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Cortelazzi et
al., San Paolo and Milan, Italy, measured serum TSH and FT4 in 29
foetuses with intrauterine growth retardation (IUGR) due to
placental perfusion defects, in 24 foetuses were affected with
malformations, in 12 with trisomy of chromosomes 13, 18, and 21,
in 15 foetuses with encephalic disorders with the exception of
anencephaly, in 11 from red cel-isoimmunized pregnancy, and in 7
thalassemic foetuses. Hundred sixty-four foetuses without any
abnormality were used as a control group. Blood samples were
collected by cordocentesis from the 17th40th week of
gestation. Results IUGR vs controls: FT4 13.4 ± 1.6 pmol/l vs
16.6 ± 5.2 pmol/l (p = 0.01). Serum TSH in IUGR were in upper
normal range 5.0 ± 1.8 mU/l (normal range 0.37.1 mU/l).
Foetuses affected with chromosomal alterations had significantly
higher (p = 0.01) TSH concentrations (mean 6.0 ± 2.3 mU/l) than
controls (3.3 ± 1.7 mU/l) between 15th24th weeks, while
their FT4 levels were within normal range. In all the other
pathological groups thyroid function was normal as compared to
controls. The authors conclude that the low FT4 of IUGR foetuses
at the end of gestation may represent a beneficial adaptation to
starvation leading to a decrease in metabolic rate and oxygen
consumption as seen in postnatal non-thyroidal illness.
Furthermore, the high TSH levels in foetuses with chromosomal
alterations during gestation may represent a precocious evidence
of a hypothalamic pituitary thyroid-axis disorder.
Parkes et al., Cardiff, UK, studied 57 women
without previous history of thyroid disease at 16 weeks of
gestation, 21/57 were negative for TPO antibodies and 15/21 were
euthyroid, 2/21 hypothyroid, and 4/21 hyperthyroid. 36/57 were
TPO antibody positive, 23/36 euthyroid, 7/36 hypothyroid, and
6/36 hyperthyroid. Thyroid stimulating antibodies (TSAB) and
thyroid stimulating blocking antibodies (TBAB) were measured by
luminescent assays. 6/57 Samples had positive TSAB and 1/57
positive for TSAB and TBAB. All these 7 patients had thyroid
dysfunction and TPO antibodies. When these 7 sera were tested as
purified IgG, the 6 TSAB positive sera became negative. Purified
IgG of the patient with positive TSAB and TBAB remained positive.
The authors stress the importance of using purified IgG for
assessing the true prevalence of stimulating and blocking
antibodies in pregnancy. Nøhr et al., Aalborg, Denmark, studied
the effect of iodine supplementation to pregnant women from an
area with mild iodine deficiency. Twenty-two women received 150
µg iodine during pregnancy and postpartum, 24 only during
pregnancy, while 26 patients received placebo. The results of
this study were that iodine supplementation of 150 µg during
pregnancy and the postpartum period was safe. There was no
significant increase in incidence or severity of postpartum
thyroid dysfunction in women found to be TPO-Ab positive at
screening. Furthermore, this study confirmed that screening for
TPO-Ab in early pregnancy predicts the risk for development of
postpartum thyroid dysfunction, as thyroid dysfunction occurred
in 35% of women with TPO-Ab levels <200 U/l, 55% between
200900 U/l, and 75% >900 U/l. Furthermore, titer of
TPO-Ab correlated with severity of postpartum thyroid
dysfunction. (Comment: As it has recently been reported, N Engl J
Med, August 1999, that a mildly lowered FT4 during pregnancy may
result in impaired cognitive function of offspring, this report
again stresses the necessity to screen pregnant women as early as
possible on the presence of TPO-Ab.)
Mariotti et al., Rome, Italy, measured the
prevalence of TPO-Ab and Islet-cell antibodies (ICA) in 2294
pregnant women at delivery. The prevalence of TPO-Ab was 11.9%
and of ICA 2.6%. There was no overall relationship between the
presence of thyroid autoantibodies and ICA. However, in sera with
high titers of ICA, the concomitant presence of TPO-Ab was 35.3%
(6/17) whereas when ICA titres were low, the prevalence was 7.1%
(3/42), being statistically significant differences.
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