Pleural Effusion and Fibrosis during Treatment with Methysergide

Hindle, William H.; Posner, E; Sweetnam, M. T.; Tan, Rubin

doi:10.1136/bmj.1.5696.605

Cited by 44 publications

(12 citation statements)

References 4 publications

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“…This syndrome occurred during the use of the ergoline drug, methysergide. Since that time, other cases have been reported during the use of methysergide [4][5][6][7][8][9][10][11][12][13][14][15][16], as well as other ergolines, such as bromocriptine [17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32], dopamine agonists [33,34], and ergotamine [12,[35][36][37][38][39][40].…”

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confidence: 99%

Pleuropulmonary changes induced by ergoline drugs

Pfitzenmeyer¹,

Foucher²,

Dennewald³

et al. 1996

Eur Respir J

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Classic ergolines, such as bromocriptine, methysergide and ergotamine, can induce chronic pleuropneumonitis. We present the cases of eight patients who developed similar changes whilst on other ergolines.In this retrospective case study spanning 1985-1995, clinical data, radiological material, pulmonary function, bronchoalveolar lavage and histopathology were reviewed. Earlier literature on ergoline-induced pleuropulmonary changes was reviewed.Eight middle-aged to elderly individuals of both sexes developed pleuropulmonary changes during long-term therapy with regular dosages of nicergoline (n=4), dihydroergocristine (n=3), or dihydroergotamine (n=1). Bibasilar pleural thickening with or without pleural effusion was present on chest radiographs and computed tomographic (CT) scans in six cases. Increased erythrocyte sedimentation rate was seen in most. Pure interstitial pneumonitis developed in two patients on dihydroergocristine and was reversible in each. Bronchoalveolar lavage was performed in four cases and was abnormal in all, but demonstrated no consistent pattern. Most patients exhibited lung restriction. The outcome was favourable showing slow improvement in all cases following discontinuation of the ergoline. Slight residual pleural thickening was seen in five out of the six cases with pleural involvement.Nicergoline and dihydroergotamine can induce a syndrome of chronic pleural thickening/effusion that slowly improves after drug withdrawal. Dihydroergocristine can induce reversible interstitial pneumonitis. Eur Respir J., 1996Respir J., , 9, 1013

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confidence: 99%

Pleuropulmonary changes induced by ergoline drugs

Pfitzenmeyer¹,

Foucher²,

Dennewald³

et al. 1996

Eur Respir J

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“…Its pathogenesis is still unknown [2,4,5]. Pleuropulmonary complications have been reported after one month to several years of methysergide therapy, at doses ranging from 1-8 mg daily [1][2][3][4][5][6][7][8]. The present patient took a cumulative dose of approximately 630 mg, intermittently over a 21 month period, before respiratory symptoms developed.…”

Section: Discussionmentioning

confidence: 87%

“…Its use is limited because of the high incidence of gastrointestinal intolerance and dermatitis [1]. The more severe complication of retroperitoneal fibrosis has been described in 1% of patients, and vascular disease (coronary disease, Leriche's syndrome), due to fibrosis and intimal proliferation of the small vessels, has been reported incidentally [2,3].…”

Section: Discussionmentioning

confidence: 99%

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A 47 year old man with nonproductive cough and right-sided chest pain

Claes¹,

Slabbynck²,

Bedert³

et al. 1997

Eur Respir J

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A 47 yr old man was admitted to our hospital because of persisting nonproductive cough, dyspnoea on exertion and right-sided chest pain of several weeks duration. He was febrile (37.5°C) and had noticed a weight loss of 5 kg within the last 2 months. The only pertinent medical history was a cluster headache, for which he was treated intermittently with methysergide. He had taken a cumulative dose of approximately 630 mg over a 21 month period. He was working as a clerk, had no history of asbestos exposure, and smoked one packet of cigarettes per week. Clinical examination was normal, except for a dullness on percussion, diminished breath sounds, and pleural friction at the right base of the thorax.Laboratory studies showed an erythrocyte sedimentation rate (ESR) of 120 mm·h -1 , a normochromic normocytic anaemia with haemoglobin of 103 g·L -1 . Arterial oxygen tension (Pa,O 2 ) and arterial carbon dioxide tension (Pa,CO 2 ) were normal. A chest radiograph revealed a moderate pleural effusion in the right base, with a mass-like lesion in the dorsobasal part of the lung. Adenopathies were absent. Pleural fluid analysis showed a white blood cell count (WBC) of 5,200×10 6 cells·L -1 , with 99% lymphocytes, glucose 0.46 g·L -1 , pH of 7.37, total protein 40 g·L -1 , and lactate dehydrogenase (LDH) 1,520 U·L -1 . Search for malignant cells was negative, as were stains and cultures for bacteria, mycobacteria and fungi.Bronchoscopy was normal, except for an erythematous mucosa in the right lower lobe. Transbronchial biopsies and subsequent open lung biopsy disclosed nonspecific parenchymal fibrosis. Computed tomography (CT) of the thorax was taken on admission ( fig. 1) and after 5 months ( fig. 2). Pleuroscopy revealed a marked diffuse, white thickening both of the parietal and visceral pleura, with multiple fibrinous adhesions. Biopsies yielded only nonspecific fibrosis. There were no signs of malignancy, granulomas or vasculitis. Stains and cultures for bacteria, mycobacteria and fungi remained negative. CASE FOR DIAGNOSISDepts of *Pneumology and **Radiology, AZ-Middelheim, Antwerp, Belgium.

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“…Neither the patient nor his family had a history of pulmonary, cardiac or other systemic diseases. He had been a heavy smoker but stopped smoking 20 of bromocriptine (lo-15 mg daily since 1987), levodopa-carbidopa and baclofen.…”

Section: Introductionmentioning

confidence: 99%

Suggestive evidence for bromocriptine-induced pleurisy

Klaassen¹

1996

The Netherlands Journal of Medicine

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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.

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Pleural Effusion and Fibrosis during Treatment with Methysergide

Cited by 44 publications

References 4 publications

Pleuropulmonary changes induced by ergoline drugs

Pleuropulmonary changes induced by ergoline drugs

A 47 year old man with nonproductive cough and right-sided chest pain

Suggestive evidence for bromocriptine-induced pleurisy

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