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Biomedical subjects

M Noder

Publications and source records attributed to M Noder.

9 recordsLinked to original sources
PubMed1989

[Hormonal aspects of erectile dysfunction].

Organic erectile dysfunction may be due to vascular, local, neurogenic, or hormonal disturbances. Various ascertainments of basal levels of testosterone, prolactin, and other hormones produced inconsistent results, although hyperprolactinemia and hypogonadism have been shown to be associated with erectile dysfunction. Recent studies by means of the dexamethasone suppression test (DST) revealed not only clinical but also endocrinological connections between erectile dysfunction and depression. These results suggest possible multiendocrinological alterations in some of the patients suffering from erectile dysfunction, similar to those obtained in depressive disorders.

Depressive Disorder↗
PubMed1989

Triiodothyronine, thyroxine, and TSH response to dexamethasone in depressed patients and normal controls.

In view of recent investigations concerning alterations of thyroid function in depression, the pre- and postdexamethasone levels of T3, T4, and TSH of 14 patients during depression and after recovery were studied, in addition to those of 27 healthy controls. A reduction of T3 and TSH levels was shown to be dependent on the depressive state, with a tendency to lower T4 levels after recovery. Dexamethasone had a pronounced suppressive effect on TSH levels in healthy controls and in patients after recovery, but not during the depressive episode. These results point to an inadequate suppressibility of the hypothalamo-pituitary-thyroid (HPT) axis to dexamethasone during depression. There are close interrelations between the hypothalamo-pituitary-adrenal (HPA) and the HPT axes that are possibly affected during depressive illness.

Adult↗
PubMed1989

Effects of glucocorticoids on plasma catecholamines in depression.

To explore corticosteroid-catecholamine interactions in depression, plasma dopamine, norepinephrine, and epinephrine concentrations were studied both before and after dexamethasone in 16 patients during depression and after recovery, and in 28 healthy controls. Dexamethasone had a significant suppressive effect on plasma epinephrine levels in depressed patients and controls, while dopamine and norepinephrine levels were not significantly affected following dexamethasone administration. Levels of norepinephrine, epinephrine, and cortisol were positively correlated, while dopamine showed no correlation with cortisol values. These findings point to differentiated interrelations between certain catecholamines and glucocorticoids which possibly are affected during depressive illness.

Adult↗
PubMed1988

Gonadal steroid and gonadotropin response to dexamethasone: a study in sexual dysfunction and normal controls.

Numerous investigations have reported an alteration of hormonal response to dexamethasone in depressive disorder. No such data are available in psychogenic sexual dysfunction. Pre- and postdexamethasone levels of testosterone, estradiol, LH and FSH were studied in 20 male patients with sexual dysfunction and 20 male healthy controls. Dexamethasone had no influence on testosterone, estradiol, LH and FSH in normal controls. The patients showed an increase in testosterone and LH but not in FSH levels in the morning after dexamethasone administration. When compared with basal levels, the increase in postdexamethasone levels in sexual dysfunction was significant for testosterone (delta T) but not for LH (delta LH). The altered gonadal steroid and gonadotropin response to dexamethasone in sexual dysfunction might be due to disturbances of dexamethasone metabolism and glucocorticoid receptor density comparable to similar findings in depressive disorder.

Adult↗
PubMed1987

Prolactin response to dexamethasone: a study on normal controls and depressed patients.

Pre- and post-dexamethasone prolactin and cortisol levels of 40 endogenous and non-endogenous depressive patients and of 20 controls were studied. Dexamethasone had a suppressive effect on prolactin levels, which was expressed more in normal controls and in non-endogenous depressive patients than in endogenous depression. A "prolactin suppression test" by dexamethasone was constructed and provided comparable results to the usual DST. However, it failed to be a specific marker for endogenous depression. There are close relationships between various endocrine axes, which might be altered in depression.

Adolescent↗
PubMedDate not supplied

Effects of glucocorticoids on the regulation of the hypothalamic-pituitary-somatotropic system in depression.

In order to evaluate the possible effect of glucocorticoids as neuromodulators of the hypothalamic-pituitary-somatotropic system in depression, cortisol, growth hormone (GH), and insulin-like growth factor I (IGF-I) concentrations were studied before and after oral administration of 1 mg dexamethasone at 11 p.m. in 16 patients during depression and after recovery and in 28 healthy controls. While there were no significant differences in GH and IGF-I levels between depressed, recovered and control subjects, GH and IGF-I concentrations of cortisol non-suppressors were significantly elevated compared to suppressors. Moreover, post-dexamethasone cortisol, GH, and IGF-I levels were positively correlated. Dexamethasone had a stimulating effect on GH and IGF-I values in patients during depression and in cortisol non-suppressors only; this effect was absent in recovered and in control subjects and in cortisol suppressors. Thus, hypercortisolemia may be of great importance for the dysregulation of the hypothalamic-pituitary-somatotropic system reported in depression.

Adult↗
PubMedDate not supplied

Thyroid response to dexamethasone: a study on normal controls and patients with psychogenic sexual dysfunction.

Pre- and postdexamethasone triiodothyronine (T3), thyroxine (T4), and TSH levels of thirteen patients with psychogenic sexual dysfunction and thirteen controls were studied. Patients showed lowered T4 levels in comparison with the control group whereas T3 and TSH levels did not differ significantly. Dexamethasone had a suppressive effect on TSH in patients and in controls while T3 levels were suppressed in the control group only. Patients scored significantly higher on the Hamilton Depression Scale than controls. These results compared with results obtained in patients recovered from major depression might point to endocrinological as well as clinical interrelations between psychogenic sexual dysfunction and minor depression.

Adult↗