Yazarlar |
Elif Oral
İzmir Katip Çelebi Üniversitesi, Türkiye |
Zekai Halıcı
Atatürk Üniversitesi, Türkiye |
Doç. Dr. İrfan ÇINAR
Kafkas Üniversitesi, Türkiye |
Elıf Ozcan
|
Zerrin Kutlu
Atatürk Üniversitesi, Türkiye |
Özet |
Objective: This study investigated changes in urotensin-II (U-II) and endocan levels which can be used as an early biological marker of endothelial injury in the episode and remission phases of bipolar affective disorder (BAD). Methods: We compared endocan and U-II levels, which has been shown to be closely associated with neurotransmitter systems in addition to continuity of endothelial structure and inflammatory response, in patients with BAD in remission for at least one year (n=42) and in patients still in manic or depressive episodes (n=16) with healthy controls (n=30). Results: Both endocan and U-II levels were significantly higher in the bipolar patients than in the controls. Endocan and U-II levels were also significantly correlated with one another (p =0.000, r=0.833). Both endocan (p =0.000) and U-II levels (p =0.000) were significantly higher in the bipolar attack group compared to the subjects in remission, and in the remission group compared to the controls. Conclusion: In this study we determined significantly higher endocan and U-II levels in BAD compared to the controls, while serum endocan and U-II levels of patients undergoing attacks were also significantly higher than those of the controls and also those of patients in remission. |
Anahtar Kelimeler |
Bipolar disorder | Endocan | Endothelial injury | Urotensins |
Makale Türü | Özgün Makale |
Makale Alt Türü | SSCI, AHCI, SCI, SCI-Exp dergilerinde yayımlanan tam makale |
Dergi Adı | CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE |
Dergi ISSN | 1738-1088 |
Dergi Tarandığı Indeksler | SCI-Expanded |
Dergi Grubu | Q3 |
Makale Dili | İngilizce |
Basım Tarihi | 05-2019 |
Cilt No | 17 |
Sayı | 2 |
Sayfalar | 211 / 221 |
Doi Numarası | 10.9758/cpn.2019.17.2.211 |
Makale Linki | http://www.cpn.or.kr/journal/view.html?doi=10.9758/cpn.2019.17.2.211 |