Informed by a goal setting and self-regulation perspective, we tested a model of perceived career goal–progress discrepancies (i.e., perception of progress made towards achieving career goals relative to where one should be if the goals were to be attained), which proposed that negative feedback from significant others predicts career goal–progress discrepancies, which, in turn, predicts levels of career-related distress. The model also proposes that active feedback seeking strengthens the relationship between feedback from significant others and goal–progress discrepancies, and that career self-regulatory behaviours (career exploration and planning) weaken the relationship between career goal–progress discrepancies and career distress. Using a sample of 420 young adults (mean age = 20.3 years, 73% female), we found that feedback from significant others was related to both career goal–progress discrepancies and career distress, career goal–progress discrepancies were related to career distress, and goal–progress discrepancies partially mediated between feedback from significant others and career distress. Supporting the moderated effects, goal–progress discrepancies were higher at higher levels of negative feedback for those more actively seeking feedback, and career distress was lower at lower levels of discrepancy for those more engaged in exploration and planning.

Chronic fatigue immune dysfunction syndrome (CFIDS) is a heterogenousproblem with an ambiguous origin and characterized by a severedisabling physical and mental fatigue that is exacerbating by minorstrain. There has been a great deal of interest in neuroendocrinology onthis challenging syndrome and neuroendocrinologic data obtained sofar will be reviewed in this paper.Many studies had been performed to investigate the function of thehypothalamic-pituitary-adrenal (HPA) axis in CFIDS but the results arequite conflicting. Overall evidence of those neuroendocrinologic studiesand hormonal treatment will be discussed in this article.Many of the HPA axis studies indicate a reduced cortisol output andsymptom production are correlated in at least some CFIDS patients.There is some evidence for heightened negative feedback andchanges in glucocorticoid receptor function for impaired ACTH andcortisol responses. Furthermore, a mutation in the gene which controlsthe production of corticosteroid-binding globulin (CBG) which isassociated with complete loss of function of CBG was identified recentlyin CFIDS. However, there is no consensus on a specific dysfunction ofHPA axis in CFIDS. There is also some evidence suggesting alterationsin GH and HPT axis or DHEA function and abnormal serotonergicactivity in CFIDS. Serotonergic responses to stimulation were also foundto be inversely correlated with basal cortisol concentrations, and CFIDSpatients had reduced baseline cortisol and enhanced serotonergicresponses, opposite to depressed patients. In the phase of subacute,acute or chronic phase of CFIDS many variables may affect endocrinesystem such as sleep disturbances, inactivity-deconditioning,psychiatric comorbidity, medication, ongoing stress due to CFIDS itselfand grade or stage which the patient is in.To obtain clearer data of etiopathological relevance of endocrinealterations in CFIDS, it seems to be important to perform futurestudies, in the cohort of high-risk subjects and patients recoveredfrom CFIDS. These kinds of strategies may provide valuableinformation to identify whether the neuroendocrine abnormalities inCFIDS are an epiphenomena or trait markers and to find new facilitiesfor therapeutical interventions.

Leptin is a product of the obese gene and plays an important role in the regulation of body weight and food intake. Weight and appetite are frequently altered in depression. So far, inconsistent results have been reported in terms of leptin levels in depression. Therefore, the authors investigated serum leptin levels in patients with depression and in healthy controls, and whether there was any alteration throughout antidepressant treatment. Female patients showed significantly higher leptin levels than those of the control females both before and after the response to antidepressant treatment, whereas no difference was found between the male patients and the male controls. The improvement from depression with antidepressant treatment caused a further elevation on the leptin levels, in both female and male patients. These findings confirm an increase in leptin levels in depressive patients and presence of a sexual dimorphism. Moreover, clinical response to antidepressant treatment seems to have an additional increasing effect on leptin levels.

Chronic fatigue syndrome (CFS) is a disease characterized by debilitating fatigue of at least 6 months' duration. The pathophysiology and the localization of the underlying HPA axis disturbance are a matter of debate. Our aim was to evaluate the hypothalamopituitary-adrenal (HPA) axis by the 1 mu g adrenocorticotrophic hormone (ACTH) test and metyrapone test in patients with CFS and to compare the size of the adrenal glands of the patients with that of the control subjects. Twenty patients (14 females, 6 males) with CFS were included in the study. Fifteen healthy subjects (12 females, 3 males) served as matched controls. ACTH stimulation test was carried out by using 1 mu g ACTH, intravenously, as a bolus injection after an overnight fast, and blood samples for cortisol were drawn at 0, 30, and 60 minutes. Metyrapone at a dosage of 30 mg/kg was taken orally at 11:00 PM with a snack. The following morning, blood was sampled for serum 11-deoxycortisol between 8:00 and 9:00 AM. Peak cortisol responses to 1 mu g ACTH test were significantly lower in the CFS group (620.7 +/- 146.2 nmol/L) than in the control group (838.7 +/- 129.6 nmol/L) (P < 0.05). The lowest peak cortisol response after the 1 mu g ACTH test was 575.8 nmol/L in normal subjects. Nine patients with CFS had peak cortisol responses to 1 mu g ACTH test lower than 575.8 nmol/L. 11-deoxycortisol response to metyrapone was significantly lower in the patients with CFS (114.2 +/- 31.1 nmol/L) than in the healthy subjects (186.5 +/- 15.7 nmol/L) (P < 0.05). The lowest 11-deoxycortsol level after metyrapone in the controls was 168.3 nmol/L. Nineteen of 20 patients with CFS had lower 11-deoxycortisol level after metyrapone than detected in normal subjects. Eight patients had both subnormal 11-deoxycortisol response to metyrapone and subnormal cortisol response to 1 mu g ACTH test. On the other hand, 10 patients had subnormal 11-deoxycortisol response to metyrapone but normal cortisol response to 1 mu g ACTH test. Thickness of the right and left adrenal glands were similar between the patients with CFS and healthy subjects (P > 0.05). We conclude that the perturbation of the HPA axis in CFS is characterized by underactivation of the HPAaxis.

Primary fibromyalgia syndrome (PFS) is characterized by widespread chronic pain that affects the musculoskeletal system, fatigue, anxiety, sleep disturbance, headache and postural hypotension. The pathophysiology of PFS is unknown. The hypothalamic-pituitary-adrenal (HPA) axis seems to play an important role in PFS. Both hyperactivity and hypoactivity of the HPA axis have been reported in patients with PFS. In this study we assessed the HPA axis by 1 μg ACTH stimulation test and metyrapone test in 22 patients with PFS and in 15 age-, sex-, and body mass index (BMI)- matched controls. Metyrapone (30 mg/kg) was administered orally at 23:00 h and blood was sampled at 08:30 h the following morning for 11-deoxycortisol. ACTH stimulation test was carried out by using 1 μg (iv) ACTH as a bolus injection after an overnight fast, and blood samples were drawn at 0, 30 and 60 min. Peak cortisol level (659.4±207.2 nmol/l) was lower in the patients with PFS than peak cortisol level (838.7±129.6 nmol/l) in the control subjects ( p <0.05). Ten patients (45%) with PFS had peak cortisol responses to 1 μg ACTH test lower than the lowest peak cortisol detected in healthy controls. After metyrapone test 11-deoxycortisol level was 123.7±26 nmol/l in patients with PFS and 184.2±17.3 nmol/l in the controls ( p <0.05). Ninety five percent of the patients with PFS had lower 11-deoxycortisol level after metyrapone than the lowest 11-deoxycortisol level after metyrapone detected in healthy controls. We also compared the adrenal size of the patients with that of the healthy subjects and we found that the adrenal size between the groups was similar. This study clearly shows that HPA axis is underactivated in PFS, rather than overactivated.

Twenty-nine patients with DSM-IV diagnoses of schizophrenia were categorized into deficit syndrome (n=14) and non-deficit syndrome (n=15) subgroups on the basis of the Schedule for the Deficit Syndrome. The patients, who had all been free of antipsychotic medication for at least 3 weeks, and 17 sex- and age-matched normal controls were studied with single-photon emission computed tomography with Tc-99m HMPAO. Age at onset, Brief Psychiatric Rating Scale (BPRS) total scores, BPRS positive symptom subscores and duration of illness were similar between the two schizophrenic subgroups. As expected, the deficit patients had more negative symptoms than the non-deficit patients. There were no statistically significant correlations between clinical parameters and regional cerebral blood flow (rCBF) values. The deficit syndrome subgroup showed diminished rCBF in the frontal regions bilaterally, right parietal regions and right superior temporal region compared with the control groups. Deficit patients showed significantly lower rCBF perfusion ratios in the right superior and inferior frontal cortex than did the non-deficit patients. No differences were detected between the controls and the non-deficit schizophrenic patients in terms of rCBF perfusion indices. The results of the present study confirm previous reports of different patterns of rCBF in deficit vs. non-deficit schizophrenic subgroups.

This study aimed to assess the safety, tolerability, efficacy, and compliance of a risperidone long-acting injection (RLAI) formulation for the maintenance treatment of stabilized bipolar patients. A prospective, open-label trial of RLAI was conducted for 12 months. Stable bipolar patients (n = 11) were switched from their existing oral antipsychotic agents to RLAI, and injections were given every 2 weeks. The assessments were performed at baseline and at 6 and 12 months of treatment by using the Young Mania Rating Scale (YMRS), Clinical Global Impressions—Severity of Illness (CGI-S) scale, 17-item Hamilton Rating Scale for Depression (HAM-D), Brief Psychiatric Rating Scale (BPRS), and Extrapyramidal Symptom Rating Scale (ESRS). The satisfaction levels of subjects were evaluated at the end of the study period using a 10-point visual analog scale. Ten patients (90.9%) completed the trial, and no significant changes were seen in the YMRS, HAM-D, and BPRS scores throughout the study. CGI-S and ESRS scores were significantly decreased from the baseline to the post-12-month treatment score. Relapses were not reported by any of the participants. This result indicates that RLAI may be beneficial in the maintenance therapy of stable bipolar patients; however, an adequately powered, randomized, placebo-controlled trial is necessary to draw a definite conclusion about the role of RLAI in the maintenance treatment of bipolar patients.

Dexamethasone suppression (DST), thyroid-stimulating hormone (TSH) and prolactin (PRL) responses to thyrotropin-releasing hormone (TRH) and growth hormone (GH) response to L-DOPA tests were evaluated in 19 depressed inpatients before the commencement of the antidepressant treatment and after the clinical response to examine: (i) the functional relationships among the hypothalamic–pituitary–adrenal (HPA) and hypothalamic–pituitary–thyroid (HPT) axis and dopaminergic system in depression, (ii) any alterations in these hormonal functions with the antidepressant treatment. TSH responses to TRH showed a tendency to increase from pre- to posttreatment period, while TRH-induced PRL and L-DOPA-induced GH responses did not change with treatment in depressed patients who responded to the treatment. Females showed significantly higher TSH and PRL responses to TRH compared to males. No interconnections were found among the responses in DST, TRH stimulation test and L-DOPA-induced GH test in the patients. The results do not support the interrelations between the abnormalities in the HPT and HPA axes and central dopaminergic activity in depression.

Lithium (Li) carbonate has been reported to be able to cause some reversible functional changes in the kidney. In this study, the authors aimed to investigate whether the duration of Li treatment is the primary determinant of the changes in renal functioning due to the Li treatment. For this purpose, 10 Li-naı̈ve (mean age±S.D.: 34.50±4.85), 10 short-term (mean age±S.D.: 31.77±7.61) and 10 long-term (mean age±S.D.: 36.60±10.15) Li-treated bipolar patients were included in the study. Serum blood urea nitrogen (BUN) and creatinine, urine creatinine levels, creatinine clearance, urine osmolality before and after 8-h water deprivation and urine osmolality after desmopressin injection were measured in all patients. Serum BUN and creatinine levels were within the normal limits and not statistically different among the groups. Creatinine clearance of the long-term Li-treated group was significantly lower than both that of the Li-naı̈ve group and that of the short-term Li-treated group. After 8-h water deprivation and also after desmopressin injection, no difference was found among the groups in terms of urine osmolality. However, when each patient was evaluated individually in terms of their renal concentrating ability, partial nephrogenic diabetes insipidus was diagnosed in four patients on long-term and in two patients on short-term Li treatment. To our surprise, hypothalamic diabetes insipidus was also diagnosed in other two patients on long-term Li treatment. These results demonstrate that long-term Li treatment may cause impairment in renal concentrating ability, some of which may originate from the effects of Li on vasopressin on hypothalamic level, and a decrease in glomerular filtration rate (GFR). In the light of these data, we can conclude that long-term administration of Li may be a risk factor for Li-induced renal impairment, which is a progressive effect in nature.

There is a considerable inconsistency in terms of the association between alcoholism and alterations in monoamine oxidase (MAO) activity. The main objectives of this study were to investigate the changes in platelet MAO-B activity throughout the alcohol withdrawal period and whether or not MAO-B activity differed between patients with high- and low-aggression tendency. We assayed platelet MAO-B levels spectrophotometrically in 22 male inpatients with alcohol dependence in their first and fourth weeks of withdrawal and in 20 healthy controls. Patients were divided into two high- and low-aggression subgroups according to scores obtained in a Brown-Goodwin Assessment for Life History of Aggression. Our data revealed that the significantly lower platelet MAO-B activity observed during the first week of alcohol withdrawal in patients, compared to controls, did not continue in the fourth week, and that there was no relationship between aggressiveness and MAO activity. These results suggest that low platelet MAO activity may be a state marker of alcohol withdrawal period or a result of high alcohol consumption rather than a trait marker of alcoholism.

In this study, the authors aimed to test the hypothesis that electroconvulsive therapy (ECT) may cause some alterations in hypothalamic-pituitary-thyroid (HPT) axis hormones and these responses may change throughout respective ECT sessions. Nineteen depressed inpatients (8 males, 11 females; mean age+/-S.D.: 44.77+/-10.59 years) considered suitable for ECT were included in the study. Each patient was exposed to 7 ECT sessions with general anaesthesia. The blood samples for measurements of thyroid-stimulating hormone (TSH), free thyroiodothyronine (fT3) and free thyroxine (fT4) were drawn before (baseline) and after propofol, immediately after ECT, and 30 and 60 min after ECT during the first and last (seventh) ECTs. In both the first and seventh ECTs, there was a significant increase in TSH levels 30 min after ECT compared to the pre-ECT values. Additionally, a significant decrease in post-ECT fT4 values compared to the baseline values was found only during the seventh ECT. No difference was detected in the TSH, fT3 and fT4 responses to ECT between males and females, and between bipolar and unipolar depressive patients. These results show that ECT may have some effects on the HPT system. However, whether there is a relationship between these neuroendocrine responses and the therapeutic effect of ECT is not clear.