Biomedical subjects

A Yassouridis

Publications and source records attributed to A Yassouridis.

At least 19 recordsLinked to original sources

PubMed2006

Growth hormone-releasing hormone and corticotropin-releasing hormone enhance non-rapid-eye-movement sleep after sleep deprivation.

The neuropeptides growth hormone (GH)-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) regulate sleep and nocturnal hormone secretion in a reciprocal fashion, at least in males. GHRH promotes sleep and GH and inhibits hypothalamo-pituitary-adrenocortical (HPA) hormones. CRH exerts opposite effects. In women, a sexual dimorphism was found because GHRH impairs sleep and stimulates HPA hormones. Sleep deprivation (SD) is the most powerful stimulus for inducing sleep. Studies in rodents show a key role of GHRH in sleep promotion after SD. The effects of GHRH and CRH on sleep-endocrine activity during the recovery night after SD are unknown. We compared sleep EEG, GH, and cortisol secretion between nights before and after 40 h of SD in 48 normal women and men aged 19-67 yr. During the recovery night, GHRH, CRH, or placebo were injected repetitively. After placebo during the recovery night, non-rapid-eye-movement sleep (NREMS) and rapid-eye-movement sleep (REMS) increased and wakefulness decreased compared with the baseline night. After GHRH, the increase of NREMS and the decrease of wakefulness were more distinct than after placebo. Also, after CRH, NREMS increased higher than after placebo, and a positive correlation was found between age and the baseline-related increase of slow-wave sleep. REMS increased after placebo and after GHRH, but not after CRH. EEG spectral analysis showed increases in the lower frequencies and decreases in the higher frequencies during NREMS after each of the treatments. Cortisol and GH did not differ between baseline and recovery nights after placebo. After GHRH, GH increased and cortisol decreased. Cortisol increased after CRH. No sex differences were found in these changes. Our data suggest that GHRH and CRH augment NREMS promotion after SD. Marked differences appear to exist in peptidergic sleep regulation between spontaneous and recovery sleep.

Adult↗

PubMed2003

Clinical outcome after trimipramine in patients with delusional depression - a pilot study.

The treatment of delusional depression is a major challenge in psychopharmacology. Hypothalamic-pituitary-adrenocortical (HPA) overdrive may contribute, via increased dopaminergic activity, to the pathophysiology of the disorder. Trimipramine appears to be an interesting potential candidate, since it is an atypical antidepressant that is known to inhibit HPA activity. In a four-week open trial we investigated its effects in 15 inpatients with delusional depression. The dosage was increased within 7 days up to 300 - 400 mg/d and was then maintained for three weeks. Psychometric assessments and safety monitoring were conducted weekly. Assessment of the HPA activity was achieved by a combined dexamethasone suppression/corticotropin-releasing hormone stimulation (Dex/CRH) test before and after four weeks of treatment. Therapeutic response was defined as a decrease in the HAMD-score of at least 50 %. Eight out of 13 completers were rated as responders. Therapeutic response was associated with L, D-trimipramine concentrations higher than 160 ng/ml. Intent-to-treat analysis showed significant improvement in psychometric variables. Despite the high dosage, the substance was generally well tolerated, with the exception of one patient who suffered from a hypotensive reaction. Mean +/- SD concentration of L-trimipramine and D-trimipramine were 138 +/- 61 ng/ml and 119 +/- 50 ng/ml at a final dose of 346 +/- 50 mg/d. The ACTH and cortisol area under the curve in the Dex/CRH tests decreased significantly, reflecting a decrease of activity in the HPA system. We suggest that the clinical use of high-dose trimipramine in delusional depression seems to be a promising treatment strategy.

Adult↗

PubMed2002

[Deglutition disorders in neurological patients. A prospective study of diagnosis, pattern of impairment, therapy and outcome].

We performed a prospective study on 208 patients with neurogenic dysphagia who were consecutively admitted for swallowing therapy over a 3-year period. The most frequent etiology was stroke (48%). Videofluoroscopic and/or fiber optic endoscopic evaluation of swallowing were performed in 204 patients. Swallowing therapy was comprised of restitution methods, compensation, and adaptation, each of which was applied in more than 80% of the patients. Mean duration of swallowing therapy was 2 months (full oral patients 1 month, patients dependent on tube feeding or tracheostomy 2.5 and 3.5 months, respectively). Fifty-five percent of the patients initially dependent on tube feeding were full oral feeders after swallowing therapy. A target variable reflecting functional feeding status showed significant improvement after swallowing therapy, also in patients with a disease duration of more than half a year, ruling out spontaneous recovery as a sole explanation of amelioration. The following variables were the main contributors to outcome prediction: functional feeding status, Barthel index, duration of disease, and degree of aspiration as shown by endoscopy.

Adolescent↗

PubMed2001

Anxiolyticlike effects of atrial natriuretic peptide on cholecystokinin tetrapeptide-induced panic attacks: preliminary findings.

BACKGROUND: Panic attacks induced by administration of cholecystokinin tetrapeptide (CCK-4) have been evaluated as a valuable tool to investigate the neurobiological mechanisms involved in panic anxiety. The rationale to study the effects of natriuretic peptides on the CCK-4 response is derived from observations that atrial natriuretic peptide (ANP) is released during panic attacks in humans and has anxiolyticlike actions in various animal models. METHODS: A double-blind, placebo-controlled design was conducted in 9 patients with panic disorder and 9 similar healthy control subjects. After pretreatment with an infusion of 150 microg of ANP or placebo in random order, each subject received 50 microg of CCK-4. Psychopathological parameters as well as physiological measures were sampled before and after CCK-4 administration. RESULTS: After pretreatment with ANP, the number of CCK-4-induced panic attacks decreased from 8 to 6 in patients and from 5 to 2 in controls. Acute Panic Inventory ratings were significantly reduced in patients after ANP vs placebo pretreatment. Infusion of ANP significantly curtailed the CCK-4-induced release of corticotropin in patients. Heart rate variability analysis indicated a sympathetic stimulation by CCK-4 that was inhibited by ANP in patients and controls. CONCLUSIONS: The present study indicates that ANP exerts anxiolyticlike effects on CCK-4-stimulated anxiety attacks in patients with panic disorder. In addition, ANP produced an inhibition of the hypothalamopituitary-adrenocortical system and sympatholytic effects.

Adrenocorticotropic Hormone↗

PubMed2001

Increased alpha activity in REM sleep in de novo patients with Parkinson's disease.

We compared the sleep structure including a quantitative electroencephalographic (EEG) analysis and the frequency of periodic limb movements (PLM) in 17 patients with Parkinson's disease (PD; 10 men, seven women, mean age 65.9 years, mean Hoehn and Yahr stage 1.8) who had never been treated with dopaminergic agents (de novo), and 10 healthy controls (six men, four women, mean age 64.5 years). The REM sleep EEG of the PD patients was characterized by a sustained increase in the high-theta/alpha (7.8-10.5 Hz) frequency range during the first one-third (i.e., 11.00 p.m. to 01.40 a.m.) of the night. There was no significant difference in the sleep continuity and sleep architecture as well as in the PLM index between both groups. The analysis of the temporal dynamics of the observed changes suggests a dysregulation of the REM sleep homeostasis in the patients with PD.

Aged↗

PubMed2001

Neither major depression nor glucocorticoid treatment affects the cellular integrity of the human hippocampus.

In major depression, decreased hippocampal volume has been attributed to hypercortisolemia, a frequent sign of the disorder, because in animals an excess of corticosteroids has led to dendritic atrophy, astrogliosis and loss of neurons in this brain region. The present study is the first to investigate the structural integrity of the human hippocampus in major depression and following glucocorticoid treatment. Post-mortem hippocampal tissue from 15 patients who had had major depression or bipolar affective disorder, 10 patients who had been treated with glucocorticoids and 16 controls was assessed using haematoxylin-eosin, Nissl and Bodian staining. The patterns of reactive astrogliosis (glial fibrillary acidic protein, GFAP), synaptic density (synaptophysin), synaptic reorganization (growth-associated protein B-50) and early signs of Alzheimer's disease (Alz-50) were examined immunocytochemically. Multivariate analysis, with the patients' age, tissue fixation time and postmortem delay as covariates, was performed. There was no evidence of neuronal cell loss or other major morphological alterations in any of the groups, nor was there a significant change in the distribution pattern of synaptophysin or Alz-50. Changes in B-50 and GFAP staining were observed in the steroid-treated and depressed patients in areas CA1 and CA2 only. The human hippocampus in major depression and after glucocorticoid treatment does not reveal any major morphological changes or signs of neuronal cell death, but does show subtle alterations in B-50 and GFAP expression in selected parts of the pyramidal cell layer.

Adult↗

PubMed2001

Treatment of multiple sclerosis with Copaxone (COP): Elispot assay detects COP-induced interleukin-4 and interferon-gamma response in blood cells.

Copolymer-1 (Copaxone or COP) inhibits experimental allergic encephalomyelitis and has beneficial effects in multiple sclerosis. There is presently no practical in vitro assay for monitoring the immunological effects of COP. We used an automated, computer-assisted enzyme-linked immunoadsorbent spot assay for detecting COP-induced interferon-gamma (IFN-gamma)- and interleukin-4 (IL-4)-producing cells and a standard proliferation assay to assess the immunological response to COP in peripheral blood mononuclear cells from 20 healthy donors, 20 untreated multiple sclerosis patients and 20 COP-treated multiple sclerosis patients. Compared with untreated and healthy controls, COP-treated patients showed (i) a significant reduction of COP-induced proliferation; (ii) a positive IL-4 Elispot response mediated predominantly by CD4 cells after stimulation with a wide range of COP concentrations; and (iii) an elevated IFN-gamma response partially mediated by CD8 cells after stimulation with high COP concentrations. All three effects were COP-specific as they were not observed with the control antigens, tuberculin-purified protein or tetanus toxoid. The COP-induced changes were consistent over time and allowed correct identification of COP-treated and untreated donors in most cases. We propose that these criteria may be helpful to monitor the immunological response to COP in future clinical trials.

Adult↗

PubMed2000

Clinical characteristics and frequency of the hereditary restless legs syndrome in a population of 300 patients.

There is a genetic contribution to the idiopathic restless legs syndrome (iRLS). An autosomal dominant mode of inheritance is suspected, but as yet no gene has been identified. To assess the frequency and characteristics of the hereditary restless legs syndrome (RLS) in comparison to those of non-hereditary RLS, we analysed the clinical data of 300 RLS patients. All 300 patients diagnosed as RLS according to the criteria of the International RLS Study Group were examined using a standard questionnaire covering demographic data, family history, clinical symptoms, subjective sleep disturbances and course of the disease. In all patients a complete neurological examination was performed, and in selected cases electrophysiological examinations and polysomnographic studies. Family history was rated as definitely positive when at least one first-degree relative was examined and classified as RLS according to the criteria by one of the authors. If it proved impossible to contact family members to verify reports of a family history, the patients were classified as only having a "possible positive family history." 232 of the 300 patients had iRLS and 68 secondary RLS due to uremia (uRLS). 42.3% of the patients with iRLS and 11.7% of those with uRLS were classified as having "definite positive" hereditary RLS, with a further 12.6% of iRLS patients and 5.8% of uRLS patients as having "possible positive" hereditary RLS. Patients with definite hereditary RLS were significantly younger at the age of onset than those with a negative family history (35.45 vs. 47.17 years, p < 0.05). The clinical characteristics of the disease were similar in both groups, except that women with hereditary RLS experienced a worsening of symptoms during pregnancy (19.1% vs. 2.6%, p < 0.05). Our study shows that patients with hereditary RLS may experience an earlier onset of the disease. Hereditary and non-hereditary RLS present with similiar clinical signs and symptoms.

Adaptation, Psychological↗

PubMed2000

Multiple sclerosis: comparison of copolymer-1- reactive T cell lines from treated and untreated subjects reveals cytokine shift from T helper 1 to T helper 2 cells.

Copolymer 1 (COP), a standardized mixture of synthetic polypeptides consisting of l-glutamic acid, l-lysine, l-alanine, and l-tyrosine, has beneficial effects in multiple sclerosis and experimental autoimmune encephalomyelitis. We selected a panel of 721 COP-reactive T cell lines (TCL) from the blood of COP-treated and untreated multiple sclerosis patients and from healthy donors by using the split-well cloning technique. All TCL selected with COP proliferated in response to COP but not to myelin basic protein (MBP). Conversely, 31 control TCL selected with MBP proliferated in response to MBP but not to COP. We used intracellular double-immunofluorescence flow cytometry for quantitative analysis of cytokine production (IL-4, IFN-gamma) by the TCL. The majority of the COP-reactive TCL from untreated multiple sclerosis patients and normal donors predominantly produced IFN-gamma and, accordingly, were classified as T helper 1 cells (TH1). In contrast, the majority of the COP-reactive TCL from COP-treated patients predominantly (but not exclusively) produced IL-4-i.e., were TH2 (P < 0.05 as assessed by using a suitable preference intensity index). Longitudinal analyses revealed that the cytokine profile of COP-reactive TCL tends to shift from TH1 to TH2 during treatment. Interestingly, although there was no proliferative cross-reaction, about 10% of the COP-reactive TCL responded to MBP by secretion of small amounts of IL-4 or IFN-gamma, depending on the cytokine profile of the TCL. These results are consistent with a protective effect of COP-reactive TH2 cells. It is hypothesized that these cells are activated by COP in the periphery, migrate into the central nervous system, and produce immunomodulatory cytokines after local recognition of MBP.

Adolescent↗

PubMed2000

Sleep and periodic leg movement patterns in drug-free patients with Parkinson's disease and multiple system atrophy.

STUDY OBJECTIVE: To assess and compare polygraphic sleep measures and periodic leg movement (PLM) patterns in untreated patients with mild to moderate Parkinson's disease (PD), multiple system atrophy (MSA) and healthy age-matched controls. DESIGN: Polysomnographic recordings of 2 consecutive nights were performed in 10 patients with PD (mean age 65 years, mean Hoehn and Yahr stage 2.2), 10 patients with MSA (mean age 61 years) and in a control group of 10 healthy subjects (mean age 64 years). All patients and controls were free of antiparkinsonian medication and other centrally active drugs for 2 weeks prior to polysomnography. SETTING: NA. PATIENTS OR PARTICIPANTS: NA. INTERVENTIONS: NA. RESULTS: Sleep measures for the second night showed a significantly lower total sleep time, sleep efficiency and sleep period time in PD and MSA patients compared to healthy controls. PLM-indices during sleep and wakefulness were significantly higher in PD, but not in MSA patients compared to controls. Five patients with PD and 7 patients with MSA, but no control subject, showed abnormal rapid eye movement (REM) sleep features (i.e., REM sleep without atonia or behavioral manifestations typical for REM sleep behavior disorder). CONCLUSIONS: Sleep disruption and increased motor activity during REM and non REM sleep are a frequent finding in PD and MSA. An increased PLM index in untreated PD patients may be due to a dopaminergic deficit and is probably not associated with dopaminergic treatment.

Aged↗

PubMed2000

Behavioral and endocrine response to cholecystokinin tetrapeptide in patients with posttraumatic stress disorder.

BACKGROUND: Given the relationship between posttraumatic stress disorder (PTSD) and panic, it was of interest to examine whether panic provoking agents affect PTSD symptoms. We therefore investigated the behavioral and endocrine response of PTSD patients to the panicogen cholecystokinin tetrapeptide (CCK-4). METHODS: Eight patients with PTSD (DSM-IV) received 50 micrograms CCK-4 intravenously in a placebo-controlled, double-blind balanced design. Provocation of panic, anxiety, and flashbacks was assessed. Plasma adrenocorticotropin (ACTH) and cortisol levels after CCK-4 were measured and compared to healthy subjects matched for age, gender, and provoked symptoms. RESULTS: Despite significant effects of CCK-4 on anxiety and panic symptoms, no significant provocation of flashbacks emerged. CCK-4-induced panic symptoms showed an inverse correlation to trait dissociation. The ACTH response after CCK-4 was significantly lower in PTSD patients than in controls. Cortisol was similarly increased in both groups after CCK-4, but PTSD patients showed a more rapid decrease of stimulated cortisol concentrations. CONCLUSIONS: Panic symptoms or heightened anxiety are not necessarily conditioned stimuli for the provocation of posttraumatic flashbacks. Further studies in PTSD with different panicogens should be controlled for the potential interference of trait dissociation. Our hormone data show further evidence for a corticotropin-releasing hormone (CRH) overdrive and enhanced negative glucocorticoid feedback in PTSD patients.

Adrenocorticotropic Hormone↗

PubMed2000

Kinematic analysis of laryngeal movements in patients with neurogenic dysphagia before and after swallowing rehabilitation.

To examine whether kinematic analysis of laryngeal movements (which are closely linked to pharyngeal swallowing) can differentiate between normal and disturbed swallowing, we used a three-dimensional ultrasound movement recording system to measure the movements of the larynx during swallowing in 32 patients with neurogenic dysphagia caused by central nervous system lesions and in 32 age- and sex-matched healthy individuals. At the beginning of an inpatient rehabilitation swallowing program, laryngeal movements in 24 patients were highly disturbed in terms of velocity curve irregularities. After rehabilitation, the majority of patients with hitherto irregular velocity profiles exhibited laryngeal kinematics that were indistinguishable from those of 32 healthy subjects. Kinematic analysis of laryngeal movements, therefore, is suitable for monitoring motor recovery of swallowing disturbances in patients with neurogenic dysphagia while undergoing swallowing rehabilitation.

Adult↗

PubMed2000

Penetration of amitriptyline, but not of fluoxetine, into brain is enhanced in mice with blood-brain barrier deficiency due to mdr1a P-glycoprotein gene disruption.

Mice with a genetic disruption (knockout) of the multiple drug resistance (Mdr1a) gene were used to examine the effect of the absence of the drug-transporting P-glycoprotein at the blood-brain barrier on the uptake of amitriptyline (AMI) and fluoxetine (FLU) and their metabolites into the brain. One hour after intraperitoneal injection of AMI or FLU, knockout (-/-) and wild-type (+/+) mice were sacrificed and drug concentrations of brain, kidney, liver, testis, and plasma were measured. The plasma concentrations of the AMI metabolites and the brain:spleen ratios of AMI, nortriptyline (NOR), 10-OH-AMI and 10-OH-NOR were significantly higher in the -/- mice, demonstrating that AMI and its metabolites are substrates of the P-glycoprotein and that mdr1a activity at the level of the blood-brain barrier reduces the penetration of these substances into the brain. In contrast, tissue distributions of FLU and its metabolites among the various tissues tested were indistinguishable between groups. The herein reported differences in brain penetration of antidepressant drugs depending on the presence of the mdr1a gene may offer an explanation for differences in the treatment response at a given plasma concentration. Moreover, individual differences in mdr1 gene activity may account for variable response patterns at different episodes and development of therapy resistance.

ATP Binding Cassette Transporter, Subfamily B↗

PubMed1999

Dose-dependence of bacterial lipopolysaccharide (LPS) effects on peak response and time course of the immune-endocrine host response in humans.

OBJECTIVE AND DESIGN: Dose-dependence of lipopolysaccharide (LPS) effects on peak and time course parameters of the immune-endocrine host response was examined in a placebo-controlled design. SUBJECTS: Data from 42 male volunteers were included. TREATMENT: 0.4 or 0.8 ng LPS/kg body weight were applied at 7.00 p.m. METHODS: Body temperature, heart rate and leukocyte counts were quantified. Plasma levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), adrenocorticotropic hormone (ACTH), cortisol and human growth hormone (hGH) were measured. RESULTS: LPS increased significantly the levels of immune (TNF-alpha, IL-6) and endocrine (ACTH, cortisol) parameters. HGH secretion was advanced without changes in the total amount of hGH released. Dose-dependence of endotoxin's effects was significant for neuroendocrine (cortisol) and physiological (temperature, heart rate) parameters. Examination of time course parameters demonstrated that the higher dose of endotoxin prolonged the increases in temperature, IL-6 and cortisol levels. CONCLUSIONS: Our data show that increases in the dosage of LPS lead to differential peak responses and changed time course patterns of the human host response.

Adrenocorticotropic Hormone↗

PubMed1999

Modelling and exploring human sleep with event history analysis.

In this paper we propose the use of statistical models of event history analysis for investigating human sleep. These models provide appropriate tools for statistical evaluation when sleep data are recorded continuously over time or on a fine time grid, and are classified into sleep stages such as REM and nonREM as defined by Rechtschaffen and Kales (1968). In contrast to conventional statistical procedures, event history analysis makes full use of the information contained in sleep data, and can therefore provide new insights into non-stationary properties of sleep. Probabilities of or intensities for transitions between sleep stages are the basic quantities for characterising sleep processes. The statistical methods of event history analysis aim at modelling and estimating these intensities as functions of time, taking into account individual sleep history and assessing the influence of factors of interest, such as hormonal secretion. In this study we suggest the use of non-parametric approaches to reveal unknown functional forms of transition intensities and to explore time-varying and non-stationary effects. We then apply these techniques in a study of 30 healthy male volunteers to assess the mean population intensity and the effects of plasma cortisol concentration on the transition between selected sleep stages as well as the influence of elapsed time in a current REM period on the intensity for a transition to nonREM. The most interesting findings are that (a) the intensity of the nonREM-to-REM transitions after sleep onset in young men shows a periodicity which is similar to that of nonREM/REM cycles; (b) 30-45 min after sleep onset, young men reveal a great propensity to pass from light sleep (stages 1 or 2) into slow-wave sleep (SWS) (stages 3 or 4); (c) high cortisol levels imposed additional impulses on the transition intensity of (i) wake to sleep around 2 h after sleep onset, (ii) nonREM to REM around 6 h later, (iii) stage 1 or stage 2 sleep to SWS around 2, 4 and 6 h later and (iv) SWS to stage 1 or stage 2 sleep about 2 h later. Moreover, high cortisol concentrations at the beginning of REM periods favoured the change to nonREM sleep, whereas later their influence on a nonREM change became weak and weaker. As sleep data are also available as event-oriented data in many studies in sleep research, event history analysis applied additionally to conventional statistical procedures, such as regression analysis or analysis of variance, could help to acquire more information and knowledge about the mechanisms behind the sleep process.

Adult↗

PubMed1999

Dehydroepiandrosterone response to the adrenocorticotropin test and the combined dexamethasone and corticotropin-releasing hormone test in patients with multiple sclerosis.

Basic and clinical research suggest that disturbed neuroendocrine function may be involved in the pathogenesis and course of autoimmune diseases including multiple sclerosis (MS). Dehydroepiandrosterone (DHEA) in this connection is of particular interest as it appears to have effects on the immune system. Moreover, DHEA levels are decreased in chronic inflammatory diseases. To further investigate the role of DHEA in MS, we administered the adrenocorticotropin (ACTH) stimulation test and the combined dexamethasone and corticotropin-releasing hormone (DEX-CRH) test to 24 patients with active MS (13 women, 11 men; age 39 +/- 2 years, mean +/- SEM; Expanded Disability Status Scale, EDSS score 4.4 +/- 0. 4, mean +/- SEM; 12 with acute relapse, 12 with chronic progression) and to 18 healthy controls matched for age and sex (8 women, 10 men; age 37 +/- 3 years). There were no statistically significant differences in the plasma cortisol response to ACTH between any groups. In the DEX-CRH test, plasma cortisol concentrations showed higher values before (DEX-pretreated) and after CRH stimulation in the MS patients than in the controls (AUC(cortisol) 738.3 +/- 154.5 vs. 295.7 +/- 55.8; p < 0.05), this finding was more pronounced in chronic progressive patients. DHEA concentrations were decreased in MS patients (AUC (DHEA) 14.4 +/- 1.6 vs. 23 +/- 2.4; p < 0.05) and cortisol/DHEA ratios were increased in the patients compared to the controls (p < 0.05). There was a positive correlation between the EDSS score and maximum cortisol/DHEA ratio (r = 0.45; p = 0.031). As with the hypothalamic-pituitary-adrenal axis system, our results suggest a dysfunction in the DHEA secretion in patients with MS.

Adrenocorticotropic Hormone↗

PubMed1999

Prediction of medium-term outcome by cortisol response to the combined dexamethasone-CRH test in patients with remitted depression.

OBJECTIVE: Current hypotheses hold that mechanisms underlying abnormal hypothalamic-pituitary-adrenocortical (HPA) function are causal factors in the precipitation of depression. If this is the case, then normalization of initially disturbed HPA regulation should indicate a good prognosis and persistent HPA dysregulation should be associated with a greater likelihood of relapse or chronicity. METHOD: The combined dexamethasone/corticotropin-releasing hormone test was administered twice to inpatients with major depression (N = 40), once after initiation of treatment and once after remission, shortly before discharge. RESULTS: Patients with a high cortisol response on both occasions or with a substantially increased cortisol response at discharge were at much higher risk for relapse within the next 6 months than those with low cortisol responses. CONCLUSIONS: An easy-to-administer neuroendocrine test allows the prediction of medium-term outcome in patients with remitted depression.

Adult↗

PubMed1998

A follow-up study for estimating the effectiveness of a cross-gender hormone substitution therapy on transsexual patients.

This follow-up study was carried out to validate the effectiveness of cross-gender hormone therapy embedded in a multistep treatment concept for transsexual patients. This therapy described in detail by the authors elsewhere and presented briefly below provides cross-gender hormone substitution to obtain an assimilation of secondary sex characteristics to the desired sex as quickly as possible. Personal and social background data of 46 male-to-female (M-to-F) and 42 female-to-male (F-to-M) patients passing through different stages of the treatment concept were included. In the Endocrinological Outpatient Clinic of the Max-Planck-Institute/Munich the effectiveness of cross-gender hormone replacement therapy as well as frequency and distribution of side effects were examined by follow-up examination of endocrinological parameters. Cross-gender hormones were administered either parenterally or orally. Blood samples were collected routinely after 2 to 6 months depending on the duration of hormone substitution and complication rate. The incidence of hyperprolactinemia in estrogen-treated M-to-F transsexuals lies in the range of studies published before, whereas the number of patients developing galactorrhea is significantly lower in our patients. The incidence of thromboembolic events during the time of cross-gender hormone treatment in our patients is negligible. Changes in hematological parameters are observed under cross-gender hormone therapy. With the cross-gender hormone regimen performed by us it is possible to generate less side effects in the treatment of transsexual patients than described before.

Female↗