Dynamic thiol and disulphide homoeostasis in fibromyalgia

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dc.authoridneselioglu, salim/0000-0002-0974-5717
dc.contributor.authorKaratas, Gulsah
dc.contributor.authorGunduz, Ramazan
dc.contributor.authorHaskul, Ismail
dc.contributor.authorUstun, Betul
dc.contributor.authorNeselioglu, Salim
dc.contributor.authorKaratas, Fatih
dc.contributor.authorAkyuz, Mufit
dc.date.accessioned2024-09-29T16:09:38Z
dc.date.available2024-09-29T16:09:38Z
dc.date.issued2020
dc.departmentKarabük Üniversitesien_US
dc.description.abstractIntroduction: Thiol and disulphide levels are biomarkers that provide useful information about oxidative stress and antioxidant capacity, showing a different homoeostasis in inflammatory and proliferative diseases. We aimed to clarify the possible aetiology of this disease by using thiol and disulphide levels in patients with fibromyalgia, the basis of which has not yet been clearly elucidated. Material and methods: A total of 156 individuals: 86 patients with fibromyalgia and 70 age-matched controls were included in this prospective non-randomised case-control study. Demographic characteristics including smoking status, body mass index (BMI), the duration of complaints, and pain levels were carefully recorded. Dynamic thiol-disulphide homoeostasis in blood samples was determined by an automatic-spectrophotometric method. The Mann-Whitney U and Student's t-test were used to determine the differences between the groups. Results: Sex, BMI, and smoking status were similar between the groups (p = 0.62, p = 0.09, and p = 0.64, respectively). While native thiol levels were found to be high in patients with fibromyalgia (p = 0.018), disulphide levels and the rates of disulphide/native thiol and disulphide/total thiol were significantly low (p = 0.049, p = 0.007, and p = 0.007, respectively). Correlation analysis showed no significant relationship between thiol-disulphide levels and duration of complaints or pain level. Conclusions: Thiol-disulphide balance in fibromyalgia was found to be similar to benign proliferative diseases, suggesting that the underlying mechanism is more likely to be of proliferative pattern rather than inflammatory. Additionally, fibromyalgia is not directly associated with increase in oxidative stress. The molecular mechanisms need to be elucidated.en_US
dc.identifier.doi10.5114/aoms.2019.87052
dc.identifier.endpage602en_US
dc.identifier.issn1734-1922
dc.identifier.issn1896-9151
dc.identifier.issue3en_US
dc.identifier.pmid32399108en_US
dc.identifier.scopus2-s2.0-85085392776en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage597en_US
dc.identifier.urihttps://doi.org/10.5114/aoms.2019.87052
dc.identifier.urihttps://hdl.handle.net/20.500.14619/7685
dc.identifier.volume16en_US
dc.identifier.wosWOS:000529817100016en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTermedia Publishing House Ltden_US
dc.relation.ispartofArchives of Medical Scienceen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectfibromyalgiaen_US
dc.subjectinflammatoryen_US
dc.subjectthiolen_US
dc.subjectdisulphideen_US
dc.subjectproliferativeen_US
dc.titleDynamic thiol and disulphide homoeostasis in fibromyalgiaen_US
dc.typeArticleen_US

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