甲状腺功能过高与失智症有关


  【24drs.com】根据新研究,甲状腺功能过高,即便检验数据在正常范围内,仍与发生失智症的可能性增加有关,校正心血管疾病风险因素后也是如此,这或许是失智症和阿兹海默氏症一个可能的新治疗目标。
  
  第一作者、荷兰鹿特丹Erasmus大学医学中心的Layal Chaker医师表示,在我们的研究中,我们发现不只是甲状腺功能高与失智症风险增加有关,甲状腺数值正常但功能偏高者也有关。
  
  这些研究发现的临床影响是,可以将验血即可测得的甲状腺功能纳入作为失智症的筛检与风险预测。
  
  虽然以前的研究认为甲状腺失能对失智症有影响,评估甲状腺功能之各种影响的研究有限。
  
  这篇研究发表于2015年国际甲状腺研讨会与美国甲状腺协会年会(2015ITC/ATA),为了这篇新的前瞻研究,Chaker医师等人评估了参与「Rotterdam Study」研究的9,495名研究对象,平均年龄64.9岁,皆有甲状腺功能测量结果与失智症评估资料,平均追踪7.8年间,有603人发生失智症。
  
  校正年龄、性别、心血管疾病风险因素等变项之后,甲状腺刺激素(TSH)值比较高的人— 一般有甲状腺功能低下的典型征兆— 失智症风险比较低(HR 0.76, 95% CI 0.64–0.91);同时,游离四碘甲状腺素(T4)值比较高 — 症状为甲状腺亢进— 与失智症风险显著较高有关(HR, 1.04; 95% CI, 1.01–1.07)。
  
  女性的TSH值比较高和失智症的绝对10年风险从6%降低到近3%有关;不过,在男性没有发现类似影响。
  
  针对与甲状腺功能有关之脑部结构的MRI后续评估显示,年长研究对象的游离T4值较高与器质容积较小有关(每减少2.1 mL与游离T4增加 1-pmol/L有关),但是未发现与海马回容积的关联。
  
  Chaker医师表示,即便校正特别显著的心血管风险因素之后,甲状腺功能和失智症之间的关联依旧存在。
  
  她解释,虽然有许多生物机转可以解释甲状腺状态和失智症风险的关联,令我们惊讶的是,其中不包括血管机转。
  
  已知甲状腺功能与心血管风险增加有关,且心血管风险因素也和失智症风险增加有关,在生物学上提供两者之间可能有关联的一个解释,不过,在我们的研究对象中,我们并未发现可解释此关联的血管机转。
  
  Chaker医师指出,这篇研究对甲状腺与失智症关联的拼图提供了重要的线索。研究结果对甲状腺功能和失智症关联提供了更多可能的重要观点,且可提供作为新的治疗目标。
  
  至于性别上的差异,研究者最初假设,男性和女性的自体免疫甲状腺病变盛行率因素可以解释这个差异,但是并非如此。
  
  我们不知道男性和女性之间为何有这些差异,而可能的解释之一是因为性荷尔蒙的差异,不过,我们无法在我们的研究中评估这项假设。
  
  会议共同主持人、意大利外科医学科学与生物技术、罗马大学的Marco Centanni医师同意,这篇研究发现的性别差异是显著的;一个新的议题是,甲状腺过量的影响只有在女性是显著的,其它某些关键因素可能可以调控这个影响,雌激素即有此可能。
  
  他指出,即使是甲状腺功能高但不一定大于正常时,也有此差异存在。
  
  这并不奇怪,因为脑萎缩可能与细胞死亡和细胞凋亡的速率有关,而这机转可能是由三碘甲状腺素(T3)所调控。
  
  发表于会议中的另一篇海报提供了一些证据支持此关联,研究者报告指出首度使用一项以质谱检测为基础的技术,评估脑脊液中的甲状腺素值的研究结果。
  
  他们发现,在35名研究对象中 —包括15名诊断有阿兹海默氏症者、10名罹患额颞叶失智症(FTD)、10人具有正常认知功能— 在阿兹海默氏症患者、额颞叶失智症患者、正常认知功能者之间,脑脊液(CSF)中的甲状腺素值并无显著差异。
  
  不过,与疾病严重度之关联有某些征兆。
  
  意大利Pisa大学的作者们写道,当我们探讨脑脊液(CSF)中的甲状腺素值是否与疾病严重度和病程之临床指标有关时,获得有趣的结果。他们结论表示,他们的研究结果认为阿兹海默氏症病程和甲状腺激素新陈代谢的局部变化确实有关。
  
  资料来源:http://www.24drs.com/
  
  Native link:Urine Tests Miss Sexually Transmitted Infections

High Thyroid Function Linked to Dementia

By Nancy A Melville
Medscape Medical News

ORLANDO, Florida — High-functioning thyroid levels, including those falling within the normal range, show an association with an increased likelihood of dementia, even after adjustment for cardiovascular disease risk factors, suggesting a possible target for dementia and Alzheimer's disease therapies, according to new research.

"In our study we show that not only high but also high-normal thyroid function is related to an increased risk of dementia," first author Layal Chaker, MD, of Erasmus University Medical Center, in Rotterdam, the Netherlands, told Medscape Medical News.

"The clinical implications [of the findings] could include the use of thyroid function, an easily obtained measure in serum, in screening for and risk prediction of dementia."

While previous research has suggested a role of thyroid dysfunction in dementia, studies evaluating the multiple aspects of thyroid function have been lacking.

Vascular Factors Don't Explain Thyroid-Dementia Link

For the new prospective study, presented here at the 2015 International Thyroid Congress and Annual Meeting of the American Thyroid Association (ITC/ATA, Dr Chaker and colleagues evaluated 9495 participants with a mean age of 64.9 who were enrolled in the Rotterdam Study, with measurements available on thyroid function as well as dementia assessment.

Over a mean follow-up of 7.8 years, 603 patients developed dementia.

After adjustment for variables including age, sex, and cardiovascular disease risk factors, those with higher thyroid-stimulating-hormone (TSH) levels — typically a sign of an underactive thyroid — had a lower risk of dementia (HR 0.76, 95% CI 0.64–0.91).

Meanwhile, higher levels of free thyroxine 4 (T4) — a sign of an overactive thyroid — were associated with a significantly higher risk of dementia (HR, 1.04; 95% CI, 1.01–1.07).

Higher TSH levels in women were linked to an absolute 10-year risk of dementia that was decreased from 6% to nearly 3%; however, a similar effect was not seen in men.

Further assessment in the form of MRI of brain structures related to thyroid function showed that higher free T4 levels in older participants were associated with smaller parenchymal volumes (?2.1 mL per 1-pmol/L increase of free T4), but no link was observed with hippocampal volumes.

The fact that the link between thyroid function and dementia was seen even after adjustment for cardiovascular risk factors was particularly notable, Dr Chaker said.

"Even though there are several mechanisms biologically that can explain a relation between thyroid status and dementia risk, we were surprised to see that vascular mechanisms are seemingly not one of them," she explained.

"Thyroid function is known to increase cardiovascular risk, and cardiovascular risk factors are also linked to an increased risk of dementia, providing a biologically plausible explanation for the link. However, we do not find that vascular mechanisms explain this relation in our population."

Important Clues in Thyroid-Dementia Puzzle

The study could provide important clues in the thyroid-dementia puzzle, Dr Chaker added.

"This finding provides more insight into the possible importance of other pathways connecting thyroid function to dementia and could provide new targets for therapeutic agents," she said.

In terms of the gender differences, the researchers initially hypothesized that differences in prevalence of autoimmune thyroid pathology between men and women might explain the findings, but this was not the case.

"We do not know why these differences exist between women and men, but one of the explanations might be due to differences in sex hormonal profiles. However, we were unfortunately not able to assess this hypothesis in our study."

Session comoderator Marco Centanni, MD, of the University of Rome, Medicosurgical Sciences and Biotechnologies, Italy, agreed that the gender differences observed in the study are notable.

"A novel issue is that the effects of thyroid excess are evident only in women, suggesting that this effect is mediated by some other key factor, which may possibly be estrogen exposure," he told Medscape Medical News.

He added that the differences seen even with high-normal levels of thyroid function are not necessarily unusual.

"It is not surprising, since brain atrophy may depend on the rate of cell death and apoptosis, mechanisms that can be regulated by triiodothyronine (T3)."

First Research to Use Mass Spectrometry for Thyroid Hormone in CSF

A poster presented at the meeting provided some additional evidence in support of the association, with researchers reporting on the first use of a mass-spectrometry–based technique to assay thyroid hormone levels in cerebrospinal fluid.

They found that in 35 subjects — including 15 with a diagnosis of Alzheimer's disease, 10 with frontotemporal dementia (FTD), and 10 with normal cognitive function — there were no significant differences in cerebrospinal fluid (CSF) thyroid hormones between the Alzheimer's disease patients, those with frontotemporal dementia, or the individuals with normal cognitive function.

However, there were some signs of a link with disease severity.

"Interesting results were obtained when we investigated whether CSF thyroid hormones were related to clinical indices of disease severity and progression," wrote the authors, with the University of Pisa, in Italy.

The findings "suggest the existence of a link between Alzheimer's disease progression and local alterations of thyroid hormone metabolism," they concluded.

Dr Chaker and the University of Pisa authors had no relevant financial relationships.

2015 International Thyroid Congress and Annual Meeting of the American Thyroid Association. Abstracts 5 and 771, presented October 19, 2015.

    
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