Browsing by Author "Buzadžić, Ivana (38661047900)"

Introduction: Sham-controlled low-frequency repetitive transcranial magnetic stimulation (rTMS) was used in patients with pharmacoresistant major depressionas anadded treatment along with partial sleep deprivation (PSD). In addition, the potential predictive role of brain-derived neurotrophic factor genetic polymorphism on treatment response was analyzed.; Methods: We recruited 19 female patients (48.3 ± 8.6 years old) with treatment-resistant unipolar major depression (Hamilton Depression Rating Scale [HDRS] score ≥20) who were on a stable antidepressant treatment. They received either 1-Hz rTMS or sham stimulation over the right dorsolateral prefrontal cortex (intensity of 110% of the threshold; 3000 stimuli per protocol; and 10 daily sessions). Additionally, PSD was applied once per week during the treatment. The patients were evaluated (HDRS and Clinical Global Impression Scale) by a blind rater at baseline (B) and after 2 and 3 weeks (W2 and W3) of treatment for short-term outcome. Long-term evaluations were performed after 12 (W12) and 24 weeks (W24) for patients who received active stimulation.; Results: Eleven patients in the active group showed a significant HDRS score reduction from 30.09 ± 3.53 (B) to 16.73 ± 5.71 (W3) compared to the lack of therapeutic response in the sham-treated patients. The long-term follow-up for the active group included 64% of the responders at W12 and 55% at W24. Full remission (HDRS ≤10) was achieved in 5 of 11 patients. Four of these 5 patients with long-term sustained remission expressed the Val66Val genotype.; Conclusion: Our study suggests a clinically relevant response, persisting for up to 6 months, from 1-Hz rTMS over the right dorsolateral prefrontal cortex and PSD in patients with pharmacoresistant major depression. The brain-derived neurotrophic factor Val66Val homozygous genotype may be related to a better treatment outcome. Copyright © 2014 by Lippincott Williams & Wilkins.

Introduction: Sham-controlled low-frequency repetitive transcranial magnetic stimulation (rTMS) was used in patients with pharmacoresistant major depressionas anadded treatment along with partial sleep deprivation (PSD). In addition, the potential predictive role of brain-derived neurotrophic factor genetic polymorphism on treatment response was analyzed.; Methods: We recruited 19 female patients (48.3 ± 8.6 years old) with treatment-resistant unipolar major depression (Hamilton Depression Rating Scale [HDRS] score ≥20) who were on a stable antidepressant treatment. They received either 1-Hz rTMS or sham stimulation over the right dorsolateral prefrontal cortex (intensity of 110% of the threshold; 3000 stimuli per protocol; and 10 daily sessions). Additionally, PSD was applied once per week during the treatment. The patients were evaluated (HDRS and Clinical Global Impression Scale) by a blind rater at baseline (B) and after 2 and 3 weeks (W2 and W3) of treatment for short-term outcome. Long-term evaluations were performed after 12 (W12) and 24 weeks (W24) for patients who received active stimulation.; Results: Eleven patients in the active group showed a significant HDRS score reduction from 30.09 ± 3.53 (B) to 16.73 ± 5.71 (W3) compared to the lack of therapeutic response in the sham-treated patients. The long-term follow-up for the active group included 64% of the responders at W12 and 55% at W24. Full remission (HDRS ≤10) was achieved in 5 of 11 patients. Four of these 5 patients with long-term sustained remission expressed the Val66Val genotype.; Conclusion: Our study suggests a clinically relevant response, persisting for up to 6 months, from 1-Hz rTMS over the right dorsolateral prefrontal cortex and PSD in patients with pharmacoresistant major depression. The brain-derived neurotrophic factor Val66Val homozygous genotype may be related to a better treatment outcome. Copyright © 2014 by Lippincott Williams & Wilkins.

The introduction of antipsychotic medication in the 1950s forever changed the outlook on the treatment of schizophrenia, although there is still a large proportion of patients who do not reach functional recovery. At least 30% of patients do not respond to clozapine, the tricyclic dibenzodiazepine with complex pharmacological actions, which was proven to be more effective than any other antipsychotic in the treatment of schizophrenia. According to most of the therapeutic guidelines for schizophrenia, clozapine is the third line therapy for patients who did not respond to other antipsychotics. Large inter-individual variability exists for clozapine bioavailability and plasma steadystate concentrations and clearance. Clozapine is metabolized by the cytochrome P450 oxidase enzyme family (CYP450). Cytochrome P450 1A2 (CYP1A2), which is polymorphically expressed in humans, is the main enzyme of clozapine metabolism. This case report addresses the influence of CYP1A2∗1F genetic polymorphism on cloza - pine metabolism, explains the primary non-response of a young patient with schizophrenia due to increased gene expression in homozygous genotype ∗1F/∗1F (increased metabolism of clozapine) and underlies the importance of personalizing schizophrenia treatment by means of genetic and other molecular tools, at least in the cases of "treatment resistance". © by Nadja P. Marić 2015.

The introduction of antipsychotic medication in the 1950s forever changed the outlook on the treatment of schizophrenia, although there is still a large proportion of patients who do not reach functional recovery. At least 30% of patients do not respond to clozapine, the tricyclic dibenzodiazepine with complex pharmacological actions, which was proven to be more effective than any other antipsychotic in the treatment of schizophrenia. According to most of the therapeutic guidelines for schizophrenia, clozapine is the third line therapy for patients who did not respond to other antipsychotics. Large inter-individual variability exists for clozapine bioavailability and plasma steadystate concentrations and clearance. Clozapine is metabolized by the cytochrome P450 oxidase enzyme family (CYP450). Cytochrome P450 1A2 (CYP1A2), which is polymorphically expressed in humans, is the main enzyme of clozapine metabolism. This case report addresses the influence of CYP1A2∗1F genetic polymorphism on cloza - pine metabolism, explains the primary non-response of a young patient with schizophrenia due to increased gene expression in homozygous genotype ∗1F/∗1F (increased metabolism of clozapine) and underlies the importance of personalizing schizophrenia treatment by means of genetic and other molecular tools, at least in the cases of "treatment resistance". © by Nadja P. Marić 2015.