TY - JOUR
T1 - Thyroid Dysfunction in Patients with Pulmonary Artery Hypertension (PAH)
T2 - The Effect of Therapies Affecting the Prostanoid Pathway
AU - Menon, Aravind A.
AU - Sahay, Sandeep
AU - Braverman, Lewis E.
AU - Farber, Harrison W.
N1 - Funding Information:
AA.M and L.E.B have no conflicts of interest to disclose. S.S has received consultant fees from Actelion Pharmaceuticals and speaker fees from Actelion Pharmaceuticals, Bayer AG and United Therapeutics Corporation. H.W.F. has received research grants from Gilead; Actelion Pharmaceuticals US Inc; and United Therapeutics Corporation and consulting fees from Gilead; Actelion Pharmaceuticals US, Inc; United Therapeutics Corporation; Bayer AG; Arena, Boehringer-Ingelheim; and Bellerophon. He also has served on a speaker’s bureau or given presentations on behalf of Actelion Pharmaceuticals US, Inc; Gilead; and Bayer AG. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Publisher Copyright:
© 2019, Springer Science+Business Media, LLC, part of Springer Nature.
PY - 2019/12/1
Y1 - 2019/12/1
N2 - Introduction: Epoprostenol, a synthetic prostaglandin I2 (PGI2) analog, has been the mainstay of treatment for severe pulmonary arterial hypertension (PAH) for the last two decades. Treprostinil, another synthetic prostaglandin analog, and selexipag, an oral selective Inositol Phosphate (IP) prostacyclin receptor agonist, have also been approved for treatment of PAH. Prostacyclin and its analogs cause a variety of side effects in patients with PAH; however, thyroid dysfunction is rarely reported. Methods: After treating an index case of thyroid dysfunction occurring after initiation of epoprostenol, we reviewed our databases of PAH patients treated with epoprostenol, treprostinil or selexipag to identify the occurrence of this association. Results: We identified six cases of thyroid dysfunction in our cohort: five after initiation of an intravenous prostacyclin (epoprostenol) and one after initiation of an oral prostacyclin receptor agonist (selexipag). Four of the patients presented with hyperthyroidism and two with a large autoimmune goiter. Graves’ disease was seen in three patients, Hashimoto’s disease in two patients and thyrotoxicosis in one patient. Conclusion: Therapy with medications targeting the prostacyclin pathway is a potential risk factor for the development of symptomatic thyroid disease.
AB - Introduction: Epoprostenol, a synthetic prostaglandin I2 (PGI2) analog, has been the mainstay of treatment for severe pulmonary arterial hypertension (PAH) for the last two decades. Treprostinil, another synthetic prostaglandin analog, and selexipag, an oral selective Inositol Phosphate (IP) prostacyclin receptor agonist, have also been approved for treatment of PAH. Prostacyclin and its analogs cause a variety of side effects in patients with PAH; however, thyroid dysfunction is rarely reported. Methods: After treating an index case of thyroid dysfunction occurring after initiation of epoprostenol, we reviewed our databases of PAH patients treated with epoprostenol, treprostinil or selexipag to identify the occurrence of this association. Results: We identified six cases of thyroid dysfunction in our cohort: five after initiation of an intravenous prostacyclin (epoprostenol) and one after initiation of an oral prostacyclin receptor agonist (selexipag). Four of the patients presented with hyperthyroidism and two with a large autoimmune goiter. Graves’ disease was seen in three patients, Hashimoto’s disease in two patients and thyrotoxicosis in one patient. Conclusion: Therapy with medications targeting the prostacyclin pathway is a potential risk factor for the development of symptomatic thyroid disease.
KW - Epoprostenol
KW - Hyperthyroidism
KW - Prostanoids
KW - Pulmonary hypertension
KW - Selexipag
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U2 - 10.1007/s00408-019-00283-8
DO - 10.1007/s00408-019-00283-8
M3 - Article
C2 - 31696306
AN - SCOPUS:85074819984
SN - 0341-2040
VL - 197
SP - 761
EP - 768
JO - Lung
JF - Lung
IS - 6
ER -