Chakrabarti Sumit Kumar, Ghosh Sujoy, Banerjee Sandip, Mukherjee Satinath, Chowdhury Subhankar
Department of General Medicine, NRS Medical College and Hospital, Jadavpur, Kolkata, West Bengal, India.
Department of Endocrinology, IPGME & R and SSKM Hospital, Jadavpur, Kolkata, West Bengal, India.
Indian J Endocrinol Metab. 2016 Sep-Oct;20(5):674-678. doi: 10.4103/2230-8210.190555.
The available data concerning oxidant stress and antioxidant capacity in hypothyroidism are scanty and inconclusive. While some authors suggest that tissues may be protected from oxidant damage because of a hypometabolic state in hypothyroidism, others report increased oxidative stress in hypothyroidism. Selenium acts as a cofactor for the thyroid hormone (TH) deiodinases that activate and then deactivate various THs and their metabolites. Selenium may inhibit thyroid autoimmunity.
The study was designed, first, to study the impact of oxidative stress in patients of primary hypothyroidism due to autoimmune thyroiditis, by estimation of serum malondialdehyde (MDA) as a biomarker of oxidative stress. Second, to study the change in MDA level pre- and post-L-thyroxine treatment. Finally, to look into the possible role of selenium supplementation on oxidative stress in autoimmune hypothyroidism.
Patients attending endocrine outpatient department (OPD) services of IPGMER and SSKM hospital were considered for the study. Sixty treatment-naive adult patients (age > 18 years) with hypothyroidism were included in the study. The patients were divided into two groups, each comprised thirty patients. One group was treated with L-thyroxine and placebo (Group A). The other group received L-thyroxine replacement along with selenium (100 mcg twice a day) as antioxidant supplementation (Group B). The patients were blinded about selenium and placebo. The study duration for both groups was 6 months. The starting dose of L-thyroxine was 1.6 mcg/kg body weight free thyroxine (FT4), and thyroid-stimulating hormone (TSH) was repeated after 12 weeks. L-thyroxine dose adjustments were done if needed. MDA was assessed at the beginning and at the end of the study, i.e., after 6 months of treatment. The control cohort was composed of thirty healthy adults. Only overt hypothyroidism (OH) cases were included in the study.
Normality of data was determined using Anderson-Darling test, Shapiro-Wilk test, and QQ plot. values were calculated using ANOVA and Bonferroni tests for normally distributed data. Correlation analysis was carried out using Pearson correlation test. < 0.05 considered to be statistically significant.
After treatment in Group A patients, FT4 showed a significant increment while TSH value decreased. MDA level reduced after treatment, ( < 0.001). After treatment in Group B patients, FT4 showed increment while TSH value decreased ( < 0.05). After treatment, there was a drop in estimated MDA level ( < 0.001). MDA level shows a significant drop in both groups after treatment. In Group B, there is more decline in the MDA percentage but did not reach statistical significance. By performing repeated measure MANOVA, no significant difference was found in the MDA levels between the two groups. MDA reduction when expressed as percentage showed reduction of 39.5% in patients of Group A. Similarly, Group B patients showed a percentage reduction of 45.4%.
Oxidative stress compounds hypothyroidism. Hypothyroidism is a state of increased oxidative stress. In this study, biomarker, MDA level is high in treatment-naive primary hypothyroid patients. After treatment with L-thyroxine, the stress marker is reduced to a significant extent. MDA can be used as a useful biomarker to measure and monitor oxidative stress. The role of the addition of antioxidant in the form of selenium remained inconclusive.
关于甲状腺功能减退症中氧化应激和抗氧化能力的现有数据稀少且尚无定论。一些作者认为,由于甲状腺功能减退症患者处于低代谢状态,组织可能受到保护免受氧化损伤,而另一些人则报告甲状腺功能减退症患者的氧化应激增加。硒作为甲状腺激素(TH)脱碘酶的辅助因子,可激活然后失活各种TH及其代谢产物。硒可能抑制甲状腺自身免疫。
本研究旨在,首先,通过评估血清丙二醛(MDA)作为氧化应激的生物标志物,研究自身免疫性甲状腺炎所致原发性甲状腺功能减退症患者氧化应激的影响。其次,研究左旋甲状腺素治疗前后MDA水平的变化。最后,探讨补充硒对自身免疫性甲状腺功能减退症氧化应激的可能作用。
本研究纳入了在IPGMER和SSKM医院内分泌门诊就诊的患者。60例未经治疗的成年甲状腺功能减退症患者(年龄>18岁)被纳入研究。患者分为两组,每组30例。一组接受左旋甲状腺素和安慰剂治疗(A组)。另一组接受左旋甲状腺素替代治疗并同时补充硒(每日两次,每次100微克)作为抗氧化剂补充(B组)。患者对硒和安慰剂不知情。两组的研究持续时间均为6个月。左旋甲状腺素的起始剂量为1.6微克/千克体重游离甲状腺素(FT4),12周后复查促甲状腺激素(TSH)。必要时进行左旋甲状腺素剂量调整。在研究开始时和结束时,即治疗6个月后评估MDA。对照组由30名健康成年人组成。本研究仅纳入明显甲状腺功能减退症(OH)病例。
使用Anderson-Darling检验、Shapiro-Wilk检验和QQ图确定数据的正态性。对于正态分布的数据,使用方差分析和Bonferroni检验计算P值。使用Pearson相关检验进行相关分析。P<0.05被认为具有统计学意义。
A组患者治疗后,FT4显著升高而TSH值降低。治疗后MDA水平降低(P<0.001)。B组患者治疗后,FT4升高而TSH值降低(P<0.05)。治疗后,估计的MDA水平下降(P<0.001)。两组治疗后MDA水平均显著下降。在B组中,MDA百分比下降更多,但未达到统计学意义。通过进行重复测量多变量方差分析,两组之间的MDA水平未发现显著差异。以百分比表示时,A组患者的MDA降低了39.5%。同样,B组患者的百分比降低了45.4%。
氧化应激加重甲状腺功能减退症。甲状腺功能减退症是氧化应激增加的状态。在本研究中,未经治疗的原发性甲状腺功能减退症患者的生物标志物MDA水平较高。用左旋甲状腺素治疗后,应激标志物显著降低。MDA可作为测量和监测氧化应激的有用生物标志物。以硒形式添加抗氧化剂的作用仍无定论。