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Hudig et al., Amsterdam, The Netherlands, studied the effects of
T3 on amiodarone-induced increase in plasma LDL cholesterol in rats. The
reason for this study was that amiodarone increases plasma cholesterol
in man due to an induced decreased number of liver LDL receptors. They
found that administration of T3, reverses the amiodarone-induced plasma
LDL cholesterol increase, and also the decrease in liver LDL receptor gene
expression. Their finding suggests, that some of the effects of amiodarone
are mediated by T3-dependent pathways and that amiodarone acts as a thyroid
hormone antagonist.
Martino et al., Pisa, Italy, performed color flow doppler sonography
(CFDS) in 5 non-goitrous thyrotoxic women with elevated FT4 and FT3, undetectable
TSH, absent thyroid antibodies and TSH receptor antibodies, and undetectable
serum TG levels, all suspected of suffering from thyrotoxicosis factitia
(due to surreptitious ingestion of excess thyroid hormone), and compa-red
the results of CFDS in untreated Graves' disease patients. All patients
with Graves' disease showed a pattern of hypervascularity and increased
peak systolic velocity (PSV), but the patients with suspected thyrotoxicosis
factitia showed absent hypervas-cularity and significantly lower PSV as
compared to Graves' disease and at the lower normal level of PSV in euthyroid
normal subjects. (Comment: Although the first line of approach, when thyrotoxicosis
factitia is suspected, is to detect serum TG as it is low or absent in
these cases, its estimation is difficult, if not impossible, when TG antibodies
are present. In that case CFDS may be an important tool for establishing
the diagnosis.)
Van Wassenaar et al. evaluated neurodevelopmental outcome in
infants < 30 weeks of gestation, when supplemented with T4, as transient
hypothyroxinemia of very preterm infants may cause developmental delay
and neurological dysfunction. The study was done in 200 infants < 30
weeks'gestational age in a randomized double-blind placebo-controlled trial.
Daily administration of 8 µg T4 per kilogram of birth weight or placebo
was started 12-24 hours after birth and discontinued 6 weeks later. Ultimately
82 children remained in the T4 group and 75 in the placebo group. At 24
months of age abnormal neurological outcome was reduced in the T4 group
as a whole compared to the placebo group. In infants < 27 weeks however,
mental development was significantly better in the T4 treated group versus
placebo, but the reverse was true in infants > 27 weeks i.e. a better result
in the placebo group. The authors conclude that T4 supplementation to infants
< 30 weeks gestation cannot be advised on the basis of these results.
They suggest that a new trial, including only infants < 27 weeks gestation,
should be performed for confirmation of their results.
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