SAT-459 A Grave Complication: Pulmonary Arterial Hypertension

There is currently emerging evidence that thyroid disease can have an impact on pulmonary pathologies but a direct causation, as opposed to correlation, is yet to be established. We present a unique case of newly diagnosed Graves’ disease with pulmonary sequalae. 69 year old non-smoking female with no known medical history presented to the hospital with acute onset of chest tightness, shortness of breath and palpitations. She had been experiencing night sweats and 10 lbs weight loss in the 3 weeks preceding hospitalization. She did not endorse any pertinent family history. On exam, she presented with tachycardia. The rest of the physical exam remained unchanged. Complete blood count and comprehensive metabolic panel did not reveal any abnormalities. Her TSH was suppressed below lab capability of measurement (<0.015). Free T4 was 5.97 ng/dL, and total T3 was 492 ng/dL. Subsequently obtained TPO antibody level was > 1000 IU/ml and TSI was 29.3 IU/L. EKG showed atrial fibrillation with RVR. Thyroid U/S showed that the thyroid gland was diffusely enlarged to the upper limit of normal but no nodules. CT chest showed diffuse ground glass opacities. She was treated with propranolol, and methimazole after resolution of acute symptoms. She was placed on diuretics to treat symptoms of pulmonary edema secondary to uncontrolled atrial fibrillation and high output heart failure. On outpatient follow up she continued to have mild shortness of breath on exertion. She had normal systolic and diastolic function of heart but an elevated PAP of 38mm Hg on a transthoracic echocardiogram, and her pulmonary function tests were within normal limits for her age. A follow up CT chest, 6 weeks after discharge, showed no resolution of ground glass opacities. Current literature shows that there might be pulmonary effects of hyper-thyroidal diseases; such as ventilation disorders, OSA, CSA, and pleural effusions. A 2002 study revealed a strong association of hyperthyroidism with pulmonary hypertension. A 2016 literature review established that there is specifically an association of Graves’ disease with pulmonary arterial hypertension. Both of these studies have had a small patient group. Our case perhaps adds credence to the fairly less known affiliation of hyperthyroidism with pulmonary disease. A unique finding in our patient - unresolving ground glass opacities, suggests a possible thyroid related interstitial lung disease. As with our case, there needs to be an increased awareness in the among clinicians to further work up both thyroid related pulmonary hypertension and interstitial lung disease possibly related to uncontrolled thyroid pathology. Increased vigilance to include hyperthyroidism as a differential for pulmonary hypertension can lead to better clinical outcomes for patients, with less possible invasive and expensive testing of other causes of pulmonary hypertension.