woensdag 14 augustus 2013

Mogelijk verband autisme en tekort schildklierhormoon in zwangerschap

Transient gestational hypothyroxinemia in rodents induces cortical neuronal migration brain lesions resembling those of autism. We investigated the association between maternal hypothyroxinemia (gestational weeks 6–18) and autistic symptoms in children.

Association of gestational maternal hypothyroxinemia and increased autism risk
GC Román, A Ghassabian, JJ Bongers-Schokking, VWV Jaddoe, A Hofman, YB de Rijke, FC Verhulst,
H Tiemeier - Article first published online: 13 aug 2013. DOI: 10.1002/ana.23976. Annals of Neurology

Autism four times likelier when mother's thyroid is weakened
Houston Methodist, 13 aug 2013

Interview met Henning Tiemeier in NRC

Schildklier en zwangerschap: Generation R op Schildkliertje

Erasmus MC Rotterdam
Neurobiological pathways to childhood psychopathology - proefschrift dr. Akhgar Ghassabian
Onderzoeksresultaten Generation R op PubMed

Methods

The mother-and-child cohort of the Generation R Study (Rotterdam, the Netherlands) began prenatal enrollment between 2002 and 2006. At a mean gestational age of 13.4 weeks (standard deviation = 1.9, range = 5.9–17.9), maternal thyroid function tests (serum thyrotropin [TSH], free thyroxine [fT4], and thyroid peroxidase [TPO] antibodies) were assessed in 5,100 women. We defined severe maternal hypothyroxinemia as fT4 < 5th percentile with normal TSH. Six years later, parents reported behavioral and emotional symptoms in 4,039 children (79%) using the Pervasive Developmental Problems (PDP) subscale of the Child Behavior Checklist and/or the Social Responsiveness Scale (SRS). We defined a probable autistic child by a PDP score > 98th percentile and SRS score in the top 5% of the sample (n = 81, 2.0%).


The association emerged from a study of more than 
4,000 Dutch mothers and their children, 
and it supports a growing view that autism spectrum disorders 
can be caused by a lack of maternal thyroid hormone, 
which past studies have shown is crucial to the migration 
of fetal brain cells during embryo development.


Results

Severe maternal hypothyroxinemia (n = 136) was associated with an almost 4-fold increase in the odds of having a probable autistic child (adjusted odds ratio = 3.89, 95% confidence interval [CI] = 1.83–8.20, p < 0.001). Using PDP scores, children of mothers with severe hypothyroxinemia had higher scores of autistic symptoms by age 6 years (adjusted B = 0.23, 95% CI = 0.03–0.37); SRS results were similar. No risk was found for children of TPO-antibody–positive mothers (n = 308).

Interpretation

We found a consistent association between severe, early gestation maternal hypothyroxinemia and autistic symptoms in offspring. Findings are concordant with epidemiological, biological, and experimental data on autism. Although these findings cannot establish causality, they open the possibility of preventive interventions.

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