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Ergot derivatives are used to treat migraine headache and enhance uterine contraction post partum. Ergots are produced by the fungus Claviceps purpurea, which may grow on rye and other grains. Natural or synthetic ergot drugs include ergotamine (Cafergot, Ergomar, Gynergen, and Ergostat), methysergide (Sansert), dihydroergotamine (DHE-45), and ergonovine (Ergotrate). Some ergoloid derivatives (dihydroergocornine, dihydroergocristine, and dihydroergocryptine) have been used in combination (Hydergine and Deapril-ST) for the treatment of dementia. Bromocriptine (Parlodel [See Bromocriptine]) and pergolide (Permax) are ergot derivatives with dopamine agonist activity that are used to treat Parkinson disease. Bromocriptine is also used to treat hyperprolactinemic states.

  1. Mechanism of toxicity

    1. Ergot derivatives directly stimulate vasoconstriction and uterine contraction, antagonize alpha-adrenergic and serotonin receptors, and may dilate some blood vessels via a CNS sympatholytic action. The relative contribution of each of these mechanisms to toxicity depends on the particular ergot alkaloid and its dose. Sustained vasoconstriction causes most of the serious toxicity; reduced blood flow causes local tissue hypoxia and ischemic injury, resulting in tissue edema and local thrombosis, worsening ischemia, and causing further injury. At a certain point, reversible vasospasm progresses to irreversible vascular insufficiency and limb gangrene.

    2. Pharmacokinetics (see Table II–61). Ergot alkaloids are extensively metabolized and highly tissue-bound, the latter characteristic accounting for protracted clinical ergot poisoning after the drug is stopped. Ergotism has occurred in people with HIV taking protease inhibitors as well as ergots for migraine, presumably owing to inhibition of ergot metabolism.

  2. Toxic dose. Death has been reported in a 14-month-old child after acute ingestion of 12 mg of ergotamine. However, most cases of severe poisoning occur with chronic overmedication for migraine headaches rather than acute single overdoses. Daily doses of 10 mg or more of ergotamine are usually associated with toxicity. There are many case reports of vasospastic complications with normal therapeutic dosing.

  3. Clinical presentation

    1. Ergotamine and related agents. Mild intoxication causes nausea and vomiting. Serious poisoning results in vasoconstriction that may involve many parts of the body. Owing to persistence of ergots in tissues, vasospasm may continue for up to 10–14 days.

      1. Involvement of the extremities causes paresthesias, pain, pallor, coolness, and loss of peripheral pulses in the hands and feet; gangrene may ensue.

      2. Other complications of vasospasm include coronary ischemia and myocardial infarction, abdominal angina and bowel infarction, renal infarction and failure, visual disturbances and blindness, and stroke. Psychosis, seizures, and coma occur rarely.

      3. Iatrogenic neonatal ergot poisoning has occurred when methylergonovine meant for the mother after delivery was administered mistakenly to the baby. Manifestations of poisoning included respiratory failure, cyanosis, peripheral ischemia, oliguria, and seizures.

    2. Bromocriptine intoxication may present with hallucinations, paranoid behavior, hypertension, and tachycardia. Involuntary movements, hallucinations, and hypotension are reported with pergolide.

    3. Chronic use of methysergide occasionally causes retroperitoneal fibrosis.

  4. Diagnosis is based on a history of ergot use and clinical findings of vasospasm.

    1. Specific levels. Ergotamine levels are not widely available, and blood concentrations do not correlate well with toxicity.

    2. Other useful laboratory studies include CBC, electrolytes, BUN, ...

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