Suggestive evidence for bromocriptine-induced pleurisy

Abstract

Pleurisy of initially unknown origin was found in a patient who was treated with bromocriptine for Parkinson's disease for 6 years. At presentation, bilateral pleural thickening existed that caused severe restriction of pulmonary function. There were an elevated erythrocyte sedimentation rate, polyclonal hypergammaglobulinaemia, increased levels of acute phase proteins and anaemia. After withdrawal of the bromocriptine the patient's complaints as well as the laboratory parameters markedly improved. Further loss of pulmonary function did not occur. However, the pleural thickening did not resolve, not even upon subsequent corticosteroid treatment, probably due to fibrosis. Together, these findings strongly suggest a causative role of bromocriptine. The results of the laboratory studies suggested an immunopathogenetic mechanism, but in vitro lymphocyte-proliferation studies and skin patch tests with bromocriptine were negative. Bromocriptine should be considered as a cause of pleurisy. The drug must be stopped immediately upon the occurrence of pleural thickening in order to prevent impairment of pulmonary function. In addition, periodic laboratory and X-ray studies in patients on long-term bromocriptine treatment should be considered.

Pleural disease during treatment with bromocriptine in patients previously exposed to asbestos

“…In 1981, RINNE [2] reported that, out of 123 patients on long-term therapy with this drug, seven had developed pleuropulmonary reactions. Since then, to our knowledge, 30 cases of bromocriptine-induced adverse reactions in the lung and/or pleura have been reported in the literature [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18]. Interestingly, ergot alkaloids other than bromocriptine can cause similar lesions in the chest [19].…”