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Carbamazepine ( CBZ ), sold under the tradename Tegretol, among others, is a medication used primarily in the treatment of epilepsy and neuropathic pain.
Common side effects include nausea and drowsiness.
Carbamazepine was discovered in 1953 by Swiss chemist Walter Schindler.
1 Medical uses
2 Adverse effects
4 Mechanism of action
6 Environmental impact
7 Brand names
8 See also
10 External links
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Carbamazepine is typically used for the treatment of seizure disorders and neuropathic pain.
In the United States, the FDA -approved medical uses are epilepsy (including partial seizures, generalized tonic-clonic seizures and mixed seizures ), trigeminal neuralgia, and manic and mixed episodes of bipolar I disorder.
The drug is also claimed to be effective for ADHD.
As of 2014, a controlled release formulation was available for which there is tentative evidence showing fewer side effects and unclear evidence with regard to whether there is a difference in efficacy.
In the US, the label for carbamazepine contains warnings concerning:
effects on the body’s production of red blood cells, white blood cells, and platelets : rarely, there are major effects of aplastic anemia and agranulocytosis reported and more commonly, there are minor changes such as decreased white blood cell or platelet counts, but these do not progress to more serious problems.
increased risks of suicide
increased risks of hyponatremia and SIADH
risk of seizures, if the person stops taking the drug abruptly
risks to the fetus in women who are pregnant, specifically congenital malformations like spina bifida, and developmental disorders.
Common adverse effects may include drowsiness, dizziness, headaches and migraines, motor coordination impairment, nausea, vomiting, and/or constipation. Alcohol use while taking carbamazepine may lead to enhanced depression of the central nervous system.
Carbamazepine has a potential for drug interactions ; caution should be used in combining other medicines with it, including other antiepileptics and mood stabilizers.
Valproic acid and valnoctamide both inhibit microsomal epoxide hydrolase (MEH), the enzyme responsible for the breakdown of carbamazepine-10,11 epoxide into inactive metabolites. By inhibiting MEH, valproic acid and valnoctamide cause a build-up of the active metabolite, prolonging the effects of carbamazepine and delaying its excretion.
Grapefruit juice raises the bioavailability of carbamazepine by inhibiting CYP3A4 enzymes in the gut wall and in the liver.
Serious skin reactions such as Stevens–Johnson syndrome or toxic epidermal necrolysis due to carbamazepine therapy are more common in people with a particular human leukocyte antigen allele, HLA-B*1502.
Carbamazepine is relatively slowly but well absorbed after oral administration. Its plasma half-life is about 30 hours when it is given as single dose, but it is a strong inducer of hepatic enzymes and the plasma half-life shortens to about 15 hours when it is given repeatedly. This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (December 2014) ( Learn how and when to remove this template message )
Mechanism of action
Carbamazepine is a sodium channel blocker.
Carbamazepine was discovered by chemist Walter Schindler at J.R. Geigy AG (now part of Novartis ) in Basel, Switzerland, in 1953.
In 1971, Drs. Takezaki and Hanaoka first used carbamazepine to control mania in patients refractory to antipsychotics ( lithium was not available in Japan at that time). Dr. Okuma, working independently, did the same thing with success. As they were also epileptologists, they had some familiarity with the antiaggression effects of this drug. Carbamazepine was studied for bipolar disorder throughout the 1970s.
Main article: Environmental impact of pharmaceuticals and personal care products
Carbamazepine has been detected in wastewater effluent. : 227
Carbamazepine is available worldwide under many brand names.
Toll-like receptor 4 investigating agonist (proinflammatory) property
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