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The transient thyrotoxicosis presents at about 14 weeks postpartum followed
by transient hypothyroidism at a median of 19 weeks. Very occasionally
the hypothyroid state is seen before the thyrotoxicosis. PPT is usually
associated with the presence of antithyroid antibodies. In one series from
Wales(16) the condition was not seen in antibody negative women. Anti thyroperoxidasse
(TPO) antibody is normally found, occasionally accompanied by anti thyroglobulin
(Tg) antibody. In less than 5% anti-Tg is the only marker. In a study of
152 antibody +ve women (as ascertained at 16 weeks gestation) compared
with 239 control women studied monthly for 12 months postpartum it was
found that PPT occurred in 50% of the antibody positives of whom 19% were
thyrotoxic alone, 49% hypothyroid alone and the remaining 32% thyrotoxic
followed by hypothyroidism. Examples of the clinical course are shown in
Fig. 1.
| Figure 1a: |
Figure 1b:
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Figure 1c:
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Figure 1a, 1b, 1c:
Course of transient postpartum thyrotoxicosis (Figs. 1a and b) and transient postpartum
hyper- and hypothyroidism (Fig. 1c). Blood samples were obtained weekly postpartum. Note
signi-ficant rise in TPO antibody titre postpartum. RAIU = radioiodine uptake.
Although the clinical manifestations of the thyrotoxic state are not
usually severe in PPT, lack of energy and irritability are particularly
prominent even in antibody +ve women who do not develop thyroid dysfunction.
In contrast the symptomatology of the hypothyroid phase may be profound.
Many classic hypothyroid symptoms occur before the onset of thyroid hormone
reduction and persist even when recovery is seen in hormone levels. Thus,
despite the transitory nature of the condition in many cases, there is
significant clinical morbidity.
Early accounts of PPT noted an anecdotal association of depression with
thyroid dysfunction during the postpartum period. More recently, depressive
symptomatology has been quantitated by Harris et al(17) in a large number
of postpartum anti-TPO positive women and compared to an age matched control
group of anti-TPO negative postpartum women. The data clearly show an increase
of mild to moderate depression in the antibody positive women irrespective
of thyroid status. Some indication of the excess of depressive symptomatology
was seen as early as 6 weeks postpartum. There is no clear explanation
for these findings but it is possible that antibodies could modulate neurotransmitter
function and it is known that there are cytokine receptors in the brain(18).
The possibility that thyroid antibodies are a marker for a specific genotype
related to depression also requires investigation. A large double-blind
randomised placebo controlled trial of thyroxine 0.1mg per day administered
from 6 weeks to 24 weeks in anti-TPO positive women (as ascertained at
16 weeks gestation) has failed to show any significant effect of T4 on
the frequency and severity of depressive symptomatology(19).
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