Galantamine Hydrobromide (3 brand names, 3 dosage forms, 1 route)
Available dosage forms: TABLET, CAPSULE, EXTENDED RELEASE, SOLUTION.
Routes of administration: ORAL.
Brand Names
- GALANTAMINE HYDROBROMIDE
- RAZADYNE
- RAZADYNE ER
Indications and Usage
Galantamine hydrobromide extended-release capsules are indicated for the treatment of mild to moderate dementia of the Alzheimer’s type.
Contraindications
Galantamine hydrobromide extended-release capsules are contraindicated in patients with known hypersensitivity to galantamine hydrobromide or to any excipients used in the formulation.
Adverse Reactions
Serious adverse reactions are discussed in more detail in the following sections of the labeling: Serious Skin Reactions [see Warnings and Precautions (5.1)] Cardiovascular Conditions [see Warnings and Precautions (5.3)] Gastrointestinal Conditions [see Warnings and Precautions (5.4)] Genitourinary Conditions [see Warnings and Precautions (5.5)] Neurological Conditions [see Warnings and Precautions (5.6)] Pulmonary Conditions [see Warnings and Precautions (5.7)] Deaths in Patients with Mild Cognitive Impairment (MCI) [see Warnings and Precautions (5.8)]
Mechanism of Action
Although the etiology of cognitive impairment in Alzheimer’s disease (AD) is not fully understood, it has been reported that acetylcholine-producing neurons degenerate in the brains of patients with Alzheimer’s disease. The degree of this cholinergic loss has been correlated with degree of cognitive impairment and density of amyloid plaques (a neuropathological hallmark of Alzheimer’s disease). Galantamine, a tertiary alkaloid, is a competitive and reversible inhibitor of acetylcholinesterase. While the precise mechanism of galantamine’s action is unknown, it is postulated to exert its therapeutic effect by enhancing cholinergic function. This is accomplished by increasing the concentration of acetylcholine through reversible inhibition of its hydrolysis by cholinesterase. If this mechanism is correct, galantamine’s effect may lessen as the disease process advances and fewer cholinergic neurons remain functionally intact. There is no evidence that galantamine alters the course of the underlying dementing process.
Overdosage
Because strategies for the management of overdose are continually evolving, it is advisable to contact a poison control center to determine the latest recommendations for the management of an overdose of any drug. As in any case of overdose, general supportive measures should be utilized. Signs and symptoms of significant overdosing of galantamine are predicted to be similar to those of overdosing of other cholinomimetics. These effects generally involve the central nervous system, the parasympathetic nervous system, and the neuromuscular junction. In addition to muscle weakness or fasciculations, some or all of the following signs of cholinergic crisis may develop: severe nausea, vomiting, gastrointestinal cramping, salivation, lacrimation, urination, defecation, sweating, bradycardia, hypotension, respiratory depression, collapse and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Tertiary anticholinergics such as atropine may be used as an antidote for galantamine hydrobromide overdosage. Intravenous atropine sulfate titrated to effect is recommended at an initial dose of 0.5 mg to 1.0 mg i.v. with subsequent doses based upon clinical response. Atypical responses in blood pressure and heart rate have been reported with other cholinomimetics when coadministered with quaternary anticholinergics. It is not known whether galantamine and/or its metabolites can be removed by dialysis (hemodialysis, peritoneal dialysis, or hemofiltration). Dose-related signs of toxicity in animals included hypoactivity, tremors, clonic convulsions, salivation, lacrimation, chromodacryorrhea, mucoid feces, and dyspnea. In one postmarketing report, one patient who had been taking 4 mg of galantamine daily for a week inadvertently ingested eight 4 mg tablets (32 mg total) on a single day. Subsequently, she developed bradycardia, QT prolongation, ventricular tachycardia and torsades de pointes accompanied by a brief loss