Pre-eclampsia and later hypothyroidism

It is believed that pre-eclampsia is probably caused by excess production of antiangiogenic factors such as soluble fms-like tyrosine kinase 1 (sFlt-1). Blood levels of sFlt-1 increase in late pregnancy, and the increase is much greater in women with pre-eclampsia. People treated with antiangiogenic factors for cancer may develop hypothyroidism. Now, data from US and Norwegian studies have confirmed that women who have had pre-eclampsia may have an increased risk of hypothyroidism associated with excess production of antiangiogenic factors.

Data were analyzed from 141 women in the US Center for Personalized Education for Physicians (CPEP) study of 1992–1995 and from 7,121 women in the Norwegian Nord-Trondelag Health Study of 1995–1997. In the CPEP study, serum Thyroid Stimulating Hormone (TSH) levels increased by a factor of 2.4 after the onset of preeclampsia, compared with a 1.5-fold increase in non-pre-eclamptic controls. There was a greater fall in levels of free triiodothyronine with preeclampsia. The increase in TSH levels was strongly associated with high sFlt-1 levels towards the end of pregnancy.

In the Norwegian study, women who had pre-eclampsia in their first pregnancy were 1.7 times more likely to have a raised TSH level later. This rise in TSH was not accompanied by thyroid peroxidase antibodies, suggesting that it was not due to autoimmune thyroid disease. Pre-eclampsia in both first and second pregnancies increased the risk still further (nearly six-fold).

Increase in sFlt-1 levels in pre-eclampsia may be associated with subclinical hypothyroidism with a risk of later clinical hypothyroidism.

Levine R et al. Pre-eclampsia, soluble fms-like tyrosine kinase 1, and the risk of reduced thyroid function: nested case-control and population based study. BMJ 2009; 339: 1355–1359 (b4336); North RA, Taylor RN. Subclinical hypothyroidism after pre-eclampsia. Ibid: 1323–1324 (editorial).