ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2019) 63 P1222 | DOI: 10.1530/endoabs.63.P1222

Screening of transient pulmonary hypertension in patients with Graves' disease

Héla Marmouch, Haythem Jenzri, Houssem Mrabet, Hamza Fekih & Ines Khochtali

Internal Medicine, Endocrinology Department, University Hospital, Monastir, TUNISIA, Monastir, Tunisia.

Introduction: Hyperthyroidism produce changes in cardiac contractility, blood pressure, and systemic or pulmonary vascular resistance. In almost all cases these cardiovascular changes are reversible when the underlying thyroid disorder is recognised and treated. Pulmonary hypertension (PAH) has been associated with hyroid dysfunction, but primaraly with hyperthyroidism. The vast majoity of patients with this form of PAH are usually older with toxic multinoduar goitre. The aim of this study was to determine the clinical correlates of PAH in patients with Graves’ disease (GD).

Methods: Our study is prospective and concerning patients with GD referred for echography before using any treatment. PAH hasbeen diagnosis when pulmonary artery systolic pressure was elevated.

Results: Our study concerned 36 patients. It is 22 women and 14 men. The average age is 35. Among 36 consecutive patients with GD referred for echography, 7 patients (19,44%) had PAH measered by Doppler echocardiography (pulmonary artery systolic pressure >35 mmHg). The search for anti-phospholipid antibodies was negative. The patients with PAH had significantly higher pulmonary vascular resistance (PVR), cardiac output, and TSH receptor anti-body (TRAb) compared to those without. Pulmonary artery systolic pressure may had a good correlation with TRAb, but was not related to free T4. All these patients have a reversible pulmonary hypertension after treatment.

Discussion: In addition to the effect of thyroid hormone on the cardiovascular system, auto-immune mediated pulmonary vascular remodelling may play a role in Graves’s disease-linked elevated pulmonary artery systolic pressure. An auto-immune processus inducing endothelial damage with GD may play a key role. Future studies should focus on discovering the immunogenetic overlap.

Conclusion: Study highlights the importance of considering hyperthyroidism as an origin of idiopathic PAH, and demonstrates the potential reversibility of its complications. At present, thyroid function tests should be considered in the invertigation of all patients.

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