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Strategies to accelerate recruitment to NHMRC multi‐centre clinical trials

Maternal auto-antibodies may cross the placenta and stimulate the fetal thyroid TSH receptor, causing excess thyroid hormone production, fetal hyperthyroidism and tachycardia that may lead to fetal hydrops. Conversely, and more rarely, these autoantibodies may also inhibit the fetal thyroid TSH receptor and cause hypothyroidism. In addition, antithyroid drugs cross the placenta and may inhibit fetal thyroperoxidase, causing inhibition of fetal thyroid hormone production, hypothyroidism and so potential neurological damage. Huel et al. have identified ultrasound features that may help differentiate thyroid function including thyroid vascular pattern (hypothyroid – peripheral vascularisation and hyperthyroid – central vascularisation), fetal heart rate (hyperthyroid – tachycardia) and bone maturation (hypothyroid – delayed and hyperthyroid – accelerated). However, FBS should still be considered to elucidate the cause of a fetal goitre prior to commencing treatment. Fetal hypothyroidism secondary to maternal antithyroid drug use treated with reduction of maternal drug dose and/or fetal therapy with T4 or T3 has previously been reported. In addition, fetal/neonatal hyperthyroidism as a consequence of maternal thyroid disease has been well described. However, reports of the fetus and infant being affected by both hypoand hyperthyroidism are rare. Rosenfeld et al. report on a register of women treated with PTU in pregnancy and summarise two cases of fetal hypothyroidism and subsequent neonatal hyperthyroidism. To our knowledge, this is the first case with clinical details of such a case with demonstrable maternal antibodies in the neonate. In this case, despite a relatively low dose of PTU and very high maternal antibodies, the fetus became significantly hypothyroid in utero secondary to maternal PTU (inhibition by maternal antibodies is unlikely due to rapid onset hyperthyroidism in the postnatal period). As maternal PTU dosage was decreased and the drug has a short half life, it is likely that drug levels were negligible in the neonate shortly following delivery. Conversely, maternal auto-antibodies may persist for several months and this neonate had very high levels of maternal antibody soon after birth that lead to symptomatic hyperthyroidism once the effects of PTU were eliminated. This case highlights the need to consider both hypoand hyperthyroidism as causes of fetal goitre, the benefit of antenatal sampling to confirm the diagnosis, and the need for ongoing neonatal surveillance.