Ahirwar Ashok Kumar, Singh Archana, Jain Anju, Patra Surajeet Kumar, Goswami Binita, Bhatnagar M K, Bhattacharjee Jayashree
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Rom J Intern Med. 2017 Dec 1;55(4):212-221. doi: 10.1515/rjim-2017-0023.
Endothelial dysfunction has been considered as one of the important factors in pathogenesis of Metabolic Syndrome (Met S). Subclinical hypothyroidism (SCH) has also been reported to be associated with Met S. The aim of our study is to evaluate the association of raised TSH with mediators of endothelial dysfunction in Met S with Subclinical hypothyroidism as compared to healthy controls.
Study population consisted of 100 subjects, out of which 50 were cases of Met S and 50 were healthy controls. Met S group were further divided into two, based on the presence & absence of SCH. Serum insulin, T3, T4, TSH were measured by chemiluminescence based immunoassay (CLIA). Serum nitric oxide (NO) levels were measured by Modified Griess's method and serum endothelin-1 (ET-1) levels were measured by ELISA.
Out of 50 cases of Met S, SCH was diagnosed in 22. The mean serum TSH levels were significantly higher in Met S cases as compared to healthy controls (5.7 ± 1.2 μIU/mL vs. 2.3 ± 1.6 μIU/mL, P <0.0001). Mean serum NO levels were significantly lower in Met S cases as compared to healthy control (15.4 ± 10 μM vs. 21 ± 10 μM, p = 0.009). Mean serum ET-1 levels were significantly higher in Met S cases as compared to healthy controls (2.68 ± 1.7 fmol/mL vs. 2.1 ± 0.84 fmol/mL, p = 0.011). On Pearson's correlation analysis, TSH showed positive correlation with ET-1 (r = 0.341, p = 0.001) and negative correlation with NO (r = -0.331, p = 0.001). Binary logistic regression analysis showed that TSH, NO and ET-1 has significant odd's ratio for predicting Met S.
Met S cases were screened for thyroid abnormalities and found to have 44% of SCH along with co-existing endothelial dysfunction. Raised TSH in SCH could cause endothelial dysfunction which may lead to Met S and associated co-morbidities. Present study gives new insight in linking endothelial dysfunction and raised TSH in Met S. Therefore, Met S cases should be screened for SCH and treated appropriately to attenuate endothelial dysfunction and associated comorbidities in Met S.
内皮功能障碍被认为是代谢综合征(Met S)发病机制中的重要因素之一。据报道,亚临床甲状腺功能减退(SCH)也与代谢综合征有关。我们研究的目的是评估与健康对照组相比,亚临床甲状腺功能减退合并代谢综合征患者中促甲状腺激素(TSH)升高与内皮功能障碍介质之间的关联。
研究人群包括100名受试者,其中50例为代谢综合征患者,50例为健康对照。根据是否存在亚临床甲状腺功能减退,将代谢综合征组进一步分为两组。采用基于化学发光的免疫分析法(CLIA)测定血清胰岛素、T3、T4、TSH。采用改良的格里斯法测定血清一氧化氮(NO)水平,采用酶联免疫吸附测定法(ELISA)测定血清内皮素-1(ET-1)水平。
在50例代谢综合征患者中,22例被诊断为亚临床甲状腺功能减退。与健康对照组相比,代谢综合征患者的平均血清TSH水平显著升高(5.7±1.2μIU/mL对2.3±1.6μIU/mL,P<0.0001)。与健康对照组相比,代谢综合征患者的平均血清NO水平显著降低(15.4±10μM对21±10μM,p=0.009)。与健康对照组相比,代谢综合征患者的平均血清ET-1水平显著升高(2.68±1.7fmol/mL对2.1±0.84fmol/mL,p=0.011)。经Pearson相关性分析,TSH与ET-1呈正相关(r=0.341,p=0.001),与NO呈负相关(r=-0.331,p=0.001)。二元逻辑回归分析显示,TSH、NO和ET-1对预测代谢综合征具有显著的比值比。
对代谢综合征患者进行甲状腺异常筛查,发现44%的患者患有亚临床甲状腺功能减退,并伴有内皮功能障碍。亚临床甲状腺功能减退中TSH升高可导致内皮功能障碍,这可能会导致代谢综合征及相关合并症。本研究为代谢综合征中内皮功能障碍与TSH升高之间的联系提供了新的见解。因此,应对代谢综合征患者进行亚临床甲状腺功能减退筛查,并进行适当治疗,以减轻代谢综合征中的内皮功能障碍及相关合并症。