Exertional symptoms, dyspnea, and impaired effort tolerance are common in patients with Graves disease. Proposed explanations include high-output left heart failure, ineffective oxygen utilization, and respiratory muscle weakness. In addition, cases of pulmonary arterial hypertension (PAH) in patients with Graves disease have been reported. Vascular endothelial growth factor (VEGF) is produced by thyroid follicular epithelial cells in response to stimulation of the TSH receptor. Secreted VEGF can lead to endothelial cell proliferation and a significant increase in serum VEGF levels in Graves disease patients has been observed and the role of VEGF in PAH suggested. To evaluate the change of pulmonary artery pressure (PAP) and VEGF in Graves disease, we performed two-dimensional and Doppler echocardiography and serum VEGF using ELISA (R&D systems) in 28 untreated Graves disease patients before and after treatment (25 patients on propylthiouracil and 3 with RAI) and 10 normal controls. Pulmonary artery (PA) pressure was increased in patients with Graves disease compared to normal controls (mean 23.5 vs 29.3 mmHg, P<0.05). 44% of Graves disease (12 patients) showed PAH (PA>30 mmHg) and serum TBII level was higher in Graves disease with pulmonary arterial hypertension than normal PA (P<0.05). After treatment, PA was normalized and serum VEGF was decreased (from 314.8±81.29 to 267.8±69.15 pg/ml, P<0.05). In conclusion, 44% of untreated Graves disease showed PAH and PAP was decreased after treatment. The pathogenesis of PAH in Graves disease needs further studies.
18 - 21 May 2019
European Society of Endocrinology