甲狀腺功能過高與失智症有關


  【24drs.com】根據新研究,甲狀腺功能過高,即便檢驗數據在正常範圍內,仍與發生失智症的可能性增加有關,校正心血管疾病風險因素後也是如此,這或許是失智症和阿茲海默氏症一個可能的新治療目標。
  
  第一作者、荷蘭鹿特丹Erasmus大學醫學中心的Layal Chaker醫師表示,在我們的研究中,我們發現不只是甲狀腺功能高與失智症風險增加有關,甲狀腺數值正常但功能偏高者也有關。
  
  這些研究發現的臨床影響是,可以將驗血即可測得的甲狀腺功能納入作為失智症的篩檢與風險預測。
  
  雖然以前的研究認為甲狀腺失能對失智症有影響,評估甲狀腺功能之各種影響的研究有限。
  
  這篇研究發表於2015年國際甲狀腺研討會與美國甲狀腺協會年會(2015ITC/ATA),為了這篇新的前瞻研究,Chaker醫師等人評估了參與「Rotterdam Study」研究的9,495名研究對象,平均年齡64.9歲,皆有甲狀腺功能測量結果與失智症評估資料,平均追蹤7.8年間,有603人發生失智症。
  
  校正年齡、性別、心血管疾病風險因素等變項之後,甲狀腺刺激素(TSH)值比較高的人— 一般有甲狀腺功能低下的典型徵兆— 失智症風險比較低(HR 0.76, 95% CI 0.64–0.91);同時,游離四碘甲狀腺素(T4)值比較高 — 症狀為甲狀腺亢進— 與失智症風險顯著較高有關(HR, 1.04; 95% CI, 1.01–1.07)。
  
  女性的TSH值比較高和失智症的絕對10年風險從6%降低到近3%有關;不過,在男性沒有發現類似影響。
  
  針對與甲狀腺功能有關之腦部結構的MRI後續評估顯示,年長研究對象的游離T4值較高與器質容積較小有關(每減少2.1 mL與游離T4增加 1-pmol/L有關),但是未發現與海馬迴容積的關聯。
  
  Chaker醫師表示,即便校正特別顯著的心血管風險因素之後,甲狀腺功能和失智症之間的關聯依舊存在。
  
  她解釋,雖然有許多生物機轉可以解釋甲狀腺狀態和失智症風險的關聯,令我們驚訝的是,其中不包括血管機轉。
  
  已知甲狀腺功能與心血管風險增加有關,且心血管風險因素也和失智症風險增加有關,在生物學上提供兩者之間可能有關聯的一個解釋,不過,在我們的研究對象中,我們並未發現可解釋此關聯的血管機轉。
  
  Chaker醫師指出,這篇研究對甲狀腺與失智症關聯的拼圖提供了重要的線索。研究結果對甲狀腺功能和失智症關聯提供了更多可能的重要觀點,且可提供作為新的治療目標。
  
  至於性別上的差異,研究者最初假設,男性和女性的自體免疫甲狀腺病變盛行率因素可以解釋這個差異,但是並非如此。
  
  我們不知道男性和女性之間為何有這些差異,而可能的解釋之一是因為性荷爾蒙的差異,不過,我們無法在我們的研究中評估這項假設。
  
  會議共同主持人、義大利外科醫學科學與生物技術、羅馬大學的Marco Centanni醫師同意,這篇研究發現的性別差異是顯著的;一個新的議題是,甲狀腺過量的影響只有在女性是顯著的,其他某些關鍵因素可能可以調控這個影響,雌激素即有此可能。
  
  他指出,即使是甲狀腺功能高但不一定大於正常時,也有此差異存在。
  
  這並不奇怪,因為腦萎縮可能與細胞死亡和細胞凋亡的速率有關,而這機轉可能是由三碘甲狀腺素(T3)所調控。
  
  發表於會議中的另一篇海報提供了一些證據支持此關聯,研究者報告指出首度使用一項以質譜檢測為基礎的技術,評估腦脊液中的甲狀腺素值的研究結果。
  
  他們發現,在35名研究對象中 —包括15名診斷有阿茲海默氏症者、10名罹患額顳葉失智症(FTD)、10人具有正常認知功能— 在阿茲海默氏症患者、額顳葉失智症患者、正常認知功能者之間,腦脊液(CSF)中的甲狀腺素值並無顯著差異。
  
  不過,與疾病嚴重度之關聯有某些徵兆。
  
  義大利Pisa大學的作者們寫道,當我們探討腦脊液(CSF)中的甲狀腺素值是否與疾病嚴重度和病程之臨床指標有關時,獲得有趣的結果。他們結論表示,他們的研究結果認為阿茲海默氏症病程和甲狀腺激素新陳代謝的局部變化確實有關。
  
  資料來源: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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