Pregnancy
  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 17th–40th 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 0.3–7.1 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 15th–24th 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 200–900 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.