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Postpartum thyroiditis (PPT) including hyperor hypothyroidism or both occurs
in 50% of thyroperoxidase (TPO) Ab positive women as detected early in
gestation. Ammari et al., Cardiff, UK, found in a study in 50 women that
there is a high risk of developing PPT following a subsequent pregnancy
if PPT had occurred previously (10/12 women). However, 24% of women who
were TPO-Ab positive and who were euthyroid after the first pregnancy,
developed PPT after the second one. The importance of screening for TPO-Ab
early in gestation is stressed. The same group reported earlier that TPO-Ab
positive women have an increased risk of developing postpartum depression
as compared to TPO-Ab negative women irrespective of thyroid function.
In the present report they present results of a study in which 187 TPO-Ab
positive women received T4 treatment vs.185 TPO-Ab positive women who received
placebo and applied 4 different psychiatric tests to evaluate depression.
Only one test just showed significance in favour of less depression during
T4 substitution. The authors conclude that the results are still preliminary.
(Comment: If indeed the occurrence of postpartum depression is not related
to thyroid function, but only to the absence or presence of TPO-Ab, it
is not surprising that hardly a significant effect of T4 substitution is
seen in this study.)
Shimizu et al., Tokyo, Japan, studied 5 patients with Graves' disease
who remained euthyroid during pregnancy and who experienced a thyrotoxic
relapse 2-4 months after delivery. Three patients developed (destructive)
painless thyroiditis and all had high antibodiey titres against thyroglobulin
and TPO in the first trimester, whereas the other 2 patients, who's relapse
was due to Graves' disease, had low, or no antibodies in the first trimester
of pregnancy. Although PTU treatment during breast-feeding is considered
safe, the issue concerning the use of methimazole has not yet been clarified.
Azizi et al., Tehran, Iran, studied the effect of different doses of
methimazole on thyroid function of neonates during breast-feeding when
mothers were using 5 mg (15 newborns), 10 mg (14 newborns), and 20 mg (6
newborns) daily. In neither of these groups abnormalities in neonatal thyroid
function (TSH, T4 and T3) were found during the study period being 1 month.
(Comment: Although the authors suggest that up to 20 mg per day of methimazole
is safe, we would caution against this advise, because the study period
is too short to draw definite conclusions, although these preliminary results
are certainly welcome.)
A more elaborate study was performed by Abe et al., Sagamihara, Japan,
on the same subject. In a preliminary study in 6 lactating women, given
a single oral dose of 15 mg methimazole at 6 p.m., analysis showed that
methimazole half-life in serum was 5.4 hr and 4.2 hr in milk. Methimazole
concentrations after 12 hr were very low, both in serum in milk. Other
studies in women who underwent thyroidectomy showed that methimazole was
concentrated in the thyroid gland and there was no correlation between
intrathyroidal methimazole and serum concentrations. Based on these studies,
5 lactating women were treated with 5-15 mg methimazole administered in
a single dose in the evening. If necessary, infants were fed by breast-milk
collected during the day or by bottle-milk. Studies were done on neonatal
thyroid function for a period of 90 days and no abnormal thyroid function
in these infants was found. It is concluded that a single evening dose
of methimazole to a maximum of 15 mg is safe in breast-feeding women, provided
that night-feeding should use breastmilk collected during the day.
Laryea et al., Montreal, Canada, performed thyroid function tests in
two thousand women, 24 hr after delivery of a live baby. They found different
grades of hypothyroidism in 24, all having elevated serum TSH, but different
levels of FT4 ranging for normal into the low normal range. Transient hypothyroxinemia
is commonly found in the first 4-8 postnatal weeks in preterm infants.
Van Wassenaer et al., Amsterdam, The Netherlands, compared plasma iodothyronine
levels in 100 preterm infants treated with 8 ug/kg birthweight T4 daily
or with placebo during the first 6 postnatal weeks. In this randomized
study T4 and rT3 levels were higher in the T4 treated group, but T3 was
lower than in the placebo group, probably by inhibition of T4 secretion
by the thyroid. There was no difference in mortality or morbidity in the
two groups and the study confirms the limited role of type I deiodinase
in sustaining T3 levels in these preterm infants.
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