怀孕时甲状腺功能低下是精神分裂症危险因素?


  【24drs.com】新研究显示,怀孕时有甲状腺功能低下之孕妇的小孩,发生精神分裂症的风险大幅增加,为此疾病提供了一个潜在可改变的危险因素。
  
  研究者发现,怀孕时有低甲状腺素血症之孕妇所生的小孩,发生精神分裂症的风险增加75%,纳入此疾病的已知风险因素考量之后,关联依旧显著。
  
  第一作者、芬兰赫尔辛基大学、赫尔辛基大学医学中心精神科David Gyllenberg博士在记者会中表示,研究结果为妊娠期间的母体低甲状腺素血症改变后代之大脑发育的关联增添文献佐证;他希望这篇报告能引导未来的动物研究,探讨与精神分裂症相关的分子与细胞偏差。
  
  该研究发表于6月的生物精神医学期刊。
  
  以前的研究指出,妊娠早期缺乏甲状腺会改变大脑发育和精神分裂症是与产前脑损伤有关。研究者检视了妊娠初期到中期的母体甲状腺缺乏是否与子代的精神分裂症有关。
  
  他们使用「Finnish Prenatal Study of Schizophrenia」这项巢式病例对照研究的资料,该研究有自1983年起、芬兰超过1百万例孕妇在第一或第二孕期的血清资料,研究者也使用芬兰医院和门诊出院登记资料,以辨识2009年前诊断的精神分裂症病例或分裂情感性障碍案例,患者年龄最大者为29岁。
  
  由此,配对903对精神分裂症案例和健康对照组,都有游离甲状腺素(fT4)和促甲状腺激素(TSH)资料。
  
  分析结果显示,母亲有低甲状腺素血症(定义为 fT4 < 第10百分位与正常TSH)之研究对象的比例,精神分裂症组有11.8%、健康对照组有8.6%,胜算比(OR)为1.75 (P = .002)。
  
  当重新定义低甲状腺素血症为 fT4 < 第5百分位且正常TSH时,母亲有低甲状腺素血症的精神分裂症组有6.6%、对照组有 5.0%,OR值为1.62 (P = .055)。
  
  将检视母体fT4值作为连续变量,研究者发现,母体的fT4值每增加一对数单位,精神分裂症风险即显著降低、OR值0.54 (P = .028);TSH值并未发现有类似关联。
  
  校正母亲的精神病史、出生省份、母亲在怀孕期间抽菸等因素之后,母体的低甲状腺素血症和子代之精神分裂症的关联依旧显著,OR值为1.70 (P = .010)。
  
  研究者写道,母体的低甲状腺素血症和子代精神分裂症之关联的一个可能解释是,低甲状腺素血症造成改变胎儿的基因表现,对胎儿的脑发育产生不利影响。
  
  另一个可能的解释是,受到早产或低出生体重影响。
  
  尽管强调他们考虑早产和低出生体重可能会有影响,而非干扰因素,研究者指出,低出生体重与精神分裂症、fT4值低于中位数、低甲状腺素血症无关,认为它不会影响这个关联。
  
  荷兰鹿特丹Erasmus医学中心Henning Tiemeier博士和Tim I. M. Korevaar医师在编辑评论中形容它是篇高雅的研究,指出作者们确定了精神分裂症新的、有趣的和潜在可修改的风险因素。
  
  不过,他们指出,尽管有提议进行随机试验以确认怀孕时的低甲状腺素血症筛检和治疗是否可以改善神经发育结果,不论是甲状腺参数之选择,或神经发育结果,实在是微不足道。
  
  Tiemeier博士和Korevaar医师也指出,目前的分析、沿著之前的研究,没有评估低甲状腺素血症一个推定主要的原因:碘。他们写道,我们需要来自各国的更多研究,以显示孕妇的碘的潜在范围、调整或影响—最好是神经发育结果。
  
  耶鲁-纽哈芬医院、耶鲁大学医学院精神科主任、生物精神医学期刊编辑John H. Krystal医师也对此研究作出评论,认为研究结果显示,低甲状腺素妇女所生之子代的精神分裂症风险可能被降低。
  
  他在记者会中表示,这篇研究确认了精神分裂症风险的一个可预防性的潜在因子,母体的低甲状腺症可容易地获得诊断与有效治疗。
  
  资料来源: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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