Bupropion
From Ganfyd
Contents |
Introduction
Although used as an antidepressant for some time in the USA it had major problems in the UK as initial dose recommendations lead to seizures. The current EU license is for smoking cessation. The absence of a clear safety margin for neurotoxicty in animals may be a factor for it not being licensed for depression in the EU. Seizure risk is 1/1000 at 300mg od. It is also being developed for various indications, including obesity, when combined with naltrexone (as in contrave®).
Clinical Use
Indications
- Adjunct to smoking cessation with motivational support (Adults)
- Depression (not in EU)
Administration
Oral 150mg od to max 300mg od for smoking cessation See manufacturers literature for dosage in other indications where licensed.
Clinical Issues
Contra-indications
- Seizures, risk of seizures
- Cirrhosis
- Anorexia nervosa
- With monoamine oxidase inhibitors
- Bipolar illness
Cautions and Interactions
- Stop if clinically significant raise in blood pressure.
- Psychosis and mania reported particulary in those with predisposition
- Alcohol can cause neuropsychiatric effects
- Reduce dose in elderly, liver and kidney disease.
Side effects
- Seizures with risk proportional to dose
- Hypersensitivity reactions including angioedema and Stevens-Johnson syndrome
- Dizziness
- Insomnia
- Headache
- Rash
- Dystonia
- Ataxia
- Parkinsonism
Special advice
Pharmacology
Works as an antidepressant by selective catecholamine (noradrenaline & dopamine) reuptake inhibitor with minimal serotonin uptake inhibition. There is evidence that it acts as a noncompetitive α3β4 nicotinic antagonist[3] which may be relevant to its use in smoking cessation.
References
- ↑ Stahl SM, Pradko JF, Haight BR, Modell JG, Rockett CB, Learned-Coughlin S. A Review of the Neuropharmacology of Bupropion, a Dual Norepinephrine and Dopamine Reuptake Inhibitor. . 2004; 6(4):159-166.
- ↑ Fryer JD, Lukas RJ. Noncompetitive functional inhibition at diverse, human nicotinic acetylcholine receptor subtypes by bupropion, phencyclidine, and ibogaine. The Journal of pharmacology and experimental therapeutics. 1999 Jan; 288(1):88-92.
- ↑ Fryer JD, Lukas RJ. Noncompetitive functional inhibition at diverse, human nicotinic acetylcholine receptor subtypes by bupropion, phencyclidine, and ibogaine. The Journal of pharmacology and experimental therapeutics. 1999 Jan; 288(1):88-92.
