Sjoerd B A H A Fluitman

University Medical Center Utrecht, Utrecht, Provincie Utrecht, Netherlands

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Publications (5)23.96 Total impact

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    ABSTRACT: Objective. To determine whether polymorphisms of the dopamine D(2) receptor (DRD2) and catechol-O-methyl-transferase (COMT) receptor genes affect the efficacy of quetiapine addition to citalopram in patients with OCD. Methods. Sixty-four drug-free or drug-naïve patients meeting DSM-IV criteria for OCD were randomized to 10 weeks double-blind treatment with citalopram (60 mg/day) with quetiapine (300 -450 mg/day) or with placebo. The change from baseline to endpoint on the total Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) and the response to treatment were the primary outcome measures. Response was defined as a 25% decrease in Y-BOCS score. Responders and nonresponders were stratified according to DRD2 TaqI A and COMT Val(158)Met genotypes. Results. No significant differences in genotype distribution or allele frequencies of the COMT or DRD2 receptor were found between responders and nonresponders to citalopram with quetiapine. However, nearly half of responders to citalopram with placebo carried the Met/Met (48%) genotype of the COMT polymorphism compared to none of the nonresponders (χ(2) = 10.06, df = 2, P = 0.007). Conclusions. The Met allele load of the COMT receptor gene was associated with response to 10 weeks of treatment with citalopram in drug-free or drug-naïve OCD patients.
    International Journal of Psychiatry in Clinical Practice 03/2012; 16(4):277-83. · 0.45 Impact Factor
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    ABSTRACT: Little is known about how the biological stress response systems--the autonomic nervous system (ANS), the hypothalamic-pituitary-adrenal (HPA) axis, and the immune system--function during psychosis. Results of studies on the effect of stress on the immune and autonomic system in patients with schizophrenia are inconsistent. The present study investigates whether the stress response is impaired in medication-naive patients with a first episode of psychosis. Ten male patients with a first episode of psychosis and 15 controls were exposed to the stress of public speaking. Parameters of the ANS (heart rate and catecholamines), the HPA axis (plasma adrenocorticotropic hormone [ACTH] and cortisol), and the immune system (number and activity of natural killer [NK] cells) were measured. Peak responses were calculated to examine the relationship between stress-induced activation of the different systems. Subjective stress and anxiety before and during the task were assessed. Patients and controls displayed similar autonomic responses to acute stress. However, there was an impaired HPA axis response, slow onset and return of ACTH, and flattened cortisol response and a reduced increase in number NK cells and NK cell activity in patients with a first episode of psychosis. Furthermore, in patients, the relationship between the different stress response systems was weaker or absent compared with controls. These findings indicate that impairments in stress processing are associated with the endophenotype of psychosis and are not a result of illness progression or antipsychotic medication.
    Schizophrenia Bulletin 03/2012; 38(2):272-9. · 8.80 Impact Factor
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    ABSTRACT: Major depressive disorder is associated with alterations in the neuroendocrine as well as immune system. Few studies examined the impact of electroconvulsive therapy (ECT) on these systems in patients with major depressive disorder (MDD). In this explorative study 12 patients suffering from medication-resistant MDD or MDD with psychotic features were studied during the first, the fifth and eleventh session of ECT. Blood samples were taken immediately prior to the electrostimulus and 5, 15 and 30 min after the electrostimulus to assess various lipopolysaccharide (LPS) stimulated or T-cell mitogen induced cytokines, immune cell numbers, Natural Killer cell activity, cortisol and ACTH. Acute ECT increased the LPS-stimulated production of the cytokines IL-6 and TNF-α by peripheral monocytes but not the production of the anti-inflammatory cytokine IL-10. Acute ECT decreased T cell mitogen-induced levels of IFN-γ but IL-10 and IL-4 levels were left unaffected while NK cell activity increased momentarily but significantly. Cortisol and ACTH rose significantly after electrostimulus. Repeated ECT had no significant effect on any of the parameters. The study had a small group size. Also the patient group was heterogeneous as it consisted of patients with therapy-resistant depression with or without psychotic features. Results suggest that acute ECT is associated with transient immunological and neuro-endocrine changes, while repeated ECT does not have an additive effect on the immune and neuroendocrine functions.
    Journal of affective disorders 12/2010; 131(1-3):388-92. · 3.76 Impact Factor
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    ABSTRACT: Neurobiological research of obsessive-compulsive disorder (OCD) has rarely taken in account the context dependent evocation of obsessive-compulsive symptoms. To bypass this obstacle, this study investigated neurobiological parameters during a standardized disgust provocation paradigm in patients with OCD and healthy controls. Ten OCD patients and 10 healthy controls were exposed to 9 disgust related items using a standardized provocation paradigm. Catecholamines and cortisol in plasma and lipopolysaccharide (LPS) stimulated levels of TNF-alpha and IL-6 by peripheral leucocytes were assessed along with severity of obsessive-compulsive symptoms, disgust, and anxiety levels using Visual Analogue Scales prior, during and after a provocation paradigm. Noradrenalin levels increased, while LPS stimulated TNF-alpha and IL-6 by peripheral leucocytes decreased during exposure to disgust related objects in OCD patients but not in healthy controls. Cortisol levels were not affected by exposure neither in patients nor in controls, but overall cortisol levels of OCD patients were increased compared to controls. In conclusion, our data suggests that symptom provocation in OCD patients with contamination fear is accompanied by alterations in the immune and neuroendocrine systems but does not affect cortisol levels.
    Psychoneuroendocrinology 07/2010; 35(6):906-11. · 5.14 Impact Factor
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    ABSTRACT: To assess the efficacy of quetiapine addition to citalopram in treatment-naive or medication-free obsessive-compulsive disorder (OCD) patients. Seventy-six patients who met DSM-IV criteria for OCD and who were drug-free or drug-naive at entry were randomly assigned in a 10-week, double-blind trial with citalopram (60 mg/day) plus quetiapine (300-450 mg/day) or placebo; treatment-refractory OCD patients were excluded. Of the 76 eligible patients, 66 patients completed the trial-31 in the quetiapine and 35 in the placebo group. The change from baseline to endpoint on the total Yale-Brown Obsessive Compulsive Scale (YBOCS) and the response to treatment in the quetiapine addition compared with the placebo addition group were the primary outcome measures. Response was defined as a 35% or greater reduction on the YBOCS and a Clinical Global Impressions-Improvement (CGI-I) score at endpoint of 1 or 2. The study was conducted from November 2003 to June 2005 at the University Medical Centre Utrecht, The Netherlands. As measured by the mean reduction in YBOCS scores following an intent-to-treat, last-observation-carried-forward analysis, quetiapine addition (11.9) was significantly superior to placebo (7.8; p = .009). Quetiapine addition was also significantly superior to placebo on the CGI-I scale, with a mean +/- SD CGI-I score of 2.1 +/- 1.3 versus 1.4 +/- 1.2, respectively (p = .023). Quetiapine addition (N = 22, 69%) was also associated with a significantly greater number of patients responding to treatment compared with placebo addition (N = 15, 41%; p = .019). More patients receiving quetiapine (N = 8) than placebo (N = 2; NS) discontinued treatment due to adverse events. The combination of quetiapine and citalopram was more effective than citalopram alone in reducing OCD symptoms in treatment-naive or medication-free OCD patients. www.trialregister.nl Identifier NTR116.
    The Journal of Clinical Psychiatry 07/2009; 70(7):1001-8. · 5.81 Impact Factor