懷孕時甲狀腺功能低下是精神分裂症危險因素?


  【24drs.com】新研究顯示,懷孕時有甲狀腺功能低下之孕婦的小孩,發生精神分裂症的風險大幅增加,為此疾病提供了一個潛在可改變的危險因素。
  
  研究者發現,懷孕時有低甲狀腺素血症之孕婦所生的小孩,發生精神分裂症的風險增加75%,納入此疾病的已知風險因素考量之後,關聯依舊顯著。
  
  第一作者、芬蘭赫爾辛基大學、赫爾辛基大學醫學中心精神科David Gyllenberg博士在記者會中表示,研究結果為妊娠期間的母體低甲狀腺素血症改變後代之大腦發育的關聯增添文獻佐證;他希望這篇報告能引導未來的動物研究,探討與精神分裂症相關的分子與細胞偏差。
  
  該研究發表於6月的生物精神醫學期刊。
  
  以前的研究指出,妊娠早期缺乏甲狀腺會改變大腦發育和精神分裂症是與產前腦損傷有關。研究者檢視了妊娠初期到中期的母體甲狀腺缺乏是否與子代的精神分裂症有關。
  
  他們使用「Finnish Prenatal Study of Schizophrenia」這項巢式病例對照研究的資料,該研究有自1983年起、芬蘭超過1百萬例孕婦在第一或第二孕期的血清資料,研究者也使用芬蘭醫院和門診出院登記資料,以辨識2009年前診斷的精神分裂症病例或分裂情感性障礙案例,患者年齡最大者為29歲。
  
  由此,配對903對精神分裂症案例和健康對照組,都有游離甲狀腺素(fT4)和促甲狀腺激素(TSH)資料。
  
  分析結果顯示,母親有低甲狀腺素血症(定義為 fT4 < 第10百分位與正常TSH)之研究對象的比例,精神分裂症組有11.8%、健康對照組有8.6%,勝算比(OR)為1.75 (P = .002)。
  
  當重新定義低甲狀腺素血症為 fT4 < 第5百分位且正常TSH時,母親有低甲狀腺素血症的精神分裂症組有6.6%、對照組有 5.0%,OR值為1.62 (P = .055)。
  
  將檢視母體fT4值作為連續變量,研究者發現,母體的fT4值每增加一對數單位,精神分裂症風險即顯著降低、OR值0.54 (P = .028);TSH值並未發現有類似關聯。
  
  校正母親的精神病史、出生省份、母親在懷孕期間抽菸等因素之後,母體的低甲狀腺素血症和子代之精神分裂症的關聯依舊顯著,OR值為1.70 (P = .010)。
  
  研究者寫道,母體的低甲狀腺素血症和子代精神分裂症之關聯的一個可能解釋是,低甲狀腺素血症造成改變胎兒的基因表現,對胎兒的腦發育產生不利影響。
  
  另一個可能的解釋是,受到早產或低出生體重影響。
  
  儘管強調他們考慮早產和低出生體重可能會有影響,而非干擾因素,研究者指出,低出生體重與精神分裂症、fT4值低於中位數、低甲狀腺素血症無關,認為它不會影響這個關聯。
  
  荷蘭鹿特丹Erasmus醫學中心Henning Tiemeier博士和Tim I. M. Korevaar醫師在編輯評論中形容它是篇高雅的研究,指出作者們確定了精神分裂症新的、有趣的和潛在可修改的風險因素。
  
  不過,他們指出,儘管有提議進行隨機試驗以確認懷孕時的低甲狀腺素血症篩檢和治療是否可以改善神經發育結果,不論是甲狀腺參數之選擇,或神經發育結果,實在是微不足道。
  
  Tiemeier博士和Korevaar醫師也指出,目前的分析、沿著之前的研究,沒有評估低甲狀腺素血症一個推定主要的原因:碘。他們寫道,我們需要來自各國的更多研究,以顯示孕婦的碘的潛在範圍、調整或影響—最好是神經發育結果。
  
  耶魯-紐哈芬醫院、耶魯大學醫學院精神科主任、生物精神醫學期刊編輯John H. Krystal醫師也對此研究作出評論,認為研究結果顯示,低甲狀腺素婦女所生之子代的精神分裂症風險可能被降低。
  
  他在記者會中表示,這篇研究確認了精神分裂症風險的一個可預防性的潛在因子,母體的低甲狀腺症可容易地獲得診斷與有效治療。
  
  資料來源:http://www.24drs.com/
  
  Native link:Hypothyroidism in Pregnancy a Schizophrenia Risk Factor?

Hypothyroidism in Pregnancy a Schizophrenia Risk Factor?

By Liam Davenport
Medscape Medical News

The offspring of women with hypothyroidism during pregnancy appear to have a substantially increased risk of developing schizophrenia, offering a potentially modifiable risk factor for the disease, new research shows.

Investigators found that children born to women with hypothyroxinemia during pregnancy had a 75% increased risk of developing schizophrenia, which remained significant after taking into account known risk factors for the disease.

Lead author David Gyllenberg, MD, PhD, department of child psychiatry, University of Helsinki and Helsinki University Central Hospital, Finland, said in a press release that the findings link to "an extensive literature on maternal hypothyroxinemia during gestation altering offspring brain development."

"I hope this paper can inform future animal studies examining molecular and cellular deviations that are relevant to schizophrenia," he added.

The research was published in the June issue of Biological Psychiatry.

Possible Mechanisms

Previous research has indicated that thyroid deficiency in early gestation alters brain development and that schizophrenia is associated with prenatal brain insults. The investigators examined whether maternal thyroid deficiency during early to mid-gestation is associated with schizophrenia in offspring.

They used data from the Finnish Prenatal Study of Schizophrenia, a nested case-control study with archived maternal sera drawn during the first or second trimester from more than 1 million pregnancies in Finland since 1983. The researchers also used the Finnish Hospital and Outpatient Discharge Register to identify cases of schizophrenia or schizoaffective disorder diagnosed before 2009, at a maximum patient age of 29 years.

From this, 903 pairs of schizophrenia cases and healthy controls were identified for which assays of both free thyroxine (fT4) and thyroid-stimulating hormone (TSH) were available.

Analysis revealed the proportion of participants with maternal hypothyroxinemia, defined as fT4 < 10th percentile and normal TSH, was 11.8% among schizophrenia cases vs 8.6% among controls, at an odds ratio (OR) of 1.75 (P = .002).

When redefining hypothyroxinemia as fT4 < 5th percentile and normal TSH, the proportion of individuals with maternal hypothyroxinemia was 6.6% among cases and 5.0% among controls, with an OR of 1.62 (P = .055).

Examining maternal fT4 levels as a continuous variable, researchers found that the risk of schizophrenia significantly decreased for each log-unit increase in maternal fT4, at an OR of 0.54 (P = .028). No such relationship was seen with TSH.

The association between maternal hypothyroxinemia and schizophrenia in offspring remained significant after adjusting for maternal psychiatric history, province of birth, and maternal smoking during pregnancy, at an OR of 1.70 (P = .010).

"One potential explanation for the association between maternal hypothyroxinemia and schizophrenia is that hypothyroxinemia contributes to altered fetal gene expression, which adversely affects fetal brain development," the researchers write.

"Another possible explanation for the finding is mediation by preterm birth or low birth weight."

While highlighting that they considered preterm and low birth weight potential mediators, rather than confounders, the researchers note that "low birth weight was not related to schizophrenia, fT4 under the median, and hypothyroxinemia, suggesting that it did not mediate the association."

Novel, Intriguing

In an accompanying commentary, Henning Tiemeier, MD, PhD, and Tim I. M. Korevaar, MD, Erasmus Medical Center, Rotterdam, the Netherlands, described the study as "elegant," adding that the authors have "identified a novel, intriguing and potentially modifiable risk factor for schizophrenia."

Nevertheless, they note that, although randomized trials have been advocated to determine whether screening and treatment for hypothyroxinemia in pregnancy can improve neurodevelopmental outcomes, "neither the choice of the thyroid parameter nor the neurodevelopmental outcome is trivial."

Dr Tiemeier and Dr Korevaar also point out that the current analysis, alongside previous studies, did not assess "one major presumed cause of hypothyroxinemia": iodine. "We need more studies from different countries to show the extent to which iodine underlies, or modifies, the effects of hypothyroxinemia in pregnant women — and preferably neurodevelopmental outcomes," they write.

Also commenting on the study, John H. Krystal, MD, chairman, department of psychiatry, Yale University School of Medicine and Chief of Psychiatry, Yale-New Haven Hospital and editor of Biological Psychiatry believes that the findings show the schizophrenia risk in the offspring of mothers with low thyroxine levels could be reduced.

"This study identifies a preventable potential contributor to the risk for schizophrenia. Maternal hypothyroidism can be easily diagnosed and effectively treated," he said in a press release.

The research was supported by National Institute of Mental Health Grants, the Sigrid Juselius Foundation, Foundation for Pediatric Research in Finland, and Finnish Medical Foundation.

The authors have reported no relevant financial relationships.

Biol Psychiatry. 2016;79:950-951, 962-970.

    
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