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Communications to the Editor |

Primary Pulmonary Hypertension and Thyroid Disease Primary Pulmonary Hypertension and Thyroid Disease FREE TO VIEW

Alejandro C. Arroliga, MD, FCCP; Raed A. Dweik, MD, FCCP; Albert L. Rafanan, MD
Author and Funding Information

Affiliations: Cleveland Clinic Foundation Cleveland, OH,  Yale University School of Medicine New Haven, CT Maine Medical Center South Portland, ME

Correspondence to: Alejandro C. Arroliga, MD, FCCP, Director, Fellowship Program, Cleveland Clinic Foundation, 9500 Euclid Avenue, Dept G62, Cleveland, OH 44195-0001; e-mail: arrolia@ccf.org



Chest. 2000;118(4):1224-1225. doi:10.1378/chest.118.4.1224
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To the Editor:

We read with interest the article of Nakchbandi et al (November 1999).1We agree that an association exists between primary pulmonary hypertension (PPH) and thyroid disease. Our group recently reported a cohort of 40 patients with PPH, in whom the prevalence of hypothyroidism was 22.5%.2

The association between hyperthyroidism and pulmonary hypertension has been described since the early 1980s.3 We recently treated two patients with moderate and severe pulmonary hypertension documented by echocardiography and Grave’s disease, in which the pulmonary hypertension improved after treatment of the hyperthyroid state. Nakchbandi et al suggested that pulmonary hypertension in a patient with hyperthyroidism was probably caused by a high cardiac output, endothelial damage/dysfunction, or increased metabolism of intrinsic pulmonary vasodilating substances. We offer an alternative explanation for the presence of pulmonary hypertension in some patients with hyperthyroidism.

The relationship between the hyperthyroid state and the sympathoadrenal system is a complex one.4Electrical stimulation of the sympathetic nerves causes pulmonary vasoconstriction, reduction of pulmonary artery compliance, and increase in pulmonary vascular resistance.57 In some studies, acetylcholine can induce pulmonary vasodilator response,8 but in the presence of hyperthyroidism, it is possible that the cholinergic output is decreased and the vasodilator response is diminished. The final result is an increase in the pulmonary artery pressure and pulmonary vascular resistance in some patients with hyperthyroid state. Our proposed explanation is consistent with the transient nature of pulmonary hypertension as documented by Nakchbandi et al.1

Nakchbandi, IA, Wirth, JA, Inzucchi, SE (1999) Pulmonary hypertension caused by Grave’s thyrotoxicosis: normal pulmonary hemodynamics restored by131I treatment.Chest116,1483-1485. [CrossRef] [PubMed]
 
Curnock, AL, Dweik, RA, Higgins, BH, et al High prevalence of hypothyroidism in patients with primary pulmonary hypertension.Am J Med Sci1999;318,289-292. [CrossRef] [PubMed]
 
Shimazaki, M, Mitsuhashi, T, Hasegawa, K Idiopathic pulmonary hypertension associated with hyperthyroidism: an autopsy case.Nippon Rinsho1980;38,1783-1786. [PubMed]
 
Nilsson, OR, Karlbert, BE Thyroid hormones and the adrenergic nervous system.Acta Med Scand Supp1983;672,27-32
 
Ingram, RH, Szidon, JP, Skalak, P, et al Effects of sympathetic nerve stimulation the pulmonary arterial tree of the isolated lobe perfusedin situ.Circ Res1968;22,801-815. [CrossRef] [PubMed]
 
Kadowitz, PJ, Hyman, AL Effect of sympathetic nerve stimulation on pulmonary vascular resistance in the dog.Circ Res1972;32,221-227
 
Hyman, AL, Kadowitz, PJ Enhancement of alpha and beta-adrenoreceptor responses by elevations in vascular tone in pulmonary circulation.Am J Physiol1986;250,H1109-H1116. [PubMed]
 
Rudolph, AM, Kurland, MD, Auld, PAM, et al Effects of vasodilator drugs on normal and serotonin constricted pulmonary vessels in the dog.Am J Physiol1959;197,617-623. [PubMed]
 

Primary Pulmonary Hypertension and Thyroid Disease

To the Editor:

We appreciate the comments made by Arroliga et al. Our report describes a patient with thyrotoxicosis and resultant secondary pulmonary hypertension. As we noted in our article, evaluation of thyroid function should be considered in patients with unexplained pulmonary hypertension.

The possible explanation offered by Arroliga et al about the pathophysiology of the association is intriguing. The study of pulmonary vascular changes in patients with thyrotoxicosis has been confounded by the involvement of the cardiovascular system.1The fact that β-adrenergic receptor blockade ameliorates some of the manifestations of thyrotoxicosis suggests that catecholamines play a key role in their pathogenesis. This is most likely a result of enhanced catecholamine sensitivity, responsiveness, or both, because plasma concentrations of catecholamines have been demonstrated to be normal in these patients.2

We know of no direct evidence of decreased cholinergic output in hyperthyroidism. In actively hyperthyroid patients with myasthenia gravis, there is no correlation between the dose of anticholinesterase medication required and the level of circulating thyroid hormones.35 Further investigation is needed to establish the precise pathophysiology of the association between pulmonary hypertension and hyperthyroidism.

References
Klein, I, Ojamaa, K Thyroid hormone and the cardiovascular system: from theory to practice.J Clin Endocrinol Metab1994;78,1026-1027. [CrossRef] [PubMed]
 
Gross, G, Lues, I Thyroid-dependent alterations of myocardial adrenoreceptors and adrenoreceptor-mediated responses in the rat.Naunyn Schmiedeberg’s Arch Pharmacol1985;329,427-439. [CrossRef]
 
Drachman, DB Myasthenia gravis and the thyroid gland.N Engl J Med1962;266,330-333. [CrossRef]
 
Millikan, CH, Haines, SF Thyroid gland in relation to neuromuscular disease.Arch Intern Med1953;92,5-39. [CrossRef]
 
Teoh, R, Chow, CC, Kay, R, et al Response to control of hyperthyroidism in patients with myasthenia gravis and thyrotoxicosis.Br J Clin Pract1990;44,742-744. [PubMed]
 

Figures

Tables

References

Nakchbandi, IA, Wirth, JA, Inzucchi, SE (1999) Pulmonary hypertension caused by Grave’s thyrotoxicosis: normal pulmonary hemodynamics restored by131I treatment.Chest116,1483-1485. [CrossRef] [PubMed]
 
Curnock, AL, Dweik, RA, Higgins, BH, et al High prevalence of hypothyroidism in patients with primary pulmonary hypertension.Am J Med Sci1999;318,289-292. [CrossRef] [PubMed]
 
Shimazaki, M, Mitsuhashi, T, Hasegawa, K Idiopathic pulmonary hypertension associated with hyperthyroidism: an autopsy case.Nippon Rinsho1980;38,1783-1786. [PubMed]
 
Nilsson, OR, Karlbert, BE Thyroid hormones and the adrenergic nervous system.Acta Med Scand Supp1983;672,27-32
 
Ingram, RH, Szidon, JP, Skalak, P, et al Effects of sympathetic nerve stimulation the pulmonary arterial tree of the isolated lobe perfusedin situ.Circ Res1968;22,801-815. [CrossRef] [PubMed]
 
Kadowitz, PJ, Hyman, AL Effect of sympathetic nerve stimulation on pulmonary vascular resistance in the dog.Circ Res1972;32,221-227
 
Hyman, AL, Kadowitz, PJ Enhancement of alpha and beta-adrenoreceptor responses by elevations in vascular tone in pulmonary circulation.Am J Physiol1986;250,H1109-H1116. [PubMed]
 
Rudolph, AM, Kurland, MD, Auld, PAM, et al Effects of vasodilator drugs on normal and serotonin constricted pulmonary vessels in the dog.Am J Physiol1959;197,617-623. [PubMed]
 
Klein, I, Ojamaa, K Thyroid hormone and the cardiovascular system: from theory to practice.J Clin Endocrinol Metab1994;78,1026-1027. [CrossRef] [PubMed]
 
Gross, G, Lues, I Thyroid-dependent alterations of myocardial adrenoreceptors and adrenoreceptor-mediated responses in the rat.Naunyn Schmiedeberg’s Arch Pharmacol1985;329,427-439. [CrossRef]
 
Drachman, DB Myasthenia gravis and the thyroid gland.N Engl J Med1962;266,330-333. [CrossRef]
 
Millikan, CH, Haines, SF Thyroid gland in relation to neuromuscular disease.Arch Intern Med1953;92,5-39. [CrossRef]
 
Teoh, R, Chow, CC, Kay, R, et al Response to control of hyperthyroidism in patients with myasthenia gravis and thyrotoxicosis.Br J Clin Pract1990;44,742-744. [PubMed]
 
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