, FSH, Prolactin, 17 beta-estradiol (E2), Estrone, 17OH-P, Androstenedione, Testosterone, Cortisol (C), Dehydroepiandrosterone-S (DEA-S) were carried out in 36 hirsute women. 13 of these presented hormone levels as found in polycystic ovary syndrome (PCOS), 6 women presented a slight 21-hydroxylase deficiency (increased plasma 17-OH-P and decreased C after ACTH test with significant, p less than 0.01, increase of 17-OH-P/C and 17 women presented idiopathic hirsutism (IH). The hormonal pattern, in the basal condition, is not different in IH or in slight 21-hydroxylase deficiency. The ACTH test is able to differentiate between IH and adrenal hirsutism.

17-alpha-Hydroxyprogesterone↗
PubMed1989

[The relationship between high-density lipoproteins, thromboxane B2 and arteriosclerosis in a case of primary hypoalphalipoproteinemia].

Data in the literature suggest that cases of hypoalphalipoproteinemia involve an increase in thromboxane B2 (TXB2) together with an increased risk of atherosclerosis. A recent detailed examination of a 32-year-old man revealed clinical and biochemical features strongly indicative of that pathology. The case presented several unusual features: marked infiltration of the skin and mesenteric lymph nodes by histiocytic lipids with sufficient hyperplasia to induce acute intestinal occlusion combined with an in vivo TXB2 generation curve, subsequently inhibited by aspirin, that was comparable to the curves of the control subjects. Furthermore there were no signs of early atherosclerotic damage so that it was possible to postulate the hypothesis that despite the 50% drop in alpha-lipoprotein levels, they were still sufficient to ensure normal turnover of the other lipoproteins so that, however complex the clinical condition, it was an incomplete expression of a phenotype.

Adult↗
PubMed1988

[Endogenous opiate modulators of insulin secretion in the obese].

The effects of endogenous opiates on insulin response to oral glucose load were studied in obese subjects and in lean healthy volunteers. None of these having a family diabetes. After 3 days on an 1,800 cal./m2, 40% carbohydrate diet all subjects underwent two standard 75 g oral glucose tolerance tests (OGTT), one of which was accompanied by an i. v. administration of 10 mg of, an antagonist of opiates, the naloxone. In one group of obese impaired oral glucose tolerance test occurred. All obese, but not the lean healthy volunteers, showed: 1) increased basal plasma insulin levels, 2) higher insulin response to OGTT, 3) a decrease in insulin response to OGTT after naloxone administration, with significant differences at 60 min (p less than 0.01) and 90 min (p less than 0.025). In none of the subjects significant differences were observed in blood glucose levels after OGTT plus naloxone administration. These data suggest that increased endogenous opiates may affect insulin response to glucose in obese with impaired or normal oral glucose tolerance test. At present there seems to be no satisfactory explanation for unchanged blood glucose levels during OGTT with and without naloxone despite a decrease in insulin secretion in the obese patients.

Adolescent↗
PubMedDate not supplied

The effects of anti-convulsant drugs on adrenal function.

Since the adrenal cortex and medulla are intimately interrelated, the effects of anticonvulsant drugs may affect both of these hormonal systems. Anticonvulsants are commonly used long-term for the treatment of epilepsy, chronic pain syndromes and affective disorders. In patients where adrenal function needs to be evaluated, the clinician should be aware of the potential interactions between anticonvulsant medication and the hypothalamo-pituitary-adrenal axis. Carbamazepine, phenytoin and phenobarbitone induce the liver P450 cytochrome enzyme system and stimulate steroid clearance. Therefore, patients investigated for Cushing's syndrome may show a falsely positive dexamethasone suppression test, and patients with adrenal insufficiency on steroid replacement may require increased doses of steroids; furthermore, increased corticosteroid-binding-globulin levels are also associated with chronic anticonvulsant administration. In addition, concomitant treatment with benzodiazepines, probably acting via the GABA pathway, can also alter the ACTH/cortisol response to stressful stimuli. Direct and indirect evidence suggest that benzodiazepines, acetazolamide and magnesium sulphate can also interfere with the renin-angiotensin-aldosterone system. Finally, to our knowledge, no systemic data are yet available in the human on the effect of antiepileptics on the function of the adrenal medulla and/or catecholamine metabolism; however, as the adrenal medulla receives part of its blood supply from the cortex, it is possible that alterations of cortical hormonal composition might affect adrenal medulla function overall.

Adrenal Glands↗
PubMedDate not supplied

Thyrotoxicosis: clinical and laboratory assessment.

Thyroid hormones are triiodothyronine (T3) and thyroxine (T4). The hypophysial thyrotropic hormone, thyroid stimulating hormone (TSH) is their physiologic regulator. Thyrotoxicosis is characterized by clinical symptoms caused by high thyroid hormone concentrations. The commonest forms are: 1) toxic diffuse goiter (Basedow-Flajani-Graves disease), 2) toxic multinodular goiter, 3) toxic adenoma. Other less frequent forms are the iodide-induced, that during Hashimoto thyroiditis, that from inappropriate TSH secretion. The diagnosis is predominantly clinical and confirmed by hormone level determination associated in some cases to functional and morphofunctional tests (TRH test, scintigraphy, thyroid I uptake) and antithyroid antibody assay.

Female↗
PubMedDate not supplied

Molecular biology of thyroid neoplasms.

Thyroid tumorigenesis proceeds through the progressive accumulation of alterations in genes involved in the regulation of cell proliferation and differentiation accompanying the acquisition of phenotypic, biological and clinical characteristics of increasing malignancy and dedifferentiation. The molecular alterations specific to thyrocyte carcinogenesis are examined. Ras mutations seem to represent an early occurrence in thyroid tumorigenesis being common to both benign and malignant follicular tumors; they would represent the early mutational events able to enhance the cell proliferation. Subsequent alterations in several genes will probably result in the determination of a follicular or papillary phenotype. In particular, mutational events activating ret, met and trk thyrokinase receptors direct the tumor growth and development towards the papillary type. Progression towards a follicular phenotype would instead occur in two stages: first there is the loss of function of genes on chromosome 11q13 which may direct the tumor cell towards the phenotype of follicular adenoma, second, there is the inactivation of the probable suppressor oncogene on chromosome 3p which might be fundamental in the transition from adenoma to follicular carcinoma. Undifferentiated or anaplastic tumors are characterized by the presence of p53 gene mutations.

Cell Division↗
PubMedDate not supplied

Neuroendocrinology of mood disorders.

The neuroendocrine system, which plays an important role in regulation of mood, is dysfunctional in patients suffering from mood disorders. In order to improve the quality of life for patients, additional research is needed to define clinical implications of neuroendocrine dysfunction in mood disorders. It would be important to define which specific hormonal responses that are blunted in affective disorders contribute to mood symptoms and which medications that normalize neuroendocrine function are conditioning the impact of mood symptoms. Consideration and evaluation of endocrine status result important in psychiatric patients, both to ensure proper diagnosis and adequate treatment.

Bipolar Disorder↗