Year : 2016 | Volume
: 13 | Issue : 3 | Page : 144--145
Pulmonary hypertension: The thyroid connection
Pooja Prakash Prabhu, GD Ravindran, Jyothi Idiculla
Department of General Medicine, St. John's Medical College, Bengaluru, Karnataka, India
Pooja Prakash Prabhu
Department of General Medicine, St. John«SQ»s Medical College, Bengaluru, Karnataka
A 52-year-old female presented with exertional dyspnea and swelling of feet for 3 weeks. On examination, she was found to have tachycardia and hypertension, with a small goiter visible on her neck. All routine investigations were normal. Echocardiogram (ECHO) revealed moderate tricuspid regurgitation and severe pulmonary hypertension (PHTN). Pulmonary function tests were normal. There was no evidence of pulmonary embolism on computed tomography pulmonary angiogram. Immunology workup was negative. She was diagnosed to have hyperthyroidism, and a technetium-99 scan of the thyroid was suggestive of Graves«SQ» disease. She was treated with radio-iodine. And is euthyroid and asymptomatic. A repeat ECHO confirmed resolution of PHTN. This case is being reported to highlight the need to detect and treat hyperthyroidism, which can cause resolution of PHTN.
|How to cite this article:|
Prabhu PP, Ravindran G D, Idiculla J. Pulmonary hypertension: The thyroid connection.Thyroid Res Pract 2016;13:144-145
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Prabhu PP, Ravindran G D, Idiculla J. Pulmonary hypertension: The thyroid connection. Thyroid Res Pract [serial online] 2016 [cited 2022 May 26 ];13:144-145
Available from: https://www.thetrp.net/text.asp?2016/13/3/144/193137
Pulmonary hypertension (PHTN) is defined as sustained elevation of mean pulmonary artery pressure of >25 mm Hg at rest, or pulmonary artery systolic pressure (PASP) of more than 35 mm Hg, with a mean capillary wedge pressure, and left ventricular end-diastolic pressure of <15 mm Hg. The Dana Point Classification of PHTN broadly classifies it into primary, secondary to left heart diseases, lung pathology, chronic thromboembolism, or metabolic causes.  Thyroid dysfunction, which belongs to the last category may cause PHTN. We report a case of severe and symptomatic PHTN in a patient with Graves' disease which reversed on successful treatment of this condition.
A 52-year-old female, with no previous co-morbidities, presented with exertional dyspnea and swelling of feet of 3 weeks duration. On examination, she had tachycardia with a heart rate of 110 beats/min and blood pressure of 150/90 mm Hg. On general examination, she was found to have pedal edema and grade 2 goiter. Systemic examination was normal apart from a loud pulmonary component of the second heart sound and brisk deep tendon reflexes.
The initial investigations including complete hemogram, liver, and renal function test were normal, as were her arterial blood gas, chest X-ray, and 12-lead electrocardiogram. A two-dimensional echocardiogram (2D-ECHO) done revealed normal left ventricular systolic function with moderate tricuspid regurgitation (TR). There was PHTN with a PASP of 75 mm Hg. Pulmonary function tests were normal. There was no evidence of pulmonary thromboembolism on a computed tomography pulmonary angiogram, nor was there any evidence of deep vein thrombosis (DVT) on Doppler studies. HIV tests and immunological workup were negative.
In view of her goiter, thyroid function tests were asked for, which were suggestive of hyperthyroidism. The thyroid stimulating hormone (TSH) was suppressed at 0.02 (0.34-4.1) µIU/ml with elevated free T4: 4.39 (0.61-1.12) ng/ml and free T3: 10.4 (2.5-3.9) pg/ml. Following this, a technetium-99 scan of her thyroid was done, which showed uniform increased uptake, suggesting Graves' disease.
She was commenced on propranolol 10 mg TID and was treated with radioiodine (7 mCi) for Graves' disease. Following radio-iodine, there was a gradual resolution of her exertional dyspnea. On follow-up, she was found to be hypothyroid (TSH - 38.7 µIU/ml) at 4 months from radio-iodine therapy. She is now euthyroid, on thyroxine 75 µg/day. A repeat ECHO done 6 months later confirmed the resolution of PHTN with a PASP - 25 mm Hg, and a retrospective diagnosis of PHTN secondary to Graves' disease was made. Currently, she is asymptomatic with no dyspnea at rest, or on exertion.
Hyperthyroidism is classically associated with left ventricular dysfunction and heart failure. This disease may also at times predominantly, if not exclusively, involve the right heart. Studies show that a large proportion of patients with hyperthyroidism have elevated PASP.  In a study of 365 patients with PHTN, Li et al. reported that 85 (24%) had thyroid disease.  In another report published by Ferris et al., 26 (19%) had PHTN.  Other studies strengthening the association of hyperthyroidism and PHTN have been published with more than 40% prevalence rates of PHTN in hyperthyroidism. ,
Our patient was diagnosed with symptomatic pulmonary arterial hypertension and was also found to have Graves' disease. Hyperthyroidism per se would also have contributed to her symptom of exertional dyspnea. However, she presented with exertional dyspnea and pedal edema, had a loud P2 and was found to have severe PHTN with TR in the 2D-ECHO. Upon treatment of Graves' disease and normalization of thyroid function, PHTN resolved, and the patient was freed from her symptoms.
The etiology and pathogenesis of PHTN that has been observed in subjects with hyperthyroidism remain unclear. The proposed hypotheses are autoimmune mediated endothelial injury, increased the metabolism of nitric oxide by the hyperthyroid state, hyperdynamic circulation as well as decreased surfactant synthesis. 
Hyperthyroidism is commonly associated with hypercoagulable states and increased prevalence of DVT, as well as two- to three-fold increased prevalence of pulmonary embolism, which may also account for patients presenting with PHTN, and always needs to be excluded.
Reversibility of PHTN upon treatment of the underlying thyrotoxicosis has been demonstrated consistently in few studies. In a study done by Marvisi et al. [ 8] it was demonstrated that a more rapid drop in pulmonary arterial pressures could be achieved with antithyroid drugs, compared to partial thyroidectomy. Reddy et al. in their study reported reversibility of PHTN in hyperthyroidism following a therapy with carbimazole. However, they have not commented on resolution of symptomatology.  In our patient, normalization of the pulmonary pressures and reduction of symptoms were achieved with radioiodine therapy. Thus, Graves' disease should be recognized as a cause of PHTN and cor pulmonale in whom the etiology remains elusive, as it is a potentially reversible condition.
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