Association between Maternal HCV and Developing Thyroid Disorders

What is it about?

It has been suggested that maternal HCV (chronic hepatitis C) may increase the risk of preterm delivery, teratogenic consequences, child death, and neonatal thyroid disorders (thyroiditis or cancer). The presence of positive thyroid antibodies and macrophages is the prognostic factors of the thyroid disorders. In addition, these disorders may cause several brain disabilities and inflammatory-immune diseases in fetuses, neonates, and childhood. In general, these disturbances may delay the development and growth depending on the severity of HCV and time of its infection. However, the disruption mechanisms of HCV during the different periods of development are still uncertain. Thus, following the state of the pregnancy and the levels of maternal T3, T4, thyroid-stimulating hormone (TSH), thyroid antibodies, and serum fibrosis markers in the presence of HCV infection should be more significant to avoid or decrease the risk of teratogenic consequences and neonatal thyroid dysfunction. Hopefully, several pharmacogenomics methods will be used to recognize the activity of maternal thyroid gland during the gestation previous to the initiation of HCV treatments. Additional work is vital to determine the developmental (the metabolic pathways), molecular and biochemical disruption mechanisms of maternal HCV infection and its treatment during the fetal and neonatal development. Clinical examinations are still essential to understand the associations between the chronic HCV infection and the prevalence of maternofetal autoimmune thyroid disorders and thyroid cancer. As well, several studies are required to discover novel drugs for HCV treatment and new therapeutic approaches to improve the maternofetal and neonatal health consequences, and to decrease the morbidity and mortality in fetuses, neonates or child.

Featured Image

Why is it important?

The presence of positive thyroid antibodies and macrophages is the prognostic factors of the thyroid disorders. In addition, these disorders may cause several brain disabilities and inflammatory-immune diseases in fetuses, neonates, and childhood. In general, these disturbances may delay the development and growth depending on the severity of HCV and time of its infection. However, the disruption mechanisms of HCV during the different periods of development are still uncertain. Thus, following the state of the pregnancy and the levels of maternal T3, T4, thyroid-stimulating hormone (TSH), thyroid antibodies, and serum fibrosis markers in the presence of HCV infection should be more significant to avoid or decrease the risk of teratogenic consequences and neonatal thyroid dysfunction. Hopefully, several pharmacogenomics methods will be used to recognize the activity of maternal thyroid gland during the gestation previous to the initiation of HCV treatments.

Perspectives