Bromocriptine is an ergot derivative with potent dopaminergic agonist action (high affinity for the D2 receptor site).
· Bromocriptine is indicated for treatment of dysfunctions associated with hyperprolactinaemia, acromegaly to reduce serum growth hormone, and for idiopathic or postencepha-litic Parkinson’s disease.
· It is no longer indicated for the treatment of suppression of physiological post-partum lactation; the FDA (USA) is of the opinion that bromocriptine may cause a serious adverse effect in post-partum women.
The drug is well absorbed on oral administration and peak plasma levels are reached in about 2 hours. The plasma half-life of bromocriptine is approximately 6 to 8 hours. The volume of distribution is 1 to 4 L/kg, and plasma protein binding is to the extent of 96%. Liver is the main site of metabolism and the main route of excretion is biliary. Less than 0.1% is excreted unchanged.
Bromocriptine is a synthetic ergoline and a direct dopamine D2 agonist stimulant. Some of its activity includes inhibi-tion of the release of prolactin by the pituitary, resulting in decreased plasma prolactin concentrations. Bromocriptine, as a dopamine agonist, occupies dopaminergic receptors in the pituitary gland to inhibit prolactin secretion. The D2 receptor sites show properties related to dopaminergic behavioural and endocrine responses.
· Nausea, vomiting, vertigo, postural hypotension, nasal congestion, constipation, and mood disturbances.
· Less common problems include headache, dryness of mouth, mydriasis, hallucinations, digital vasospasm, eryth- romelalgia,* and bladder disturbances.
· Diplopia, dyskinesia, anginal pain, and ergotism have also been reported.
· Long-term therapy may result in pleural effusion, pleural and pulmonary fibrosis, retroperitoneal fibrosis, and pleu- ritic chest pain.
· Hypothermia, hypertension, myocardial infarction, stroke, and seizures have been reported in postpartum women who were given bromocriptine for lactation suppression.
· Sudden discontinuation can result in hyperpyrexia.
· Bioavailability of bromocriptine is increased if it is given along with erythromycin.
· Alcohol reduces tolerance to bromocriptine and vice versa.
· Bromocriptine has been reported to sensitise patients to acute dystonic crisis following administration of a neuro- leptic. Dopamine antagonists, such as the neuroleptics or leptic. Dopamine antagonists, such as the neuroleptics or C
· dopamine agonists when given concurrently. Life-threatening symptoms of seizures, cerebral vasospasm, ventricular tachycardia and cardiac dysfunction have been reported when bromocriptine was combined with sympa- thomimetics.
· Drowsiness, vertigo, postural hypotension, sweating, hallucina-tions, agitation, convulsions, nausea, and vomiting. Dyskinesias may occur.
· Gastric lavage can be done if the patient is seen within a short time post-ingestion (upto 2 to 3 hours). Activated charcoal may not be beneficial.
· Rest of the treatment involves supportive and symptomatic measures. Most cases of overdose with bromocriptine appear minimal and treatable with supportive care.
· Monitor CNS changes for possible dyskinesias or seizures. Specific treatment for dyskinesias primarily includes reduc-tion of dosage and supportive care.
· If the patient is hyperactive, administer diazepam 10 to 20 mg orally to adults, (no more than 0.1 mg/kg in children).
· Blood pressure and ECG must be followed up in sympto-matic patients.
· Because of the significant protein binding of bromocriptine, haemodialysis is not expected to be of benefit.