Pleuropulmonary disease during bromocriptine treatment of Parkinson's disease

McElvaney, N.G.

doi:10.1001/archinte.148.10.2231

Cited by 17 publications

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“…All ergot drugs also presumably differ from the newer dopamine agonists in their incidence of adverse reactions such as erythromelalgia 26 and fibrosis. 27 The prevalence of symptomatic pleuropulmonary fibrosis during chronic bromocriptine treatment has been estimated to be as high as 2-5% over 5 years. 27 Such complications appear infrequent with the other ergot derivatives and may affect less than 1 in 1,000 individuals treated with pergolide (Eli Lilly, data on file).…”

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confidence: 99%

Rationale for Use of Dopamine Agonists in Parkinson's Disease: Review of Ergot Derivatives

Blanchet

1999

Can. J. Neurol. Sci.

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The role and optimal timing of introduction of dopamine agonists in the symptomatic treatment of Parkinson's disease (PD) are still unsettled. Reevaluation of these issues is required in light of new experimental data published on crucial therapeutic issues revolving around the mechanisms of induction of motor response complications and cell death. In spite of suggestive animal evidence that levodopa may be harmful to compromised dopamine neurons in vivo, 1-2 there is no direct proof yet that levodopa results in irreversible dysfunction of the basal ganglia and catecholaminergic cell death in humans.3 Nonetheless, strategies to reduce (adjunct agonist therapy) or even replace (agonist monotherapy de novo) levodopa early in the disease have been explored for many years in an attempt to reduce long-term adverse effects. The advantages of direct dopamine agonists in PD include the lack of competition with dietary amino acids for absorption and absence of necessary enzymatic metabolic steps, leading to more reliable and consistent effects, a long duration of efficacy, greater potency, potential alternative modes of delivery, a reduced incidence of early motor response complications and possible neuroprotective properties. The clinical efficacy of the ergot derivatives is briefly reviewed to provide useful information for comparing their effects with newer dopamine agonists. ABSTRACT: While dopamine agonists are still traditionally used as adjunct medications to improve performance and smooth out motor response complications in advanced levodopa-treated Parkinson's disease, they are increasingly used in monotherapy or early in combination with levodopa particularly in patients under 65 years of age. Long-term studies using bromocriptine showed efficacy in lowering the cumulative levodopa dose and reducing the early incidence of levodopa-related motor response complications. New dopamine agonists have recently shown efficacy as adjunct medications in short-term trials. While we now have more options to fit our individual patients' needs and tolerance, it is important to view the new agonists in the light of the results obtained with ergot derivatives. In this article, the rationale for use and efficacy profile of the ergolines are briefly reviewed. Can. PHARMACOLOGICAL PROPERTIES

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confidence: 99%

Rationale for Use of Dopamine Agonists in Parkinson's Disease: Review of Ergot Derivatives

Blanchet

1999

Can. J. Neurol. Sci.

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“…The dosage of 1 0 mg BCR daily in the present case is comparable to the lowest dosage reported to cause signs of PPF. In previous reports on BCR-related PPF the dosage ranged from 15 to 100 mg/day, and relatively high doses were also used in case of other dopamine agonists (McElvaney et al, 1988;Bhatt et al, 1991). While previous reports have related the occurrence ofPPF to a high daily or cumulative dosage of BCR (Vergeret et al, 1984;Tomling et a/., 1986;Melmed andBraunstein, 1989, Bhatt eta/., 1991), the present case rather suggests an individual susceptibility.…”

Section: Discussionmentioning

confidence: 57%

“…Other fibrosing reactions to drugs, such as retroperitoneal fibrosis during treatment with methysergide and BCR (Demonet et al, 1986;Ward eta/., 1987;Wiggins and Skinner, 1986) and fibrosing peritonitis during practolol treatment (MylHirniemi and Leppaniemi, 1981 ), may well share a common background. The suggested aetiopathology includes serotonin-mediated or agonistic effect (Le Witt and Caine, 1981;Taal et al, 1983;Tornling et al, 1986;McElvaney et al, 1988;Kinnunen and Viljanen, 1988;Todman et al, 1990;Bhatt et al, 1991), serotonin antagonistic effect (Wiggins and Skinner, 1986), immunoallergic response (Vergeret et al, 1984;Douvier et al, 1985), and autoimmune response (Demonet et al, 1986;Ward et al, 1987). Taken that the pathogenesis in different cases is identical, it must account for: (1) delayed pleuropulmonary or retroperitoneal reactions with non-specific symptoms such as weight loss, anaemia and acute phase proteins; (2) immunological features of polyclonal hypergammaglobulinaemia and the presence of RF; (3) group (ergo lines) reactivity; ( 4) dose-effect relation, with wide variation of inter-individual sensitivity.…”

Section: Discussionmentioning

confidence: 99%

“…Laboratory findings include an elevated erythrocyte sedimentation mte (ESR) and C-reactive protein ( c m ) level with little or no leucocytosis, moderate anaemia, and raised levels of gammaglobulin and acute phase proteins. Pulmonary h c t i o n shows a restrictive pattern with a reduced vital capacity and unchanged or increased Tiffeneau index (FEV, NC), hence a proportionate reduction of diffusing capacity (Douvier et al, 1985;McElvaney et al, 1988). After discontinuation of the DA agonist, clinical improvement is rapid, but resolution of the radiographic changes is slow and usually incomplete.…”

Section: Introductionmentioning

confidence: 99%

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Low dose bromocriptine‐induced pleural effusion and pleuropulmonary fibrosis

Brunt

Boeree

1995

Euro J of Neurology

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We describe a parkinsonian patient who developed a slight asymptomatic pleural effusion during prolonged therapy with low dose bromocriptine (BCR) in addition to levodopa, following prior treatment with CQA 206-291. A moderate increase of BCR dosage prompted a severe pleuropulmonary inflammatory reaction with polyclonal activation and elevated serum liver enzymes, which normalized following withdrawal of the drug. The clinical syndrome and close relation to BCR treatment are in keeping with a diagnosis of BCR-related pleuropulmonary fibrosis (PPF). Features of this case are compared with previous reports on dopamine (DA) agonist-related PPF. This case supports earlier suggestions of polyclonal activation in DA agonist-related PPF and suggests hepatic involvement and dose dependency.

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“…Bromocriptine increases risk of pulmonary fibrosis and has lower efficacy in comparison with other dopamine agonists. 11,28 Pergolide is associated with development of cardiac valve fibrosis and valvular heart disease. 29 (It was recently withdrawn from the U.S.…”

Section: Dopamine Agonistsmentioning

confidence: 99%

Pharmacotherapy for Parkinson's Disease

Chen

Swope

2007

Pharmacotherapy

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The available pharmacotherapies for Parkinson's disease address symptomatology because no agent has been demonstrated to provide definite neuroprotection against the disease. Choice of pharmacotherapy must include consideration of short-term benefits as well as long-term consequences. Patients with mild Parkinson's disease often function adequately without symptomatic treatment. However, recent data suggest that initiation of treatment with a well-tolerated agent (e.g., the monoamine oxidase [MAO]-B inhibitor rasagiline) in the absence of functional impairment is associated with improved long-term outcomes. Consideration should also be given to many patient-specific factors, including patient expectations, level of disability, employment status, functional as well as chronologic age, expected efficacy and tolerability of drugs, and response to previous Parkinson's disease therapies. Increasingly, initial monotherapy begins with a nondopaminergic agent or, if the patient is considered functionally young, a dopamine agonist. Since Parkinson's disease is a progressive disorder, adjustments to pharmacotherapy must be expected over time. When greater symptomatic relief is desired, or in the more frail elderly patient, levodopa therapy should be considered. If motor fluctuations develop, addition of a catechol-O-methyltransferase inhibitor or MAO-B inhibitor should be considered. For management of levodopa-induced dyskinesias, addition of amantadine is an option. Surgery may be considered when patients need additional symptomatic control or are experiencing severe motor complications despite pharmacologically optimized therapy.

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Pleuropulmonary disease during bromocriptine treatment of Parkinson's disease

Cited by 17 publications

References 0 publications

Rationale for Use of Dopamine Agonists in Parkinson's Disease: Review of Ergot Derivatives

Rationale for Use of Dopamine Agonists in Parkinson's Disease: Review of Ergot Derivatives

Low dose bromocriptine‐induced pleural effusion and pleuropulmonary fibrosis

Pharmacotherapy for Parkinson's Disease

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