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Review
. 2022 Feb 10;11(4):921.
doi: 10.3390/jcm11040921.

The Role of Thyroid Disorders, Obesity, Diabetes Mellitus and Estrogen Exposure as Potential Modifiers for Pulmonary Hypertension

Affiliations
Review

The Role of Thyroid Disorders, Obesity, Diabetes Mellitus and Estrogen Exposure as Potential Modifiers for Pulmonary Hypertension

Eleni Vrigkou et al. J Clin Med. .

Abstract

Pulmonary hypertension (PH) is a progressive disorder characterized by a chronic in-crease in pulmonary arterial pressure, frequently resulting in right-sided heart failure and potentially death. Co-existing medical conditions are important factors in PH, since they not only result in the genesis of the disorder, but may also contribute to its progression. Various studies have assessed the impact of thyroid disorders and other endocrine conditions (namely estrogen exposure, obesity, and diabetes mellitus) on the progression of PH. The complex interactions that hormones may have with the cardiovascular system and pulmonary vascular bed can create several pathogenetic routes that could explain the effects of endocrine disorders on PH development and evolution. The aim of this review is to summarize current knowledge on the role of concomitant thyroid disorders, obesity, diabetes mellitus, and estrogen exposure as potential modifiers for PH, and especially for pulmonary arterial hypertension, and to discuss possible pathogenetic routes linking them with PH. This information could be valuable for practicing clinicians so as to better evaluate and/or treat concomitant endocrine conditions in the PH population.

Keywords: diabetes mellitus; estrogen; obesity; pulmonary hypertension; thyroid disorders.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Biologically plausible pathogenetic routes (indicated by arrows) linking hypothyroidism with PH. Abbreviations: dBP, diastolic blood pressure; NO, nitric oxide; SVR, systemic vascular resistance.
Figure 2
Figure 2
Biologically plausible pathogenetic routes (indicated by arrows) linking hyperthyroidism with PH. Abbreviations: CO, cardiac output; NO, nitric oxide.

References

    1. Galiè N., Humbert M., Vachiery J.L., Gibbs S., Lang I., Torbicki A., Simonneau G., Peacock A., Vonk Noordegraaf A., Beghetti M., et al. 2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS) Eur. Heart J. 2016;37:67–119. doi: 10.1093/eurheartj/ehv317. - DOI - PubMed
    1. Simonneau G., Montani D., Celermajer D.S., Denton C.P., Gatzoulis M.A., Krowka M., Williams P.G., Souza R. Haemodynamic definitions and updated clinical classification of pulmonary hypertension. Eur. Respir. J. 2019;53:1801913. doi: 10.1183/13993003.01913-2018. - DOI - PMC - PubMed
    1. Huber L.C., Bye H., Brock M. Swiss Society of Pulmonary Hypertension. The pathogenesis of pulmonary hypertension—An update. Swiss Med. Wkly. 2015;145:w14202. - PubMed
    1. Lan N.S.H., Massam B.D., Kulkarni S.S., Lang C.C. Pulmonary Arterial Hypertension: Pathophysiology and Treatment. Diseases. 2018;6:38. doi: 10.3390/diseases6020038. - DOI - PMC - PubMed
    1. Simonneau G., Galiè N., Rubin L.J., Langleben D., Seeger W., Domenighetti G., Gibbs S., Lebrec D., Speich R., Beghetti M. Clinical classification of pulmonary hypertension. J. Am. Coll. Cardiol. 2004;43:S5–S12. doi: 10.1016/j.jacc.2004.02.037. - DOI - PubMed

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