Chronic cough associated with statin use in a 74-year-old man

Case

A 74-year-old man with a remote history of a myocardial infarction presented to his family physician for routine chronic disease management. He complained of a dry cough that began approximately 15 years prior. The cough was not progressing and not associated with hemoptysis, weight loss, fever, chills, or chest pain. He complained of exertional dyspnea and fatigue in the past few years that he thought was due to physical deconditioning. He denied any typical heartburn symptoms and was not known to have any chronic lung disease or malignancy. He denied any nasal congestion or rhinorrhea.

The patient worked in a wire factory for 44 years. He was knowingly exposed to asbestos for about 20 of those years. He did not use any form of respiratory protection during his employment. He did not have any other known inhalant exposures such as bats, grain, or mould. He smoked cigarettes but quit more than 30 years prior to presentation. He had no family or personal history of chronic lung disease or lung cancer.

His past medical history included hypertension, hyperlipidemia, and ischemic heart disease, for which he was taking 40 mg of oral telmisartan once daily, 40 mg of oral atorvastatin at bedtime, and 81 mg of oral acetylsalicylic acid once daily, respectively. His other medications were vitamin D3, cholestyramine, and pantoprazole.

The patient believed his cough began when he started taking atorvastatin after his myocardial infarction, though he was prescribed telmisartan at that time. He found the cough improved if he stopped taking the atorvastatin for a few days.

On examination, he looked well. His vital signs, including respiratory rate and pulse oximetry, were normal. His cardiovascular and respiratory examination findings were unremarkable.

Investigation

Given the patient’s history of asbestos exposure, we performed computed tomography (CT) scans of the chest. There were shallow noncalcified pleural plaques bilaterally, suggesting mild changes of asbestos-related pleural disease. A minor degree of subpleural reticulation at bilateral lower lung zones without honeycombing fibrosis was seen, which may have reflected some minimal or early fibrosis changes. Evidence of remote previous granulomatous infection with tiny punctate granulomas was seen in the left lung, as was a small calcified right hilar lymph node.

Differential diagnosis

Common causes of chronic cough include asthma, gastroesophageal reflux disease, upper airway cough syndrome, or nonasthmatic eosinophilic bronchitis. The patient’s CT findings were suggestive of mild asbestos-related pulmonary disease, but he declined a referral for biopsy to definitively rule out mesothelioma. Pulmonary function testing was not available to rule out asthma or chronic obstructive pulmonary disease (given his occupational exposures). The patient’s blood eosinophil count was normal. He was known to have gastroesophageal reflux disease but his symptoms were well controlled with pantoprazole therapy. Given the history of improvement of his symptoms with discontinuation of atorvastatin, the patient was switched from 40 mg of atorvastatin to 20 mg of rosuvastatin orally at bedtime. The patient’s cough resolved a few weeks after switching to rosuvastatin.