Publication Details



Bromocriptine is an oral dopamine receptor agonist used predominantly in the therapy of Parkinson disease, but which has other activities including inhibition of prolactin and growth hormone release which has led to its use in acromegaly, infertility and galactorrhea. Bromocriptine therapy is associated with low rate of transient serum enzyme elevations during treatment and has been implicated in rare cases of acute liver injury.


Bromocriptine (broe" moe krip' teen) is a semisynthetic ergot alkaloid derivative which acts as a dopamine receptor agonist. Bromocriptine has strong agonist activity on the D2 class of dopamine receptors and partial antagonist of the D1 receptors in central nervous system. Bromocriptine was approved for use in the United States in 1978, the first in this class of agents, and has been in wide use since. Current indications are the therapy of symptomatic Parkinson disease as well as spastic disorders and extrapyramidal disorders caused by medications. Bromocriptine also has inhibitory activity on prolactin and growth hormone release, and its indications also include treatment of amenorrhea and galactorrhea related to hyperprolactinemia, female infertility, acromegaly, Cushing syndrome and premenstrual syndrome. Bromocriptine is available in tablets of 2.5 mg and capsules of 5 mg in generic forms and under the brand name of Parlodel. The recommended dose for Parkinson disease is 10 to 40 mg daily, but it must be introduced gradually and the dose titrated based upon tolerance and effect. In Parkinson disease, it is usually used in combination with levodopa/carbidopa. Common side effects include profound hypotension (with the first dose), somnolence, fatigue, vivid dreams, anxiety, confusion, hallucinations, delusions, depression, dizziness, headache, nausea and gastrointestinal upset, symptoms common with increased dopaminergic activity.


Bromocriptine has been reported to cause serum aminotransferase elevations in a small proportion of patients, but these abnormalities are usually mild, asymptomatic and self-limiting even without dose adjustment. In rare instances, more marked elevations occur that may require dose modification or discontinuation and which can recur with rechallenge. In addition, bromocriptine has been implicated in a small number of cases of clinically apparent acute liver injury, but the clinical characteristics and typical pattern of enzyme elevations has not been characterized and case reports of hepatic injury due to bromocriptine have not been published. Thus, bromocriptine is a very rare cause of clinically apparent liver injury and has not been implicated in causing acute liver failure or chronic liver injury.

Likelihood score: D (possible rare cause of clinically apparent liver injury).

Mechanism of Injury

Bromocriptine is rapidly removed from the serum by the liver with extensive first pass metabolism. Bromocriptine is metabolized to inactive forms largely by hydrolysis and excreted rapidly.

Outcome and Management

Most instances of suspected hepatotoxicity of bromocriptine have been mild and self-limited. There have been no reports of acute liver failure or chronic hepatitis due to bromocriptine. There is likely cross sensitivity to hypersensitivity reactions among the different ergot alkaloids, such as pergolide.

Drug Class: Antiparkinson Agents

Other Drugs in the Subclass, Dopamine Receptor Agonists: Apomorphine, Pergolide, Pramipexole, Ropinirole, Rotigotine



Bromocriptine – Generic, Parlodel®


Antiparkinson Agents


Product labeling at DailyMed, National Library of Medicine, NIH



References updated: 20 July 2017

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    (Expert review of hepatotoxicity published in 1999; among anticholinergic agents, "only trihexyphenidyl has been incriminated in hepatic injury"; other antiparkinsonism drugs discussed include levodopa, lergotrile [no longer available], pergolide and bromocriptine).
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    (Retrospective analysis of experience in treating 92 patients with Parkinson disease using bromocriptine and levodopa for up to 30 months, serum enzyme elevations occurred in 6 patients [7%] which were transient in 4, required dose modification in 1 and stopping in 1; no clinically apparent liver injury).
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    (Among 899 cases of drug induced liver injury from the US enrolled in a prospective database between 2004 and 2012, none were attributed to an agent used to treat Parkinson disease).