| Philips et al., Southampton, Cardiff, and London, UK, analyzed if beside heredity, a low birth weight could as well determine the development of circulating thyroid autoantibodies. Of twins born between 1950 and 1955, representing 45 monozygous and 91 dizygous pairs, blood was taken for measurement of TPO-Ab and Tg-Ab. Overall TPO-Ab were present in 49/156 (31%) of women and in 7/116 (6%) of men. Of 26 monozygous female pairs 8 were concordant for Tg-Ab and 5 pairs discordant, resulting in a probandwise concordance rate of 76% while these values for the dizygous female pairs were 3 and 8 pairs, and 30% respectively. Similar concordance rates were found for TPO-Ab. These figures underline the importance of genetic factors in autoantibody development. Tg antibodies were more prevalent in monozygous twins than dizygous twins (30% vs 17%, p = 0.01). These latter results were explained on the notion that birth weights of monozygous twins tend to be lower than in dizygous twins. Another finding was that within the monozygous pairs, those twins who had a lower birth size, had a higher prevalence of TPO antibodies (p = 0.01). As in monozygous twins differences in birth weight are determined by the environmental conditions in utero, the authors suggest that apparently environmental factors are also of significance in development of thyroid autoantibodies in later life. Parkes et al., Cardiff, UK, did a randomized placebo controlled double blind study in that 0.1 mg T4 or placebo was administered to 335 postpartum women (known to be TPO-Ab positive at 14 weeks of gestation) between 6-24 weeks postpartum. Serum FT3, FT4 and TSH were measured at 6, 12, 16, 20, and 24 weeks postpartum. They found that before randomization about 20% of these women had a raised FT3. In the T4 treated group biochemical thyrotoxicosis developed in 68,6% which is highly significantly elevated versus the placebo group, showing hyperthyroidism in 19.2%. (Comment: What would the mechanism be of this high percentage of thyrotoxicosis in T4 treated women? Already present thyroid autonomy or induction of Graves' disease by T4? This latter phenomenon has been described.) Koutras et al., Athens, Greece, followed development of thyroid autoantibodies in two groups of pregnant women. Group A (n = 78) had an abnormal TSH (<0.3->3.7 ľU/ml), group B (n = 343) had a normal TSH (=0.3-=3.7 ľU/ml). In group A, a significantly higher prevalence of thyro |
