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Department of Internal Medicine, University Hospital Uppsala
The Department of Internal Medicine, Central Hospital Västerås, Sweden
Address all correspondence and requests for reprints to: F. Anders Karlsson, Department of Internal Medicine, University Hospital, S-751 85 Uppsala, Sweden.
In the present study we examined the influence of L-T4 and iodide on autoimmune postpartum thyroiditis. Women at risk of developing the disease were identified in early pregnancy by the presence of moderate or high titers of antibodies against thyroid peroxidase (TPOAb). They were given no treatment (n = 20), 0.1 mg L-T4 daily (n = 18), or 0.15 mg iodide daily (n = 20) for 40 weeks postpartum.
Changes in thyroid function were seen in all women, although n i nine hormone values remained within the reference ranges of erthymoid individuals. In each group of women, thyrotoxicosis occurred around 2–3 months postpartum, followed by a gradual rise of TPOAb. Subsequently, around 5–7 months postpartum, a hypothyroid phase was observed. TSH elevations (<5 mU/L) occurred in 9 of 18 women in spite of treatment with 0.1 mg L-T4 although elevations were lower than in the other two groups. Among those women who developed abnormal thyroid function, the hormone changes appeared greater in the iodide-treated group than in the control group, suggesting that in certain patients iodide may aggravate rather than ameliorate the disease.
All 58 women showed a reduction of TPOAb during pregnancy and a transient rise during the postpartum year. The extent of TPOAb elevations did not differ between the groups. Thus, the administration of L-T4 prevented hypothyroid symptoms, but did not alter the course of the postpartum thyroiditis, which appears not to be accelerated by events of target cell origin.
* This work was supported by the Swedish Medical Research Council (no. 4996), the Pharmacia Foundation, and the Swedish Life Insurance Foundation.
Received August 7, 1989.
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