Carbamazepine
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| Image:Carbamazepine.png | |
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| Carbamazepine
| |
| Systematic (IUPAC) name | |
| 5H-dibenz[b,f]azepine-5-carboxamide | |
| Identifiers | |
| CAS number | 85756-57-6 (dihydrate) |
| ATC code | N03 |
| PubChem | |
| DrugBank | |
| Chemical data | |
| Formula | C15H12N2O |
| Mol. mass | 236.269 g/mol |
| Pharmacokinetic data | |
| Bioavailability | 80% |
| Protein binding | 76% |
| Metabolism | Hepatic—by CYP3A4, to active epoxide form (carbamazepine-10,11 epoxide) |
| Half life | 25–65 hours |
| Excretion | 2–3% excreted unchanged in urine |
| Therapeutic considerations | |
| Pregnancy cat. |
C(US) |
| Legal status | |
| Routes | Oral |
Carbamazepine ("CBZ") is an anticonvulsant and mood stabilizing drug, used primarily in the treatment of epilepsy and bipolar disorder. It is also used to treat ADD, ADHD, schizophrenia and trigeminal neuralgia.
Contents |
Trade names
Carbamazepine has been sold under the names Tegretol, Biston, Calepsin, Carbatrol, Epitol, Equetro, Finlepsin, Sirtal, Stazepine, Telesmin, Timonil, Trimonil, Epimaz, and Degranol (in South Africa)[1].
History
Carbamazepine was discovered by chemist Walter Schindler at J.R. Geigy AG (now part of Novartis) in Basel, Switzerland, in 1953.[1] Schindler then synthesized the drug in 1960, before its anti-epileptic properties had been discovered.
Carbamazepine was first marketed as a drug to treat trigeminal neuralgia in 1962. It has been used as an anticonvulsant in the UK since 1965, but only approved in the U.S. since 1974.
Adverse effects
Carbamazepine renders certain methods of hormonal contraception ineffective because it is an enzyme inducer of the cytochrome P450 system which metabolises the oral contraceptive, leaving less active contraceptive in the plasma.
Common side effects include drowsiness, motor coordination impairment and/or upset stomach. Carbamazepine preparations can greatly decrease alcohol tolerance.
Less common side effects include cardiac arrhythmias, blurry or double vision and/or the temporary or mild loss of blood cells or platelets. In rare cases the latter can be life-threatening if unnoticed, so frequent blood tests are required during the first few months' use, followed by three or four tests per year. In the UK testing would be less frequent in long-term use, typically once every year or two. Underactivity of the thyroid gland may be provoked, so thyroid function tests are advisable every year or two.
Small reductions in white cell count and serum sodium are common.
There are also reports of an auditory side effect, whereby patients perceive musical notes about a semitone lower than their actual pitch (so middle C would be heard as the note B3 just below it, etc).
Oxcarbazepine, a derivative of carbamazepine, has fewer and less serious side effects.
Carbamazepine may cause SIADH (syndrome of inappropriate antidiuretic hormone), since it both increases the release and potentiates the action of ADH (vasopressin).
Carbamazepine may aggravate juvenile myoclonic epilepsy, so it is important to mention any history of jerking, especially in the morning, before starting to take this drug.
Pregnant women taking carbamazepine for seizures are putting their fetuses at increased risk for teratogenic effects and should be given folic acid supplementation and undergo prenatal ultrasonography for diagnosis.
In addition, carbamazepine has been linked to serious adverse cognitive effects, including EEG slowing[1] and cell apoptosis[1].
Mechanisms
The mechanism of action of carbamazepine and its derivatives is relatively well understood. Voltage-gated sodium channels are the molecular pores that allow brain cells (neurons) to generate action potentials, the electrical events that allow neurons to communicate over long distances. After the sodium channels open, to start the action potential, they inactivate, essentially closing the channel. Carbamazepine stabilizes the inactivated state of sodium channels, meaning that fewer of these channels are available to open, making brain cells less excitable.
Interactions
Valproic acid and valnoctamide both interact with carbamazepine, as they inhibit microsomal epoxide hydrolase (mEH), the enzyme responsible for the breakdown of carbamazepine-10,11 epoxide into inactive metabolites.[1] By inhibiting mEH, valproic acid and valnoctamide cause a buildup of the active metabolite, prolonging the effects of carbamazepine and delaying its excretion.
Carbamazepine,as CYP 450 inducer, may increase clearance of many drugs, decreasing their blood levels.
See also
Notes
External links
- Carbatrol website
- Equetro website
- TA warning
- Carbamazepine overview from PsychEducation.org
- U.S. Patent 2,948,718, August 1960
fr:Carbamazépine hr:Karbamazepin it:Carbamazepina hu:Karbamazepin nl:Carbamazepinesv:Karbamazepin
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
