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Biomedical subjects

A Yassouridis

Publications and source records attributed to A Yassouridis.

At least 37 records · Page 2Linked to original sources
PubMed1998

Transsexualism and osteoporosis.

The aim of this study was to investigate whether and to what extent our regime of cross-gender hormone replacement therapy might influence osteoporosis development in transsexual patients. We found that after long-term therapy the bone densities of our cross-gender hormone-treated transsexual groups (10 male-to-female and 10 female-to-male) did not show significant differences compared to those of the corresponding biological sex. Moreover, the bone-density during therapy pointed out very little variability and that independent of the gender-alteration (transsexuality-direction) and the age of the transsexuals. Our results indicate that for transsexual patients treated with cross-gender hormone replacement therapy the risk of developing osteoporosis is low.

Adult↗
PubMed1998

Combined treatment of schizophrenic psychoses with haloperidol and valproate.

In accordance with a previous study of adjuvant effects of the anticonvulsant carbamazepine (CBZ) on the neuroleptic treatment of schizophrenic psychoses, the effects of valproate (VPA) were tested in a randomly assigned double-blind, placebo-controlled study. Apart from a (statistically nonsignificant) psychopathological deterioration following discontinuation of VPA while on continuous neuroleptic mediation after four weeks and a statistically significant effect on "hostile belligerence", no overall therapeutic effects of the combination of haloperidol (HPD) with VPA were observed under controlled conditions. Unlike the results with CBZ, concomitant use of VPA led to an even higher consumption of haloperidol and biperiden and to a higher rate of extrapyramidal symptoms compared with the corresponding placebo group, although these differences did not attain statistical significance. In regard to use of the sedative neuroleptic chlorprothixene, there was a trend toward lower doses in the VPA group than in the placebo group. From these results, adjuvant effects like those of carbamazepine in the neuroleptic treatment of schizophrenic psychoses could not be confirmed for valproate in the present study. However, the trend toward lower doses of sedative medication and observed effects on "hostile belligerence" may indicate sedative and/or antimanic properties of valproate which have recently been demonstrated in several controlled studies.

Adult↗
PubMed1998

Neurobehavioural disturbances, rehabilitation outcome, and lesion site in patients after rupture and repair of anterior communicating artery aneurysm.

OBJECTIVE: To determine: (1) patterns of cognitive and psychiatric dysfunction; (2) those neurobehavioural parameters which mostly influence disability in activities of daily living (ADL) and handicap in occupational and psychosocial activities, and (3) underlying neuroanatomical pathology in patients after rupture and repair of anterior communicating artery (ACoA) aneurysm. METHODS: 30 patients were extensively examined by means of a comprehensive battery of neuropsychological tests, by rating of psychopathological symptoms, and by use of the functional independence measure (FIM), Glasgow outcome scale (GOS), and MRI. RESULTS AND CONCLUSIONS: (1) Three main groups were characterised by primary impairment of memory, executive functions, or of attentional performance. Within these main groups, specific patterns were identified relating to extent of primary dysfunction and associated disorders. The variety of neuropsychological disturbances is in contradiction to the existence of an "ACoA syndrome" as an entity. (2) Rehabilitation outcome proved to be mostly associated with both memory and attentional performance. (3) In neuropathological terms, lesions of the medial septum and nucleus of the diagonal band of Broca (MS/ndbB) were closely associated with memory deficits and prefrontal lesions were associated with attentional, executive, and psychopathological dysfunctions. At the same time, bilateral lesions were associated with severe disturbances. The type and severity of the above mentioned deficits were independent of the side of lesion in unilateral cases, of rectus gyrus resection, and of the Hunt and Hess grading system.

Activities of Daily Living↗
PubMed1998

Effect of flumazenil in lactate-sensitive patients with panic disorder.

OBJECTIVE: Flumazenil is a benzodiazepine receptor antagonist that has been reported to provoke panic attacks in patients with panic disorder. This study was undertaken to compare the effects of flumazenil and sodium lactate, the most widely studied panic provocation agent. METHOD: Ten patients with panic disorder were given infusions of saline, sodium lactate, and flumazenil in randomized order. Panic attacks, psychopathological changes, heart rate, and cortisol and ACTH secretion were recorded. RESULTS: Eight of the 10 patients experienced a panic attack after sodium lactate, but none did after flumazenil or saline. Cortisol and ACTH secretion were not enhanced by any of the treatments. Sodium lactate increased heart rate, whereas flumazenil had the opposite effect. CONCLUSIONS: These findings do not lend support to the view that the benzodiazepine receptors of lactate-susceptible patients with panic disorder are hypersensitive and that flumazenil can therefore act as an inverse agonist.

Adrenocorticotropic Hormone↗
PubMed1997

Influence of clonidine on psychopathological, endocrine and respiratory effects of cholecystokinin tetrapeptide in patients with panic disorder.

The influence of clonidine pretreatment on psychopathological, endocrine and respiratory effects of cholecystokinin tetrapeptide (CCK-4) was characterized. Patients with panic disorder (DSM-III-R) were given 50 micrograms CCK-4 i.v. at 1100 hours on 2 separate study days. In a randomized double-blind design they were additionally infused with 150 micrograms clonidine or placebo from 1040 to 1110 hours. After CCK-4 all patients experienced symptom attacks. No effects of clonidine on panic psychopathology or blood gas parameters were observed. After CCK-4, in the clonidine condition the pituitary release of adrenocorticotropin (ACTH) and prolactin was seemingly enhanced compared to placebo. Our results suggest that CCK-4-induced panic attacks are not suppressible by presynaptic alpha-2 receptor stimulation. Moreover, they point to a synergistic postsynaptic action of clonidine to CCK-4 upon pituitary hormone secretion. The diverging sites of action might possibly explain the discrepancies of psychopathological alterations and stress hormone secretion.

Adrenergic alpha-Agonists↗
PubMed1997

Central administration of IL-1 reduces anxiety and induces sickness behaviour in rats.

In the present study, we examined the effects of various doses of recombinant human interleukin-1beta on anxiety-like behaviour, on body temperature, and on behavioural changes typical of sick animals. First, we assessed the behaviour of rats in the elevated plus-maze before and 20 min after intracerebroventricular injection of IL-1 at six doses ranging from 0.001 to 100 ng. After treatment with 0.1 and 100 ng IL-1, animals exhibited different anxiety levels. The dose effect on behavioural performance in the plus-maze appears to be nonlinear (parabolic function), with the highest effects near a 0.1-ng dose and the lowest near doses of 0.0 and 100 ng. In a second set of experiments, we examined the effects of doses of 0.1 and 100 ng IL-1 (which had the most pronounced effects on performance in the plus-maze) on physical parameters over a 24-h period. Using radiotelemetry we measured body temperature, locomotor activity, food intake, and water consumption: a) in animals kept under basal resting conditions, and b) in animals exposed to a novel environment prior to administration of IL-1. Both doses evoked a fever response and reduced locomotor activity, but the increase in body temperature did not correlate with the decrease in locomotor activity and both effects did not occur at the time of behavioural testing. Taken together, our data indicate that central administration of IL-1 has anxiolytic-like properties.

Animals↗
PubMed1997

Autonomic reactivity and hormonal secretion in lactate-induced panic attacks.

To compare autonomic and neuroendocrine responses during lactate-induced panic attacks, heart rate variability and cortisol and atrial natriuretic hormone (ANH) levels were measured in patients with panic attacks and in healthy control subjects. In a randomized double-blind design, all subjects received either 10 ml/kg body weight of 0.5 M racemic sodium lactate or normal saline from 1100 to 1120. Spectral analysis of the R-R interval of analog electrocardiograms was performed, and total (0.001-0.45 Hz), low-frequency (0.01-0.05 Hz), midfrequency (0.05-0.15 Hz), and high-frequency power (0.15-0.45 Hz) were computed. Cortisol was measured 12 times in the period from 0900 to 1300, and ANH was measured at 1100, 1120, and 1200 by radioimmunoassay. In both panickers (n = 6) and nonpanickers (n = 8), an infusion of lactate resulted in an acceleration of heart rate, a reduction in total spectral power, and a decrease in the high- and low-frequency components of spectral power. Panickers showed a significant enhancement of the high-frequency power, whereas in nonpanickers, a shift from the mid- and high-frequency toward the low-frequency power emerged. ANH plasma concentrations during lactate infusion in panickers showed a significant increase (115 and 131% at 1120 and 1200, respectively, over concentrations at 1100) in contrast to nonpanickers (20 and 74%, respectively). No group or treatment effects on cortisol secretion emerged, which is in line with former reports. Our study supports preliminary observations that lactate-induced panic attacks enhance the release of ANH, a vasodilatator and inhibitor of sympathetic activity. Hence this hormone not only could inhibit the secretion of the stress hormone cortisol but, in parallel, could also attenuate the sympathetic stimulation to the heart. These inhibitory effects of ANH could explain the so-far-unresolved dissociation between psychopathological alterations and autonomic and endocrine responses of panic attacks.

Adult↗
PubMed1997

Corticotropin-releasing hormone inhibits melatonin secretion in healthy volunteers--a potential link to low-melatonin syndrome in depression?

Interactions between the hypothalamic-pituitary-adrenocortical (HPA) system and melatonin secretion have been demonstrated, but only the effects of melatonin on the activity of the HPA system have been studied in man. Alterations of melatonin secretion described as low-melatonin syndrome have been demonstrated in patients suffering from a major depressive episode, and an inhibitory factor on melatonin secretion has been postulated. We investigated whether corticotropin-releasing hormone (CRH), which is thought to be involved in HPA abnormalities in depressed patients, can also suppress melatonin secretion in healthy volunteers. Ten healthy male human volunteers in a double-blind study design received randomized hourly intravenous injections from 08.00 to 18.00 h that contained 10 micrograms human CRH, 1 microgram adrenocorticotropic hormone (ACTH), or placebo to simulate pulsatile hormone secretion. Plasma melatonin and cortisol responses during the treatment and nocturnal sleep electroencephalograms after the treatment were recorded. Administration of CRH reduced melatonin secretion significantly below values obtained after administration of placebo and ACTH. Cortisol secretion was significantly enhanced by ACTH in comparison to both placebo and CRH. Electroencephalographic sleep parameters revealed no treatment effects. Our findings suggest that CRH has an inhibitory effect on the pineal secretion of melatonin in normal man. A mechanism via a release of cortisol was not supported by our results. Secondary hormonal effects from changes in nocturnal sleep architecture were excluded. Further investigation of the action of CRH on melatonin secretion as well as the mutual feedback between the HPA system and the pineal gland may extend our knowledge of neuroendocrine alterations mediating the adaptive response to stress and the eventual involvement in the pathogenesis of depression.

Adult↗
PubMed1997

Corticosteroid receptor function is decreased in depressed patients.

Decreased feedback control of the hypothalamic-pituitary-adrenocortical (HPA) system as revealed by the combined dexamethasone and corticotropin-releasing hormone (DEX-CRH) test has been documented in the vast majority of patients with affective disorders. This finding was interpreted as a failure at the level of the glucocorticoid receptor (GR)-mediated feedback action, which apparently fails to restrain HPA activity in the presence of elevated plasma corticosteroid levels. To test this hypothesis we conducted the DEX/CRH test using increasing doses of DEX in order to establish a dose-response relationship. We used three different DEX doses (0.75, 1.5, 3.0 mg) in three groups of depressed patients and controls. As expected, increasing DEX doses were associated with decreasing amounts of adrenocorticotropin (ACTH) and cortisol being released after CRH injection. However, dose-response curves for both plasma ACTH and cortisol concentrations were shifted to higher area under the curve (AUC) values among patients compared to controls. Pretreatment with 0.75 and 1.5 mg DEX produced significantly higher AUC values for both plasma ACTH and cortisol values among patients. These differences became less obvious with the higher DEX doses, indicating that the dose of 1.5 mg used in the majority of clinical studies so far is well suited to differentiate between healthy controls and patients. The reported data here are consistent with the hypothesis that an altered GR capacity or function underlies the exaggerated HPA activity in depression.

Adrenocorticotropic Hormone↗
PubMed1996

No tolerance to peripheral morphine analgesia in presence of opioid expression in inflamed synovia.

Pain treatment with centrally acting opiates is limited by tolerance. Tolerance is a decreasing effect of a drug with prolonged administration of that drug or of a related (e.g., endogenous) compound acting at the same receptor. This is often associated with a downregulation of receptors. In peripheral inflamed tissue, both locally expressed opioid peptides and morphine can produce powerful analgesia mediated by similar populations of opioid receptors. We hypothesized that the chronic presence of endogenous opioids in inflamed joints might convey downregulation of peripheral opioid receptors and tolerance to the analgesic effects of intraarticular morphine. We assessed these effects after arthroscopic surgery in patients with and without histologically verified synovial cellular infiltration, and we examined synovial opioid peptides and opioid receptors by immunocytochemistry and autoradiography, respectively. We found that, despite an abundance of opioid-containing cells in pronounced synovitis, morphine is at least as effective as in patients without such cellular infiltrations, and there is no major downregulation of peripheral opioid receptors. Thus, opioids expressed in inflamed tissue do not produce tolerance to peripheral morphine analgesia. Tolerance may be less pronounced for peripherally than for centrally acting opioids, which provides a promising perspective for the treatment of chronic pain in arthritis and other inflammatory conditions.

Adolescent↗
PubMed1996

Trimipramine and imipramine exert different effects on the sleep EEG and on nocturnal hormone secretion during treatment of major depression.

In a 4-week double-blind clinical trial we compared the effects of the tricyclic antidepressants trimipramine and imipramine on the sleep EEG and on nocturnal bormone secretion in 20 male inpatients with major depression. Both treatments produced rapid significant clinical improvement in depression without severe adverse effects. However, the two drugs had markedly different neurobiologic profiles. Trimipramine enhanced rapid eye movement (REM) sleep and slow wave sleep, whereas imipramine suppressed REM sleep and showed no effect on slow wave sleep. Total sleep time and the sleep efficiency index increased under trimipramine but not under imipramine. Nocturnal cortisol secretion decreased with trimipramine but remained unchanged with imipramine. In contrast to imipramine, trimipramine induced an increase in prolactin secretion compatible with its known antagonism at dopamine (D2) receptors. Imipramine induced a decrease in growth hormone secretion during the first half of the night. Neither of the drugs induced significant changes in plasma testosterone concentration. We conclude that trimipramine is an antidepressant with sleep-improving qualities that possibly acts through inhibition of hypothalamic-pituitary-adrenocortical system activity by a yet unknown mechanism.

Adult↗
PubMed1996

Heterogeneity of hypothalamic-pituitary-adrenal system response to a combined dexamethasone-CRH test in multiple sclerosis.

The endocrine system participates in the regulation of the immune and neural systems and therefore hormonal factors probably play an important role in the development and course of multiple sclerosis (MS). Specifically, the hypothalamic-pituitary-adrenal (HPA) system seems crucial because (a) the inflammatory response is accompanied by HPA activation; (b) animal models with an inherited HPA defect are prone to developing experimental autoimmune encephalitis; and (c) most important, corticosteroids are still the most widely used treatment. We administered a recently developed neuroendocrine function test that combines dexamethasone suppression (1.5 mg orally at 2300 h) and corticotropin-releasing hormone (CRH) stimulation (100 micrograms i.v. at 1500 h the following day) and measured the response of plasma cortisol and corticotrophin (ACTH) secretion in 19 patients with an acute exacerbation of MS. These patients had a significantly higher mean plasma cortisol response than age-matched controls (peak minus baseline; 48.1 +/- 10.5 ng/ml [mean +/- SEM] versus 19.8 +/- 4.2 ng/ml; p < 0.05), but the corresponding ACTH values for the two groups were indistinguishable (13.4 +/- 1.4 pg/ml [mean +/- SEM] versus 11.3 +/- 1.4 pg/ml; n.s.). The response range in the patients was broader and we identified six patients with excessive cortisol release (peak minus baseline: 100.5 +/- 14.4 ng/ml [mean +/- SEM]), whereas four patients failed to respond at all. The hormonal response patterns were not related to previous treatments with corticosteroids or other immunosuppressants or to psychopathological features. These results point to a heterogeneity of HPA system function, most likely at the corticosteroid receptor level, which has clinical implications for all those treatments that affect the HPA system and the course of MS.

Adrenocorticotropic Hormone↗
PubMed1996

Pituitary-adrenal-system regulation and psychopathology during amitriptyline treatment in elderly depressed patients and normal comparison subjects.

OBJECTIVE: This study was done to compare the effects of 6-week treatment with amitriptyline on hypothalamic-pituitary-adrenocortical (HPA) regulation in elderly depressed patients and age-matched comparison subjects. METHOD: A combined dexamethasone-suppression/CRH-stimulation (dexamethasone/CRH) test was administered before initiation of amitriptyline treatment and at the end of weeks 1, 3, and 6 of treatment. Thirty-nine depressed inpatients, mean age = 69 years, completed the study. Fourteen normal volunteers, mean age = 67 years, served as comparison subjects. RESULTS: In relation to the comparison subjects, the depressed patients had a profoundly abnormal HPA response, in particular an exaggerated cortisol release in the dexamethasone/CRH test. This abnormality began to disappear after 1 week of treatment with amitriptyline. In contrast, amitriptyline did not affect neuroendocrine regulation in the comparison subjects at any time during the test period. CONCLUSIONS: The data suggest that amitriptyline affects HPA regulation in hypercortisolemic depression only, and they raise the possibility that normalization of its feedback control is related to the antidepressive effect of amitriptyline.

Aged↗
PubMed1995

Possible role of atrial natriuretic hormone in pituitary-adrenocortical unresponsiveness in lactate-induced panic.

OBJECTIVE: This study investigated whether lactate-induced panic attacks in patients with panic disorder would activate atrial natriuretic hormone, which could explain the missing ACTH and cortisol response found in this kind of experimentally induced panic. METHOD: Sodium lactate and placebo infusions were administered to 10 patients with panic disorder and to 10 healthy comparison subjects, and the atrial natriuretic hormone responses of the two groups were compared. RESULTS: During lactate infusion both the seven patients who had panic attacks and the eight comparison subjects who did not responded with increased plasma concentrations of atrial natriuretic hormone, but the patients had more pronounced surges of the hormone. CONCLUSIONS: Because atrial natriuretic hormone suppresses both pituitary ACTH and adrenal cortisol release, the authors suggest that the immediate rise of atrial natriuretic hormone explains the reported lack of pituitary-adrenocortical activation during lactate-induced panic.

Adrenocorticotropic Hormone↗
PubMed1994

Reduced availability of milk after central injections of corticotropin-releasing hormone in lactating rats.

Corticotropin-releasing hormone (CRH) plays a major role in activating the pituitary-adrenal axis in stress; its central application may therefore be expected to mimic stress. Since stress reportedly disrupts lactation, experiments were designed to study the effects of CRH administration upon the transfer of milk from rat mothers to their pups and to examine some of the possible underlying physiological mechanisms. CRH was administered intracerebroventricularly to primiparous rats on the 8th day of lactation immediately prior to being reunited with 8 of their overnight-separated pups. Changes in litter weights were measured for a period of up to 4 h as an index of milk procurement by the young (milk transfer); a qualitative assessment of maternal behaviour was also made. Treatment of dams with 0.1-1 nmol CRH resulted in a dose-dependent reduction in the amount of milk obtained by the pups. Conscious mothers treated with CRH initially showed intense behavioural activation; these events (mainly hyperlocomotion and grooming) in the mother resulted in reduced opportunities for nipple attachment by the pups and, thus, milk transfer. On the other hand, milk transfer was also significantly reduced in urethane-anaesthetized mothers treated with CRH, indicating that behavioural activation cannot have been the sole factor underlying the CRH-induced inhibition of milk transfer in awake dams. Although oxytocin (OT) release is stimulated by a variety of stressors, the possibility of an inhibitory effect of CRH upon OT secretion and/or disruption of the reflex arc serving milk ejection was considered. The peripheral administration of OT (100 mU/rat s.c.) did not, however, surmount the inhibitory actions of CRH upon milk transfer.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗