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At least 37 records · Page 2Linked to original sources

[Mechanism of hyocorticosteronemia action of Strongyloides ratti in the rat].

In order to explain the hypocorticosteronemia which establishes itself in rats with Strongyloides ratti parasites, we are proceeding with a functional exploration of the hypothalamo-hypophyso-corticosurrenal axis in experimentally infested rodents. The adreno-cortico-tropic-hormone test (A.C.T.H.), stress to ether and the Lysin-8-Vasopressin and Metopirone tests lead to concordant results: -- the hypothalamo-pituitary-corticosurrenal present a functional integrity which allows it to react normally to direct stimulation or to feed-back; -- the deficiency seems to relate to the hypothalamic secretion of the cortico-releasing factor; -- the cause would stem from an inhibition of the nervous mechanism which regulates this neurosecretion.

Adrenal Cortex Hormones↗

Short ACTH test in assessing hypothalamic-pituitary-adrenocortical function.

The adrenocortical response to the simple 30-minute ACTH stimulation test was compared with the hypothalamic-pituitary-adrenocortical (HPA) response to insulin-induced hypoglycaemia in 25 patients with various degrees of hypothalamic-pituitary malfunction. The correlations between the increase in plasma cortisol during insulin hypoglycaemia and that during ACTH stimulation (r = 0-66) and between peak plasma cortisol levels during the two tests (r = 0-90) were highly significant. Peak plasma cortisol levels in individual patients were similar on both tests, no patient showing any major discrepancy between the two test results. Thus the simple 30-minute ACTH stimulation test seems to be reliable in detecting imparied HPA function.

Adolescent↗

[Reactivity of the adrenals to ACTH in rats with alloxan diabetes].

Experiments were conducted on rats. A study was made of the adrenal gland ACTH reactivity under conditions of alloxan diabetes. The function of the adrenal gland increased one month after the administration of alloxan; this was indicated by an increase of their absolute and relative weight, by an elevation of the corticosterone content in the peripheral blood and the glands proper. ACTH stimulated the adrenal gland function in rats with an intact pancreas, increasing the weight of the adrenal glands, the level of corticosterones in the blood and the adrenal glands. ACTH reactivity proved to be lowered in rats with alloxan diabetes. The blood corticosterone level increased in them less and changes in the weight of the glands and of the hormone concentration in them proved to be statistically insignificant.

Adrenal Glands↗

[Anomalies of corticotropin secretion in chromophobe adenomas].

Corticotrophic secretion has been studied in several groups of subjects during metopirone test and arginine L-Dopa infusion. In animals, a net plasma ACTH increase is observed under while it is inconstant after arginine L-Dopa. In hypopituitarism, metopirone ACTH levels are low and unchanged during the tests. In chromophobe adenoma, basal ACTH levels are high, ACTH increase is normal during test and significantly higher than in controls after L-Dopa injection. Significance of these metopirone corticotrophic abnormalities is discussed.

Adenoma, Chromophobe↗

[Investigation of adrenal function with corticotrophin-(1-23)-tricosipeptide-amide (author's transl)].

The new peptide corticotrophin-(1-23)-tricosipeptide-amide (Acethropan S) was shown to be useful in the assessment of adrenal function. Both in normal subjects and patients with adrenal insufficiency, the cortisol releasing capacity could be better evaluated with a dosage of 0.5 mg than with 0.25 mg. There were no obvious side effects induced by corticotrophin-(1-23)-tricosipeptide-amide.

Adrenal Cortex Function Tests↗

[Mineralocorticoid and glucocorticoid functions of the adrenal cortex and some mechanisms of their regulation in obesity].

A study was made of 77 patients with adiposity and a group of healthy persons with normal weight. Patients with adiposity had a significant increase of blood plasma aldosterone level; of decisive role in the formation of secondary hyperaldosteronism was played by the elevation of blood renin level. Apparently activation of the renin-angiotensin system and the associated intensification of mineralocorticoid function of the adrenal glands served as one of the causes of development of arterial hypertension in persons with excessive weight. In adiposity there proved to be an increased rate of cortizol secretion and of 17-OCS excretion with the urine; as to the blood plasma cortizol concentration, it failed to show any significant difference from the normal. Apparently stable blood cortizol level in the patients with adiposity was maintained as a result of intensified ACTH secretion; in these patients reserve possibilities of the adrenocorticosteroid function of the hypophysis were diminished.

17-Hydroxycorticosteroids↗

Evaluation of pituitary-adrenal function in patients with chronic bronchial asthma following substitution of steroid treatment with disodium cromoglycate (Lomudal).

In a group of 32 steroid-dependent asthmatic patients an attempt was made to replace steroid treatment with disodium cromoglycate (Lomudal). Withdrawal of steroids was accompanied by a transitory stage of combined corticotropin-Lomudal treatment for 6 to 8 mo. Pituitary-adrenal function was assessed by ACTH and Metopirone test. Before treatment an impairment of pituitary-adrenal function was found in most of our patients, although in 26 patients a normal increment of plasma cortisol was found after ACTH stimulation. At the end of the combined treatment, 17 patients are now on Lomudal with normal pituitary-adrenal function, 9 patients need small quantities of steroids occasionally, and 6 patients are steroid-dependent.

17-Hydroxycorticosteroids↗

Growth, pulmonary, and endocrine function in chronic asthma patients on daily and alternate-day adrenocorticosteroid therapy.

Growth, pulmonary, and adrenal-pituitary function were assessed in 20 steroid-dependent asthmatic children and adolescents while they were on daily prednisone therapy. The patients were then switched to equivalent daily methylprednisolone or twice equivalent alternate-day methylprednisolone for a 3-mo period, after which time studies were repeated. The steroid regimens were then crossed so that those patients taking daily methylprednisolone were switched to alternate-day therapy and the alternate-day therapy patients were switched to daily medication for another 3-mo interval, after which studies were repeated again. Abnormal growth, bone maturation, and cataracts were identified. Mean symptom scores at each evaluation were similar. Pulmonary function tests and shunt studies showed little difference between methylprednisolone and prednisone. Endocrine function tests showed a high incidence of disturbed pituitary and adrenal function. A 3-mo period of alternate-day therapy did not alter this.

17-Hydroxycorticosteroids↗

Relationships among the secretion of ACTH, GH, and cortisol during the insulin-induced hypoglycemia test in the normal and obese child.

The behavior of the secretion of ACTH, GH, and plasma cortisol during the insulin-induced hypoglycemia test on normal and obese children was studied. The secretion of the above-mentioned hormones was determined by calculating the integrals of the curves. The mean values of the integrals of the plasma cortisol and ACTH curves do not show any significant differences between the two groups of children. The mean values of the ratios between the integrals of the plasma cortisol and ACTH curves show a significant difference between the two groups (P smaller than 0.01). Since the mean values of the integrals of the plasma cortisol curves are practically the same in both groups, the difference in the above-mentioned ratios refers to the lower values of the integrals of the ACTH curves found in the obese children. This enables us to make the hypothesis that in the obese child the function of the pituitary-adrenal axis, at least during the insulin test, does not differ from the norm thanks to the adaptation of the ACTH secretion to the greater sensitivity of the adrenal glands to this hormone. In both the groups examined there was no correlation between the secretion of ACTH and plasma cortisol, between ACTH and GH, and between plasma cortisol and GH.

Adrenocorticotropic Hormone↗

Modification of adrenal function by the anti-serotonin agent cyproheptadine.

The effect of the serotonin antagonist, cyproheptadine (Cypro), on metyrapone-induced stimulation of the pituitary-adrenal axis was evaluated in nine normal subjects. The subjects underwent standard oral metyrapone tests (750 mg every four h, for six doses) while taking no medications and while receiving oral Cypro (4 mg every six h). Cypro administration caused a significant reduction in: 1) baseline 17-hydroxycorticosteroid (17-OH) excretion (-31 +/- 7.2%), 2) the increase above baseline in 24 h 17-OH excretion on the day after metyrapone (-32 +/- 4.9%), 3) serum 11-deoxycortisol concentrations 8 h (-45 +/- 5.5%) and 24 h (-18 +/- 3.6%) after the first dose of metyrapone, and 4) plasma ACTH concentration 8 h (-32 +/- 8.2%) and 24 h (-22 +/- 8.0%) after the first dose of metyrapone. When compared with the control test, Cypro administration did not alter: 1) baseline 17-ketosteroid secretion, 2) the fall in serum cortisol concentration while taking metyrapone, 3) the serum free metyrapone concentration, 4) cortisol metabolism, 5) the adrenal response to ACTH, and 6) assay methods for measurement of serum and urinary corticosteroids. Our data suggest that Cypro can reduce pituitary-adrenal responsiveness by reducing plasma ACTH concentrations. If Cypro acts as a serotonin antagonist, our data lends support to the idea that serotoninergic mechanisms are important in the control of pituitary ACTH secretion in normal human subjects.

17-Hydroxycorticosteroids↗

Genetic subtypes of unipolar primary depressive illness distinguished by hypothalamic-pituitary-adrenal axis activity.

Serum-cortisol response to the 1 mg overnight dexamethasone suppression test was investigated in 86 patients with unipolar primary depressive illness and 80 non-depressed controls (45 with mania and 35 with schizophrenia). The depressed patients were assigned to one of three genetic subtypes according to the family psychiatric history. Resistance to suppression of serum-cortisol by dexamethasone was found in 37 of 86 (43%) depressives and none of the 80 controls. Non-suppression distinguished the three genetic subtypes of depression, being found in 23 of 28 (82%) patients with familial pure depressive disease (F.P.D.D.), 13 of 35 (37%) patients with sporadic depressive disease (S.D.D.), and 1 of 23 (4%) patients with depression spectrum disease (D.S.D.). The three genetic subtypes were further distinguished by the age of onset, with S.D.D. the oldest, and by the number of previous depressive episodes, with F.P.D.D. the most. Severity of depression did not separate the three subtypes. This is the first report of a distinct neuroendocrine abnormality which supports an objectively defined classification of unipolar primary depressive illness. It is suggested that unipolar primary depressive illness is three or more separate illnesses, each with a potentially distinctive mode of inheritance, pathophysiology, neurochemistry, clinical course, and treatment response.

Adolescent↗

A syndrome of functional hypogonadotropic hypogonadism and sterility in a male with elevated serum estradiol.

A 36-year-old male complaining of impotence was examined. He was a genotypic male. Phenotypically, he exhibited signs of long-standing estrogen excess, such as feminine body build, gynecomastia, and varicose veins. His testes were soft and borderline small, and his prostate was small and soft. However, he had a normal-sized penis, normal male hair distribution, normal sense of smell, and normal intelligence. The laboratory data were compatible with mild hypogonadotropic hypogonadism. Serum estradiol (E2) levels were consistently elevated. The patient had azoospermia and a decreased semen volume. Inappropriately low levels of luteinizing hormone and follicle-stimulating hormone responded normally to gonadotropin-releasing hormone and clomiphene citrate. Levels of both testosterone (T) and E2 increased dramatically after prolonged clomiphene medication and in response to human chorionic gonadotropin. There was no change in either T or E2 levels in response to manipulations of the pituitary-adrenal axis. It is concluded that the elevated E2 level was responsible for suppression of gonadotropins which, in turn, caused mild hypogonadism and sterility in this patient. According to the stimulation tests, the source of the elevated E2 levels was testicular.

Adolescent↗

Gastric carcinoid with ectopic production of ACTH and beta-MSH.

A 51-year-old woman with typical Cushing's syndrome of about 9 years duration was shown to have a gastric carcinoid tumor. Plasma levels of ACTH and cortisol were elevated and lacked the normal diurnal rhythm. Urinary excretion of steroids was unaffected by the administration of either metyrapone or dexamethasone. Fluctuation in urinary steroid excretion, as well as transient hypokalemic alkalosis and glycosuria suggested periodic hormonogenesis. The extirpated gastric carcinoid was shown to contain immunoreactive ACTH and beta-MSH. However, the biologic ACTH activity was undetectable by in vivo steroidogenic assay. By gel filtration, it was demonstrated that both tumor and plasma ACTH was predominately "big" ACTH. Although postoperatively she developed hypoadrenocorticism severe enough to require ACTH treatment, her pituitary-adrenal function was gradually restored. This is the first documented case of ectopic ACTH syndrome caused by gastric carcinoid in which successful cure was achieved by surgery.

Adrenal Cortex Function Tests↗