E. Esel

Changes in platelet monoamine oxidase and plasma dopamine-beta-hydroxylase activities in lithium-treated bipolar patients

The activity of monoamine oxidase (MAO) and dopamine-beta-hydroxylase (DBH), enzymes involved in monoamine metabolism, were studied in 29 bipolar patients (mean age = 33.12 years, SD = 7.27) who were treated with lithium carbonate and in 20 healthy volunteers (mean age = 30.05 years, SD = 6.04). Platelet MAO activity was higher after lithium withdrawal, whereas plasma DBH activity was lower in remitted euthymic bipolar patients compared with normal volunteers. During lithium treatment, platelet MAO activity decreased and plasma DBH activity increased compared with the lithium-withdrawal values. It was also observed that the activities of these enzymes in the bipolar patients during lithium treatment did not differ from those in the volunteers. Thus, platelet MAO and plasma DBH activities differed in unmedicated patients with bipolar affective disorder from those of healthy subjects. Treatment with lithium appeared to have a normalizing effect on MAO and DBH activity levels.

Effects of olanzapine and haloperidol on serum prolactin levels in male schizophrenic patients

It has been proposed that new atypical antipsychotics cause minimal prolactin (PRL) elevation compared to traditional antipsychotic agents because they spare dopamine blockade within the brains tuberoinfundibular tract. The aim of this study was to compare the effects of olanzapine and haloperidol on PRL secretion in male schizophrenic patients. Twenty-nine male schizophrenic inpatients were included in the study. Fifteen of them were given olanzapine in a fixed dose of 10 mg/day PO and 14 of them were given haloperidol in a fixed dose of 10 mg/day PO for 6 weeks after a 2-week drug washout period. Fifteen age-matched healthy control subjects were used as control group. PRL levels were measured both before and after the 6-week treatment period in the patients. At the end of the 6th week, the PRL values observed with olanzapine treatment were significantly less than those observed with haloperidol, but not different from those of the controls. There was a significant positive correlation between the PRL values and the severity of extrapyramidal side effects in only the haloperidol group after the six weeks treatment period. Our data indicate that short-term olanzapine treatment at doses of 10 mg/day PO causes minimal elevations in PRL secretion in male schizophrenic patients in contrast to haloperidol. This finding is consistent with the previous reports and may be attributed to olanzapines differential effects on dopamine neurotransmission.

P.2.g.011 Acute and long-term effects of electroconvulsive therapy on serum leptin level in major depressive patients

Purpose: Leptin is suggested to be involved in the pathophysiology of depression. The results of the studies concerning leptin levels in depressed patients and effects of antidepressant treatment on leptin levels have so far been inconsistent (Esel et al., 2005). However, there is no study on the effects of electroconvulsive therapy (ECT) on the leptin levels yet. Thus, the purpose of the present study was to investigate whether one session or a completed cure of ECT has any effect on the levels of this protein in depressive patients. Method: Twenty-eight inpatients who fully met the DSM-IV criteria for major depressive disorder and suitable for ECT were included in the study. Twenty-five who responded to a course of ECT were evaluated in the statistical analyses (11 males, 14 females). Twenty-three healthy subjects (11 males, 12 females) composed the control group. The patients had been drug-free for at least 1 week. They remained hospitalised and were not given any drug treatment during the whole treatment period. They did not have any physical or psychiatric disease except depression. The 17-item Hamilton Rating Scale for Depression (HRSD) was used to rate the severity of depression. HRSD scores were measured before the 1st ECT and after the therapeutic response to ECT in the patient group. A decrease of 50% or more in HRSD scores was accepted as clinical response to treatment. Each patient was totally given 7−12 ECT sessions under general anaesthesia, three times a week. In the patients, serum leptin levels were measured two days before and 10 minutes after the first ECT, and three days after the last ECT. Measurements were made only once in the control group. Serum leptin levels were determined by using immunoradiometric assay kits. Appropriate statistical tests were fulfilled by taking age and BMI as covariates. Results: Age, BMI and gender ratio of the patients were not different from those of the controls. Serum leptin levels were not different between the patient and control groups neither before nor after the treatment. No significant difference was found in serum leptin levels throughout ECT treatment in the patients. The female patients had significantly higher leptin levels compared to the male patients both before and after the treatment (approximately five fold). The same difference was present in controls, too. When male and female patients were analyzed separately, there was no significant difference in serum leptin levels between the patients and the controls and pre and post treatments. There was a positive correlation between serum leptin levels and BMI in the patients. Conclusions: The findings of present study confirmed that gender difference in leptin levels reported in healthy people is also available in depressive patients. There was no significant effect of depression or ECT on serum leptin level of either male or female patients. We may suggest that leptin and related system probably do not play any role in pathophysiology of depression or in improving effect of ECT in depression.