A 56yearold Caucasian female with a history of asthma since age 14 presented with dyspnea on exertion and productive cough for the past three days. One month prior she was hospitalized for similar symptoms and treated for an asthma exacerbation. She has had progressive dyspnea on exertion over the past several months acutely worse over the past 3 days. She also complained of chest pain and orthopnea. On review of systems she endorsed subjective fevers and an intentional 68 pound weight loss over the past year, occasional palpitations for the past month, hyperdefecation, bilateral hand tremors and anxiety for the past 4 months. On exam vital signs were normal other than tachycardia of 113 beats per minute. Physical exam revealed an anxious middleaged female with obese body habitus. No evidence of proptosis or thyromegaly. Cardiac exam was normal except for a regular tachycardia. There was no jugular venous distension. Respiratory exam revealed diffuse bilateral wheezes. There was onycholysis of the nails on bilateral hands and bilateral pitting lower extremity edema. Chest radiography demonstrated no cardiopulmonary pathology. Electrocardiogram revealed sinus tachycardia. A NTproBNP was severely elevated. Echocardiography demonstrated a left ventricle of normal size and function with mild concentric left ventricular hypertrophy. Mild left atrial enlargement and mild diastolic dysfunction were noted. There was no significant valvular disease. Right ventricular systolic pressure was estimated to be 3540 mmHg. Thyroid studies were consistent with Grave’s Disease.
Grave’s disease is the most common cause of hyperthyroidism accounting for 6080% of cases; it is more common in women. The usual presentation is anxiety, irritability, weakness, tremors, heart palpitations, heat intolerance, perspiration, and weight loss despite a normal appetite. Although dyspnea is primarily attributed to pulmonary or cardiac causes, hyperthyroidism is a welldocumented cause. The etiology is not well understood, but thought to be secondary to a combination of increased ventilatory drive and respiratory muscle weakness. Although brain natriuretic peptide is commonly used to discern between the two most common etiologies of dyspnea, pulmonary and cardiac, patients with hyperthyroidism have been noted to have an elevated BNP. This is related to direct effects of thyroid hormone on BNP irrespective of cardiac function. Furthermore, there is normalization of the BNP once the patient becomes euthyroid.
It is important to remember a severely elevated BNP is not synonymous with a diagnosis of heart failure. Thyroid disease must be considered in patients with an elevated BNP. It is important to obtain the correct diagnosis, so as not to delay the correct treatment, which differs significantly.
To cite this abstract:Christianson L, Wu W. Elevated Brain Natriuretic Peptide in a Case of Hyperthyroidism. Abstract published at Hospital Medicine 2012, April 1-4, San Diego, Calif. Abstract 97947. Journal of Hospital Medicine. 2012; 7 (suppl 2). https://www.shmabstracts.com/abstract/elevated-brain-natriuretic-peptide-in-a-case-of-hyperthyroidism/. Accessed November 22, 2019.