Pulmonary Arterial Hypertension in Graves' Disease: Role of Thyroid Autoimmunity and NEDD9.

Introduction: Pulmonary arterial hypertension (PAH) is an underrecognized cardiovascular complication of Graves' disease (GD). The role of thyroid autoimmunity and neural precursor-cell-expressed developmentally downregulated 9 (NEDD9), a profibrotic protein, in GD with PAH remains unclear. This study evaluated the prevalence, predictors of PAH, role of thyroid autoimmunity and NEDD9, and reversibility with carbimazole in newly diagnosed GD and PAH. Methods: This prospective observational study enrolled 90 newly diagnosed GD patients. PAH was defined as mean pulmonary artery pressure (mPAP) >20 mmHg and was assessed non-invasively by echocardiography. Serum FT3, FT4, TSH, and anti-thyroid peroxidase (anti-TPO) antibodies were measured using chemiluminescent immunoassay (CLIA), while TSH receptor antibodies (TRAb) and plasma NEDD9 were quantified by enzyme-linked immunosorbent assay (ELISA). Binary logistic regression identified independent predictors of PAH. Thyroid autoimmunity markers and NEDD9 were evaluated in relation to a ≥10 mmHg reduction in mPAP after carbimazole therapy. Results: Among 90 GD patients, PAH was observed in 39 (43.3%). On correlation analysis, only TRAb was positively correlated with mPAP. In binary logistic regression, TSH receptor antibody levels (OR: 1.093; 95% CI: 1.035-1.155; Conclusion: Thyroid autoimmunity significantly contributes to PAH in GD, while NEDD9 showed no association.