Amisulpride (AMS) in low dosage has been used effectively for treatment of dysthymia. Yet there is a dearth of reports on its use as an augmentation agent in therapy-resistant depression. We deal with this issue presenting case reports and a review of the literature. The addition of 50 mg amisulpride (AMS) to antidepressant therapy in seven patients with depression at different stages of treatment resistance, one of them a case of recurrent brief depression, is described in this report. Augmentation with AMS led to a profound improvement in psychopathology in most patients. The only side effects were elevation of prolactin levels and occasional weight gain. In most cases, improvement occurred early, after only 1-2 weeks of treatment. In some patients, reduction or cessation of AMS led to an immediate and intense recurrence of depressive symptoms that resembled a withdrawal syndrome. Further investigations into the clinical utility and the mode of action of AMS as an augmentation agent are warranted.
Chronic somatic comorbidities are associated with higher rates of psychiatric rehospitalization independently of psychiatric comorbidities and other clinical, sociodemographic, and lifestyle factors. Therefore, to treat psychosis effectively, it may be necessary to treat chronic somatic comorbidities promptly and adequately. Chronic somatic comorbidities should be considered equally important as the SSD, and should be brought to the forefront of psychiatric treatment and research with the SSD as one entity. The integrative approach should be the imperative in clinical practice.
Introduction
High prolactin (PRL) concentrations are found in laboratory test results of patients on majority of antipsychotic drugs. Prevalence rates and degrees of severity of hyperprolactinemia (HPRL) based on PRL concentration may depend on the presence of macroprolactin in the serum. The aim of the study was to investigate the difference between PRL concentrations before and after precipitation of macroprolactin and to examine if there were any changes in the categorization of HPRL between samples prior and after precipitation.
Materials and methods
Total of 98 female patients (median age 33; range 19-47 years) diagnosed with a psychotic disorder, proscribed antipsychotic drugs, and with HPRL were included. Total PRL concentration and PRL concentration after macroprolactin precipitation with polyethylene glycol (postPEG-PRL) were determined by the chemiluminometric method on the Beckman Coulter Access2 analyser.
Results
Total PRL concentrations (median 1471; IQC: 1064-2016 mlU/L) and postPEG-PRL concentrations (median 1453; IQC: 979-1955 mlU/L) were significantly correlated using intraclass correlation coefficient for single measurements (mean estimation 0.96; 95%CI 0.93-0.97) and average measurement (mean estimation 0.98; 95%CI 0.96-0.99), and all investigated female patient had HPRL according to PRL and postPEG-PRL concentration. The median PRL recovery following PEG precipitation was 95; IQC: 90-100%. There was substantial agreement (kappa test = 0.859, 95% CI: 0.764-0.953) between the categories of HPRL severity based on total PRL concentrations and postPEG-PRL concentrations.
Conclusion
The study demonstrated that HPRL was present in all subjects using the reference interval for total PRL concentration and postPEG-PRL concentration with no significant impact of macroprolactin presence in the serum on the categorization of patients according to severity of HPRL.
In this project, we recruited a sample of 150 patients with first episode of psychosis with schizophrenia features (FEP) and 100 healthy controls. We assessed the differences between these two groups, as well as the changes between the acute phase of illness and subsequent remission among patients over 18-month longitudinal follow-up. The assessments were divided into four work packages (WP): WP1-psychopathological status, neurocognitive functioning and emotional recognition; WP2-stress response measured by saliva cortisol during a stress paradigm; cerebral blood perfusion in the resting state (with single photon emission computed tomography (SPECT) and during activation paradigm (with Transcranial Ultrasonography Doppler (TCD); WP3-post mortem analysis in histologically prepared human cortical tissue of post mortem samples of subjects with schizophrenia in the region that synaptic alteration was suggested by WP1 and WP2; WP4-pharmacogenetic analysis (single gene polymorphisms and genome wide association study (GWAS). We expect that the analysis of these data will identify a set of markers that differentiate healthy controls from patients with FEP, and serve as an additional diagnostic tool in the first episode of psychosis, and prediction tool which can be then used to help tailoring individualized treatment options. In this paper, we describe the project protocol including aims and methods and provide a brief description of planned post mortem studies and pharmacogenetic analysis.
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