Gene fluctuation predicted thyroid disease in premature babies

Misregulation of gene expression in premature births may affect genes involved in fetal growth and thyroid function, according to research presented at the Joint 15th International Congress of Endocrinology and 14th European Congress of Endocrinology Meeting.

Luca Persani, MD, PhD, associate professor of endocrinology at the University of Milan, Italy, and Institute of Endocrine Sciences Istituto Auxologico Italiano IRCCS, and researchers investigated patterns of blood DNA methylation in 31 babies with congenital hypothyroidism (CH) born prematurely, according to their gestational age, growth percentile and levels of thyroid stimulating hormone (TSH).

“We found that far less of the DNA of premature babies with congenital hypothyroidism is methylated, that is, far less is found in the ‘off position.’ The analysis was performed on blood cell DNA and therefore caution should be given in the interpretation of such results. However, a number of the potentially affected genes we found are involved in fetal growth and thyroid hormone metabolism, which gives us a preliminary indication that this could be related to premature birth and could predispose children to congenital hypothyroidism,” Persani said.

Persani and colleagues said 95% of the gene-specific methylation analyses were hypomethylated, and 70% were represented by CpG sites in non-coding regions of DNA.

Based on suggested data, genomic fluctuation caused by global hypomethylation could be linked to premature birth and fetal growth delay, they said.  Additionally, the team concluded thyroid defects could be caused by “an increased expression of predisposing-genes, rather than a reduced expression of protective-genes.”

Persani said research has barely scratched the surface, and further investigation will be conducted to determine whether the deregulation is a cause or effect of premature birth.

Disclosure: The researchers report no relevant financial disclosures.