A 75-year-old male, with long-standing Parkinson's disease and benign prostatic hyperplasia, was brought into the emergency department after syncope. He had felt dyspnea, but denied any other prodromal symptoms and did not have involuntary movements or urinary or fecal incontinence. 
He did not have any other chronic diseases, habits, or allergies, and his medications were levodopa/carbidopa 250/25 mg qid, bromocriptine 30 mg daily, amantadine 100 mg bid, alprazolam 2.5 mg daily, and tamsulosin 0.4 mg daily.
He had been admitted to the hospital 3 times during the last 4 months with bilateral recurrent pleural effusions, dyspnea, and episodes of noncardiogenic acute pulmonary edema of unknown etiology. 
When he was admitted, he referred to dyspnea and pleuritic chest pain. The physical examination showed signs of respiratory distress, oxygen saturation was 88% in room air, and the vital signs were within normal limits, without jugular venous distension or edema. Heart sounds were normal, without murmurs, and he had no audible breath sounds on the lower half of the right lung and lower third of the left lung field, without crackles, wheezing, or rhonchi bilaterally. 
The chest X-ray confirmed a big pleural effusion on the right side and a moderate one on the left (Figure 1). The pleural effusion on the right-hand side was drained and was found to be an exudate, rich in normal lymphocytes, with normal values of adenosine deaminase activity and no neoplastic cells. The pleural biopsy revealed fibrosis and moderate inflammatory infiltrate with lymphocytes, plasmocytes, and neutrophils, without granulomas, neoplastic cells, or amyloid; the bacterial cultures and polymerase chain reaction for M. tuberculosis were negative.
The complete blood count, liver enzymes, creatinine, ionogram, brain (BNP natriuretic peptide), and hormone (thyroid-stimulating TSH) were normal and only the erythrocyte sedimentation rate was elevated. Blood cultures and urinalysis were negative. The PPD test (purified protein derivative) was negative (3 mm). The peripheral blood flow cytometry showed only an augmentation of NK cells, suggestive of cell activation. The transthoracic echocardiogram and EKG showed no relevant changes. The analysis of the 24-hour Holter and a 2-week electrocardiographic event recorder showed only one short episode of supraventricular tachycardia. The immunological study revealed only positive antinuclear antibodies (1/160), with immunoglobulins, complement, rheumatoid factor, antidouble stranded DNA antibodies, and antineutrophil cytoplasmic antibodies within normal values. The electroimmunoassays and detection of serum-free light chains were negative. A computerized axial tomography scan of the thorax, abdomen, and pelvis did not reveal any important changes either, with the exception of the pleural effusion and pleural thickening (Figure 2).
This case was very intriguing, because there was no apparent cause for the chronic exudative lymphocytic bilateral pleural effusions and for the episodes of pulmonary edema without heart or lung diseases.
We then decided to investigate the drugs that the patient was taking and found out that bromocriptine and other classic ergolines, such as methysergide and ergotamine, had been linked to chronic pleural effusions, generally exudates, and pleuropulmonary fibrosis. 
After failure of other treatments and drainages in avoiding recurrence of the pleural effusion, we decided to stop the bromocriptine. 
Within less than a month, the considerable bilateral pleural effusion disappeared (Figure 3), and the patient did not have recurrence of the pleural effusions or acute pulmonary oedema episodes since then, for more than a year now.