ABSTRACT
OBJECTIVE: Oxidative stress may be an important pathogenic mechanism in the obesity and metabolic syndrome. The aims of this study was to assess the possible association between the oxidative stress related Glutathione S-Transferase genes (GST-M1, GST-T1, and GST-P1) variants and the olanzapine-induced weight gain in Korean schizophrenic patients. METHODS: We categorized 78 schizophrenic patients into two groups the more than 7% weight gain from baseline (weight gain > or =7%) and the less weight gain (weight gain or =7% compared to subjects with body weight gain 0.05). No significant difference in GST-P1 genotype and allele frequencies were observed between the groups (p>0.05). MDR analysis did not show a significant interaction between the three GST gene variants and susceptibility to weight gain (p>0.05). CONCLUSION: These findings do not support a relationship between the genetic variants of three GST genes (GST-M1, -T1 and -P1) and weight gain in Korean schizophrenic patients receiving olanzapine treatment.
Subject(s)
Humans , Benzodiazepines , Body Weight , Body Weight Changes , Cohort Studies , Gene Frequency , Genotype , Glutathione , Glutathione Transferase , Multifactor Dimensionality Reduction , Obesity , Oxidative Stress , Weight GainABSTRACT
Bupropion is a selective norepinephrine and dopamine reuptake inhibitor with no serotonergic activity, and is therefore an antidepressant with unique pharmacological properties. There are some reports that selective serotonin reuptake inhibitors (SSRIs) or mirtazapine can induce adverse effects including restless legs syndrome (RLS) and that bupropion can reverse these adverse effects. Here, we report about a patient with a major depressive disorder who exhibited RLS after being treated with pregabalin and mirtazapine. This adverse effect disappeared after having switched from mirtazapine to bupropion. Bupropion inhibits the reuptake of dopamine and increases dopamine neurotransmission in both the nucleus accumbens and the prefrontal cortex. This pharmacological profile can be effective in patients with RLS related to dopamine hypoactivity. However, the limitations of this single case report mean that further investigations with larger samples are needed.
Subject(s)
Humans , Bupropion , Depressive Disorder, Major , Dopamine , gamma-Aminobutyric Acid , Mianserin , Norepinephrine , Nucleus Accumbens , Prefrontal Cortex , Restless Legs Syndrome , Selective Serotonin Reuptake Inhibitors , Synaptic Transmission , PregabalinABSTRACT
Bupropion is a selective norepinephrine and dopamine reuptake inhibitor with no serotonergic activity, and is therefore an antidepressant with unique pharmacological properties. There are some reports that selective serotonin reuptake inhibitors (SSRIs) or mirtazapine can induce adverse effects including restless legs syndrome (RLS) and that bupropion can reverse these adverse effects. Here, we report about a patient with a major depressive disorder who exhibited RLS after being treated with pregabalin and mirtazapine. This adverse effect disappeared after having switched from mirtazapine to bupropion. Bupropion inhibits the reuptake of dopamine and increases dopamine neurotransmission in both the nucleus accumbens and the prefrontal cortex. This pharmacological profile can be effective in patients with RLS related to dopamine hypoactivity. However, the limitations of this single case report mean that further investigations with larger samples are needed.