Predictive value of oxidative stress biomarkers in drug-free patients with bipolar disorder. (3rd October 2022)

• Record Type: Journal Article
• Authors: Guidara, Wassim; Messedi, Meriam; Naifar, Manel; Charfi, Nada; Grayaa, Sahar; Maalej, Mohamed; Maalej, Manel; Ayadi, Fatma
• Is Part Of: Nordic journal of psychiatry. Volume 76:Number 7(2022)
• Page Start: 539
• Page End: 550
• Publication Date: 2022-10-03
• Subjects: Bipolar disorder -- oxidative stress -- homocysteine -- CombiROC; Psychopharmacology -- Periodicals; Psychotherapy -- Periodicals; Psychiatry -- Periodicals; Psychiatry -- Scandinavia -- Periodicals; 616.89
• DOI: 10.1080/08039488.2021.2016954
• Languages: English
• ISSNs: 0803-9488

Abstract

Abstract: Objective: Oxidative stress is one of the primary etiological mechanisms of bipolar disorder (BD). Methods: The present study was conducted over a period of 24 months on Tunisian on 34 drug‑free male patients with BD (mean age: 34.5 years) and 101 age and gender matched controls (mean age: 34.20 years) were enrolled in the study. Results: Plasma reduced glutathione (GSH) and total thiols levels were significantly decreased in patients compared to controls (respectively p < .001; p = .009). In addition, malondialdehyde (MDA), advanced oxidation protein products (AOPP), protein carbonyls (PC) and homocysteine (Hcys) concentrations and glutathione peroxidase (GSH-Px) activity were significantly increased in patients compared to controls ( p = .002; p < .001; p = .001; p < .001 and p = .016, respectively). The binary logistic regression analysis revealed that MDA, AOPP and Hcys could be considered as independent risk factors for BD. When using CombiROC analysis, a remarkable increase in the area under the curve (AUC) with higher sensitivity (Se) and specificity (Sp) for MDA, AOPP, PC, GSH-Px and Hcys combined markers was observed. Conclusions: Overall, the identification of the predictive value of these five selected biomarkers related to oxidative stress in drug free patients should lead to a better identification of the etiological mechanism of BD.