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Imbalance of T-helper 1/T-helper 2 cytokines and impaired glucose tolerance among patient with acute coronary syndrome


 Department of Endocrinology, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, China

Correspondence Address:
Zhao-Hui Mo,
Department of Endocrinology, Third Xiangya Hospital, Central South University, 138 Tong Zi Po Road, Changsha 410013, Hunan Province
China
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Source of Support: None, Conflict of Interest: None

Purpose: The balance between T helper (Th) cells Th1- and Th2-related cytokines plays a key role in the clinical process of acute coronary syndrome (ACS) and type 2 diabetes mellitus (T2DM) or impaired glucose tolerance (IGT). The objective of this study was to assess the status of Th1/Th2 cytokines in patients with ACS and T2D or IGT. Methods: A total of 201 ACS patients were enrolled in the study. All ACS patients were divided into three groups: Group I-patients with normal glucose tolerance (NGT), Group II-patients with IGT and Group III-patients with T2D. We measured circulating Th1/Th2-type cytokines (interleukin [IL]-4, IL-13, interferon-gamma [IFN-γ], and tumor-necrosis factor-alpha [TNF-α]) using enzyme-linked immunosorbent assay and calculated the ratio of Th1/Th2. Results: Significant elevations in serum levels of IL-4, IL-13, IFN-γ, and TNF-α were found in ACS-T2D and ACS-IGT groups compared to that in both ACS-NGT group and healthy individuals. Higher serum levels of IL-4, IL-13, and TNF-α were found in ACS-NGT group than that in the control group. Furthermore, IL-4 and IFN-γ concentrations were significantly higher in ACS-T2D patients than in ACS-IGT patients. IFN-γ/IL-4, IFN-γ/IL-13, and TNF-α/IL-4 ratios as markers of Th1/Th2 ratio were significantly higher for the ACS-T2D group and ACS-IGT group as compared to that in the ACS-NGT group and control group (P < 0.05). Conclusion: Shifts in the balance of Th1/Th2 toward a predominance of Th1 may represent more severe inflammatory status in ACS patients with type T2D or IGT.


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    -  Zhao SL
    -  Mo ZH
    -  He HH
    -  Zhao LL
    -  Xie YH
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