{"title":"Oxidative stress markers predict treatment outcomes in patients with generalized anxiety disorder treated with selective serotonin reuptake inhibitors","authors":"lijun cui, jingjing lu, zhongxia shen, jielin zhu, huanxin chen, shengliang yang, shikai wang, xinhua shen","doi":"10.1101/2024.09.07.24313247","DOIUrl":null,"url":null,"abstract":"Introduction: The etiology of generalized anxiety disorder (GAD) has not been fully understood, and oxidative stress may potentially contribute to its pathogenesis. However, there is no published evidence concerning the possible influence of oxidative stress on antidepressant treatment outcomes. This study investigated the ability of oxidative stress markers to predict treatment outcomes in GAD patients treated with selective serotonin reuptake inhibitors (SSRIs).\nMethods: One hundred-one GAD patients and 100 healthy controls (HCs) were included in this study. The 101 GAD patients were selected for treatment with escitalopram (n=52) or sertraline (n=49) for eight weeks. Hamilton Anxiety Rating Scale (HAM-A) assessments were conducted before and after treatment. The serum levels of eight oxidative stress makers, malondialdehyde (MDA), lipid hydroperoxides (LPO), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), cortisol, high-density lipoprotein (HDL), and nitric oxide (NO) were measured using enzyme-linked immunosorbent assays (ELISA) before and after SSRI treatment in GAD patients and at the time of HCs enrollment.\nResults: The serum levels of MDA, cortisol, and LPO were higher in GAD patients than in HCs (all p<.001), while SOD, GSH-Px, and CAT were lower than in HCs (all p<.001). The baseline MDA, LPO, NO, and cortisol levels were positively correlated with anxiety severity, while GSH-Px was negatively correlated. After eight weeks of SSRI treatment, the GSH-Px levels increased, and MDA and LPO decreased (all p<.05). Alterations in MDA levels co-varied with changes in anxiety measures (all p<.05). The ability of the receiver operating characteristic (ROC) area of the baseline MDA levels to predict the SSRI endpoint treatment response was 0.804 (p<.05).\nConclusion: The pathogenesis of GAD might involve oxidative stress. Moreover, serum MDA levels might predict treatment response to SSRIs. However, more research is warranted to confirm these findings.","PeriodicalId":501388,"journal":{"name":"medRxiv - Psychiatry and Clinical Psychology","volume":"34 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"medRxiv - Psychiatry and Clinical Psychology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/2024.09.07.24313247","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction: The etiology of generalized anxiety disorder (GAD) has not been fully understood, and oxidative stress may potentially contribute to its pathogenesis. However, there is no published evidence concerning the possible influence of oxidative stress on antidepressant treatment outcomes. This study investigated the ability of oxidative stress markers to predict treatment outcomes in GAD patients treated with selective serotonin reuptake inhibitors (SSRIs).
Methods: One hundred-one GAD patients and 100 healthy controls (HCs) were included in this study. The 101 GAD patients were selected for treatment with escitalopram (n=52) or sertraline (n=49) for eight weeks. Hamilton Anxiety Rating Scale (HAM-A) assessments were conducted before and after treatment. The serum levels of eight oxidative stress makers, malondialdehyde (MDA), lipid hydroperoxides (LPO), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), cortisol, high-density lipoprotein (HDL), and nitric oxide (NO) were measured using enzyme-linked immunosorbent assays (ELISA) before and after SSRI treatment in GAD patients and at the time of HCs enrollment.
Results: The serum levels of MDA, cortisol, and LPO were higher in GAD patients than in HCs (all p<.001), while SOD, GSH-Px, and CAT were lower than in HCs (all p<.001). The baseline MDA, LPO, NO, and cortisol levels were positively correlated with anxiety severity, while GSH-Px was negatively correlated. After eight weeks of SSRI treatment, the GSH-Px levels increased, and MDA and LPO decreased (all p<.05). Alterations in MDA levels co-varied with changes in anxiety measures (all p<.05). The ability of the receiver operating characteristic (ROC) area of the baseline MDA levels to predict the SSRI endpoint treatment response was 0.804 (p<.05).
Conclusion: The pathogenesis of GAD might involve oxidative stress. Moreover, serum MDA levels might predict treatment response to SSRIs. However, more research is warranted to confirm these findings.