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There are two concerns about ATDs when used in the treatment of hyperthyroidism during pregnancy:
1. That they produce foetal hypothyroidism and goitre.
2. That they have teratogenic effects.
Fully functional thyroid tissue is not present until 10 weeks' gestation. Therefore ADT treatment is unlikely to have an adverse effect on foetal thyroid function unless it begins after 10 weeks of pregnancy [Editor's note: annecdotal evidence suggests that this same argument applies to inadvertent administration of radioactive iodine during early pregnancy.]
Ironically, because it is less effective at controlling hyperthyroidism, PTU may be less
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likely than MMI to have an adverse effect on foetal thyroid function. This sentiment is echoed elsewhere, allbeit for a different (and debatable) reason.
Although risks to the foetal thyroid from moderate doses of ATDs appear to be small, the use of higher doses of carbimazole in combination with thyroxine to prevent hypothyroidism should be avoided.
In terms of teratogenicity, PTU has traditionally been 'preferred' over MMI. Part of the reason for this 'prejudice' has been the reported association of MMI with aplasia cutis, a rare foetal scalp defect. However, this association has recently been questioned; moreover, aplasia cutis is not seen as a contraindication for MMI's use in pregnancy. Similarly, the reported association between MMI and more serious congenital malformations such as tracheosophageal fistulas has recently been questioned. |
