Study on the relationship between hyperthyroidism and vascular endothelial cell damage.

The aim of the research is to explore the relationship between hyperthyroidism, iodine, antithyroid drugs (propylthiouracil) and vascular endothelial injury. In total, 136 SD rats were randomly allocated into the control group, the hyperthyroidism group, the hyperthyroidism propylthiouracil group, the hyperthyroidism low iodine group, the high iodine group, and the endothelial injury group. Rats were raised for 60 days. Afterward, indicators concerning endothelial damage were determined, including the von Willebrand Factor (vWF), thrombomodulin (TM), nitric oxide (NO), endothelin 1 (ET-1), and P-selectin, as well as the plant hemagglutinin sample type oxidized low-density lipoprotein receptor 1 (LOX-1) from the aorta and the number of endothelial progenitor cells (EPCs) in whole blood. The hyperthyroidism group had significantly higher values for vWF, TM, NO, ET-1, and P-selectin in serum and a higher number of EPCs in whole blood compared with the control group, similar to the LOX-1 expression in abdominal aorta. The hyperthyroidism low iodine group had significantly higher values for vWF, ET-1, and P-selectin in serum and a higher number of EPCs in whole blood compared with those of the control group, as was the case for LOX-1 expression in the abdominal aorta. The hyperthyroidism propylthiouracil group had significantly higher values for FT4 in the serum compared with those in the control group. The electron microscope showed that hyperthyroidism caused a certain degree of endothelial injury to the abdominal aorta in rats. Hyperthyroidism can damage the vascular endothelium and is a high-risk factor for cardio-cerebrovascular disease. Propylthiouracil could be used in the treatment of hyperthyroidism, thus protecting endothelial cells from damage.

Subclinical thyroid disease and single nucleotide polymorphisms in reproductive-age women in areas of Shanxi Province, China, where iodine exposure is excessive.

BACKGROUND AND OBJECTIVES: When iodine intake is in excess, a susceptible population that has a genetic predisposition will have an increased risk of hypothyroidism or autoimmune thyroiditis. This study evaluated the vulnerability to iodine excess and subclinical thyroid disease through screening of single nucleotide polymorphisms (SNPs) in reproductive-age women to provide evidence to be used for the prevention of subclinical thyroid disease. METHODS AND STUDY DESIGN: In Shanxi province, four areas where a range of iodine exposures from low to high were chosen in each region, 60 women were anticipated to enrol, including 20 pregnant women, 20 lactating women, and 20 non-pregnant, non-lactating women. Genotyping was performed using whole-blood samples, and the genotypes of 21 SNPs were determined and compared among areas with different water iodine and between controls and patients with subclinical thyroid disease. RESULTS: In total, 241 participants were enrolled. Among the 21 candidate SNPs, no difference was found among areas with various water iodine, whereas, TG (rs2252696), TSHR (rs4903957), CTLA-4 (rs231775), CAPZB (rs1472565), PDE4D (rs27178), and HLA (rs2517532) were significantly associated with various subclinical thyroid diseases; in particular, the PDE4D (rs27178), ad hoc TT allele, was associated with all examined subclinical thyroid diseases. CONCLUSIONS: Vulnerability to subclinical thyroid diseases is influenced by the presence of gene polymorphisms. There is a need for screening of suspected genes to effectively prevent and reduce the occurrence of thyroid diseases. People with the TT allele in PDE4D (rs27178) should be made aware of an increased risk of subclinical thyroid disease.