bromocriptine
Regulatory sources consulted
Approved indications
- Prevention or suppression of postpartum lactation only when clinically indicated; hyperprolactinemic disorders, prolactinomas, acromegaly, and Parkinson disease.
Contraindications
Absolute
- Hypersensitivity to bromocriptine, excipients, or other ergot alkaloids.
- Uncontrolled hypertension, hypertensive disorders of pregnancy, postpartum or puerperal hypertension.
- For lactation suppression: coronary artery disease or other severe cardiovascular disease, or severe psychiatric history or symptoms.
- For long-term treatment, cardiac valvulopathy shown by echocardiography.
Clinical warnings
- Major warning · It may cause hypotension, somnolence, or sudden sleep onset. Do not drive if these occur. Prolonged or high-dose use is associated with pleural, pulmonary, pericardial, or retroperitoneal fibrosis and valvulopathy. — CIMA/AEMPS, ficha técnica 54633
- Major warning · Routine lactation suppression is not recommended. During the postpartum period, monitor blood pressure and severe neurologic, cardiovascular, or psychiatric symptoms. — CIMA/AEMPS, ficha técnica 54633
- Major warning · Rare postpartum reports include hypertension, myocardial infarction, seizures, stroke, and severe psychiatric disorders. Seizures or stroke may be preceded by severe headache or transient visual disturbances. Stop bromocriptine and assess immediately for hypertension, chest pain, severe, progressive, or persistent headache with or without visual disturbances, or evidence of central nervous system toxicity. — CIMA/AEMPS, ficha técnica 54633
Drug interactions
- HighStrong CYP3A4 inhibitors or macrolides
Mechanism: They may substantially increase bromocriptine exposure.
Recommendation: Avoid or use with close monitoring and adjustment.
CIMA/AEMPS, ficha técnica 54633https://cima.aemps.es/cima/dochtml/ft/54633/FT_54633.html
- ModerateDopamine antagonists such as antipsychotics, metoclopramide, or domperidone
Mechanism: They may reduce bromocriptine efficacy.
Recommendation: Avoid if possible or monitor response.
CIMA/AEMPS, ficha técnica 54633https://cima.aemps.es/cima/dochtml/ft/54633/FT_54633.html
Adverse events
Common (≥1%)
Nausea, vomiting, or constipation · Headache, fatigue, or vertigo · Nasal congestion
Rare but serious
Valvulopathy or cardiopulmonary fibrosis · Arrhythmia · Gastrointestinal bleeding · Psychotic disorder · Postpartum hypertension · Postpartum myocardial infarction · Postpartum seizures or stroke · Severe postpartum psychiatric disorder
Pregnancy and lactation
It may restore fertility; use reliable contraception if pregnancy is not desired. It should not be used during breastfeeding when lactation is to be maintained because it suppresses milk production.
Recent literature (PubMed)
Pituitary adenomas are neoplasms of the pituitary adenohypophyseal cell lineage and include functioning tumors, characterized by the secretion of pituitary hormones, and nonfunctioning tumors. Clinically evident pituitary adenomas occur in approximately 1 in 1100 persons. Pituitary adenomas are classified as either macroadenomas (≥10 mm) (48% of tumors) or microadenomas (<10 mm). Macroadenomas may cause mass effect, such as visual field defects, headache, and/or hypopituitarism, which occur in about 18% to 78%, 17% to 75%, and 34% to 89% of patients, respectively. Thirty percent of pituitary adenomas are nonfunctioning adenomas, which do not produce hormones. Functioning tumors are those that produce an excess of normally produced hormones and include prolactinomas, somatotropinomas, corticotropinomas, and thyrotropinomas, which produce prolactin, growth hormone, corticotropin, and thyrotropin, respectively. Approximately 53% of pituitary adenomas are prolactinomas, which can cause hypogonadism, infertility, and/or galactorrhea. Twelve percent are somatotropinomas, which cause acromegaly in adults and gigantism in children, and 4% are corticotropinomas, which secrete corticotropin autonomously, resulting in hypercortisolemia and Cushing disease. All patients with pituitary tumors require endocrine evaluation for hormone hypersecretion. Patients with macroadenomas additionally require evaluation for hypopituitarism, and patients with tumors compressing the optic chiasm should be referred to an ophthalmologist for formal visual field testing. For those requiring treatment, first-line therapy is usually transsphenoidal pituitary surgery, except for prolactinomas, for which medical therapy, either bromocriptine or cabergoline, is usually first line. Clinically manifest pituitary adenomas affect approximately 1 in 1100 people and can be complicated by syndromes of hormone excess as well as visual field defects and hypopituitarism from mass effect in larger tumors. First-
Pyometra is a common disease in intact bitches and queens and occurs, although less frequently, in most other female pets. In bitches and queens, the illness is generally diagnosed within 4 months after estrus, in middle-aged to older individuals. Complications such as peritonitis, endotoxemia, and systemic inflammatory response syndrome are not uncommon and associated with more severe illness. Ovary-sparing surgical options such as hysterectomy could be considered in individuals with high-risk for detrimental side effects of spaying or without infection of the uterus but has not yet been evaluated for safety in pyometra.
Prolactinomas are the commonest form of pituitary neuroendocrine tumor (PitNET), representing approximately half of such tumors. Dopamine agonists (DAs) have traditionally been the primary treatment for the majority of prolactinomas, with surgery considered the second line. The aim of this review is to examine the historical and modern management of prolactinomas, including medical therapy with DAs, transsphenoidal surgery, and multimodality therapy for the treatment of aggressive prolactinomas and metastatic PitNETs, with an emphasis on the efficacy, safety, and future directions of current therapeutic modalities. DAs have been the mainstay of prolactinoma management since the 1970s, initially with bromocriptine and more recently with cabergoline. Cabergoline normalizes prolactin in up to 85% of patients and causes tumor shrinkage in up to 80%. Primary surgical resection of microprolactinomas and enclosed macroprolactinomas performed by experienced pituitary neurosurgeons have similar remission rates to cabergoline. Aggressive prolactinomas and metastatic PitNETS should receive multimodality therapy including high dose cabergoline, surgery, radiation therapy (preferably using stereotactic radiosurgery where suitable), and temozolomide. DAs remain a reliable mode of therapy for most prolactinomas but results from transsphenoidal surgery in expert hands have improved considerably over the last one to two decades. Surgery should be strongly considered as primary therapy, particularly in the setting of microprolactinomas, non-invasive macroprolactinomas, or prior to attempting pregnancy, and has an important role in the management of DA resistant and aggressive prolactinomas.
Pyometra is a common disease in intact bitches and queens and occurs, although less frequently,in most other female pets. The illness is generally diagnosed within 4 months after estrus, in middle-aged to older bitches and queens. Hormonal and bacterial factors are important for the disease development, and progesterone plays a key role. The diagnosis is based on case history, clinical signs, and findings on physical examination, laboratory analyses and diagnostic imaging. Pyometra is potentially life-threatening and considered a medical emergency. Surgical ovariohysterectomy is the safest and most efficient treatment, but purely pharmacologic options are possible in less severe cases. Huntington disease (HD) is a progressive disorder of motor, cognitive, and psychiatric manifestations. HD typically manifests in adult life with mean age of onset around 40-50 years, although childhood onset and late onset do occur. Early manifestations include subtle changes in eye movements and coordination, minor involuntary movements, difficulty with mental planning, and often a depressed or irritable mood. As the disease progresses, chorea becomes more prominent, voluntary activity becomes increasingly difficult, dysarthria and dysphagia worsen, and intermittent outbursts of aggressive behaviors and social disinhibition may increase. In later stages, motor disability becomes severe and affected individuals are often totally dependent, mute, and incontinent. The median survival after onset is 15 to 18 years. The diagnosis of HD can be established in a proband with characteristic clinical, neuroimaging, and family history findings and a heterozygous CAG trinucleotide repeat expansion in HTT identified by molecular genetic testing. Treatment of manifestations: Pharmacologic therapy for chorea includes typical and atypical neuroleptics, benzodiazepines, tetrabenazine, deutetrabenazine, or valbenazine. Hypokinesia and rigidity can be treated with pharmacologic and/or nonpharmacologic