ObjectiveSSRIs are some of the most widely prescribed medications in the world. In addition to their effectiveness, SSRIs were reported to be associated with the side effects of weight gain, sexual dysfunction, drug interactions, extrapyramidal symptoms and discontinuation symptoms. However, the effects of SSRIs on metabolic parameters are poorly understood.MethodsThis study aims to describe the effects of SSRIs on the metabolic parameters of drug-naive first episode patients with generalized anxiety disorder. Ninety-seven female patients aged 20-41 years without any metabolic or psychiatric comorbidity were included in the study. Fluoxetine, sertraline, paroxetine, citalopram and escitalopram were randomly given to the patients. Metabolic parameters, including BMI, waist circumference and the levels of fasting glucose, total cholesterol, triglyceride, HDL, LDL and blood pressure, were measured before and after 16 weeks of treatment.ResultsIn the paroxetine group, there was a significant increase in the parameters of weight, BMI, waist circumference, fasting glucose, total cholesterol, LDL and triglyceride after 16 weeks of treatment. There were significant increases in the levels of triglyceride in the citalopram and escitalopram groups. In the sertraline group, the total cholesterol level increased after treatment. In the fluoxetine group, there were significant reductions in the parameters of weight, total cholesterol and triglyceride.ConclusionTo our knowledge, this study is the first to prospectively describe metabolic syndrome abnormalities in patients with first episode generalized anxiety disorder. Although the effectiveness of the different SSRIs is similar, clinicians should be more careful when prescribing SSRIs to patients who have cardiac risk factors. Larger and lengthier controlled clinical trials are needed to explore the associations between SSRI use and metabolic syndrome.

BackgroundSecond generation antipsychotics (SGAs) are currently the most prescribed drugs in the treatment of schizophrenia. Despite their advantages, which include greater improvement in negative symptoms, cognitive function, prevention of deterioration, quality of life, and fewer extrapyramidal symptoms, the concern regarding metabolic abnormalities which might cause cardiovascular diseases during treatment with SGAs have been rising. Paraoxonase 1 (PON1) is an enzyme mostly located on high-density lipoprotein particles, and has been shown to protect or inhibit lipoprotein oxidation. Growing evidence suggests that PON1 plays a key role in the pathophysiology of atherosclerosis.MethodsIn the present study, we measured serum PON1 activity and serum levels of total cholesterol (TC), triglyceride, high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) in patients with schizophrenia, who had been treated with either olanzapine or quetiapine, and in healthy controls. Thirty five patients who had been treated with olanzapine, 29 patients who had been treated with quetiapine, and 32 age, sex, and smoking status-matched healthy control (HC) participants were enrolled. Serum PON1 activity and serum levels of TC, triglyceride, HDL-C, and LDL-C were measured.ResultsSerum PON1 activity in the olanzapine group was significantly lower than that of HC and quetiapine groups. Furthermore, serum levels of TC and LDL-C in the olanzapine group were significantly higher than those of quetiapine and HC groups. Interestingly, there was a positive correlation between PON1 activity and HDL-C levels in the olanzapine group.ConclusionThese findings suggest that serum PON1 activity in patients treated with olanzapine was lower than that of HC and quetiapine groups, and that PON1 may play a role in the metabolic side effects associated with olanzapine treatment. A further study to examine the relationship between serum PON1 activity and cardiovascular and metabolic side effects during treatment with SGAs will be of great interest.

Objective: Oxidative stress is among the major components of cardiovascular disease pathogenesis. Thiols play a significant role in prevention of oxidative stress in the cell. The purpose of this study is to investigate the relationship between the severity of coronary artery disease and disulphide/native thiol ratio, also determine if this ratio can be used as a marker of oxidative stress in this population. Methods: A total number of 107 patients with angiographically established coronary artery disease and 26 control subjects with normal coronary arteries were enrolled. The mean Gensini score of patients were calculated (mean=30) and a score of 29 or below was considered as mild and a score of 30 or higher coronary artery disease as severe. Serum total, native thiol was measured and the disulphide and disulphide/native thiol ratio were calculated as described by Erel&Neselioglu. Results: Patients with mild and severe coronary artery disease had significantly lower native thiol levels and higher disulphide/native thiol ratio levels when compared to the control subjects. Also severe disease's disulphide/native thiol ratio were higher than mild. Conclusion:The increased disulphide/native thiol ratio related with the severity of coronary artery disease, may reflect the augmented oxidative stress in coronary artery disease.

In this study we determined that left ventricular systolic function is preserved in patients with uSpA. Although frequency of diastolic dysfunction was similar in both groups, deterioration of some diastolic parameters in the uSpA group might be considered for possible cardiac involvement in patients with uSpA.

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