Pleuropulmonary fibrosis after long-term treatment with the dopamine agonist pergolide for Parkinson Disease

Our plain-English summary of Pleuropulmonary fibrosis after long-term treatment with the dopamine agonist pergolide for Parkinson Disease, by R. Tintner, P. Manian, P. Gauthier, et al (Archives of Neurology, 2005).

The study

• Authors: R. Tintner, P. Manian, P. Gauthier, J. Jankovic
• Journal: Archives of Neurology
• Published: 2005;62(8):1290-5
• Type of article: Case report
• Cited by: 32 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Dopamine agonists are increasingly used in the treatment of Parkinson disease, but they may cause serious adverse effects. In December 1983, symptoms of Parkinson disease developed in a 55-year-old man with no history of pulmonary disease, smoking, or asbestos exposure. He began treatment with dopamine agonists bromocriptine mesylate (in 1984) and pergolide mesylate (in 1989). In late 2000, pulmonary symptoms developed. Chest radiographs and computed tomographic findings showed a mass in the right upper lobe and effusion. A biopsy specimen showed pleural and parenchymal fibrosis. This syndrome resolved after cessation of pergolide therapy and a switch to pramipexole dihydrochloride. This case draws attention to the association of long-term ergot dopamine agonist therapy with pleuropulmonary fibrosis, which can develop as late as 11 years after the initiation of therapy. We also review evidence that the risk of this complication is substantially lower with the newer nonergot dopamine agonists.

In plain English

This article was a case report of one man with Parkinson disease, plus a review of published reports of fibrosis linked to the drug pergolide. He had no history of lung disease, smoking, or asbestos exposure. The only prior exposure or risk factor the authors named was 5 earlier years of bromocriptine treatment. His Parkinson symptoms began in December 1983, at age 55. He took bromocriptine from 1984 and was switched to pergolide in August 1989. Both are ergot-type dopamine agonist drugs. In August 2000 he developed a cough, shortness of breath and fluid around the lung (pleural effusion). Chest CT showed a mass in the right upper lobe and pleural plaques. A biopsy showed fibrosis of the pleura, which was believed consistent with a reactive process. Pergolide was replaced with pramipexole, and he had no return of lung symptoms through July 2002. The authors wrote that the published pergolide cases had occurred within 3 years. They also cited later reports of fibrosis after 11 years and after more than 6 years. They concluded that pergolide was the likely cause, though bromocriptine may have contributed.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Case report of a single patient, with a review of previously published case reports of fibrosis associated with pergolide
• Who was studied: One man whose Parkinson disease symptoms began in December 1983 at age 55, treated in Houston, Texas. He had no history of pulmonary disease, smoking, or asbestos exposure.
• Exposure: The drug bromocriptine (an ergot dopamine agonist) from September 1984 to August 1989, then the drug pergolide (also an ergot dopamine agonist) from August 1989, started at 1.5 mg/d. The article's table lists a maximum pergolide dosage of 4 mg/d for this patient. The authors stated he had no prior exposures or risk factors for pleuropulmonary fibrosis except the earlier 5-year bromocriptine exposure.
• Main results:
  • In August 2000, about 11 years after pergolide was started, the patient developed a cough and shortness of breath and was diagnosed with pleural effusion.
  • Chest computed tomography showed a mass in the right upper lobe of the lung and pleural plaques.
  • Biopsy of the pleura showed fibrinous and fibrous pleuritis. The findings were believed to be consistent with a reactive process.
  • After pergolide was replaced by pramipexole, the patient continued without recurrence of pulmonary signs or symptoms through July 2002.
  • In the authors' review, ten cases of serosal membrane fibrosis associated with pergolide had been reported, and in the reported cases symptoms occurred within 3 years of starting treatment. In this case the complication took 11 years to develop.
  • The authors also cited a Japanese report of pericardial fibrosis in another patient after 11 years, published after the first abstract report of this case.
  • The authors also cited a newsletter report of fibrosing alveolitis in a 48-year-old woman who had taken pergolide for more than 6 years.
• The authors' conclusion: The authors concluded that their report provides evidence that ergot dopamine agonists such as pergolide can induce pulmonary fibrosis, and possibly other serosal fibrotic syndromes, even after more than a decade of treatment. They wrote that the timing strongly suggested pergolide was the causative agent. They also wrote that the risk of fibrosis with long-term ergot exposure is so minimal and usually reversible that it should not outweigh the potential benefits.
• Limitations the authors state:
  • The patient's earlier 5-year treatment with bromocriptine, an ergot drug also associated with fibrotic syndromes, may have played a contributory role.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Pleural plaques and thickening.

Medical terms in this study, explained in our Lexicon: Fibrosis, Asbestos Exposure, Chest X-Ray, Biopsy, Interstitial Fibrosis.

Related studies

• Rounded atelectasis and respiratory compromise secondary to pergolide use — C.I. Bloom, G.E. Wilson (2009)
• Pleural disease during treatment with bromocriptine in patients previously exposed to asbestos — G. Hillerdal, J. Lee, et al. (1997)
• Asbestos-related pleural and lung fibrosis in patients with retroperitoneal fibrosis — T. Uibu, R. Järvenpää, et al. (2008)
• Asbestos-related pleuropulmonary diseases: evaluation with low-dose four-detector row spiral CT — M. Remy-Jardin, A. Sobaszek, et al. (2004)
• Chest imaging and lung function impairment after long-term occupational exposure to low concentrations of chrysotile — D. Spyratos, D. Chloros, et al. (2012)
• Mesothelial cell proliferation: a nonspecific response to lung injury associated with fibrosis — I.Y. Adamson, J. Bakowska, et al. (1994)

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