Carbamazepine aplastic anemia with

Aplastic anemia and agranulocytosis have been reported in association with carbamazepine therapy. The risk of developing these reactions is 5 to 8 times greater than in the general population. Consider discontinuation of the drug if any evidence of significant bone marrow depression develops. 

The anticonvulsant therapeutic range for plasma concentrations of carbamazepine is 4 to 12 pg/mL. Hematological assessment in patients on carbamazepine therapy is appropriate because aplastic anemia and agranulocytosis have been reported in association with its use. 

Considerable concern exists regarding the occurrence of idiosyncratic blood dyscrasias with carbamazepine, including fatal cases of aplastic anemia and agranulocytosis. Most of these have been in elderly patients with trigeminal neuralgia, and most have occurred within the first 4 months of treatment. The mild and persistent leukopenia seen in some patients is not necessarily an indication to stop treatment but requires careful monitoring. The most common idiosyncratic reaction is an erythematous skin rash other responses such as hepatic dysfunction are unusual. 

Aplastic anemia occurred in one patient who had recovered 7 years earlier from bone-marrow aplasia ascribed to carbamazepine (SEDA-20, 63). Severe pure red cell aplasia in a patient with heterozygous beta-thalassemia reversed rapidly after lamotrigine withdrawal however,... 

The therapeutic concentration range for optimal pharmacological effect of carbamazepine is 4 to 12p,g/mL. Toxicity associated with excessive carbamazepine ingestion occurs at plasma concentrations in excess of 15p.g/mL and is characterized by symptoms of blurred vision, paresthesia, nystagmus, ataxia, drowsiness, and diplopia. Side effects unrelated to plasma concentration include development of an urticarial rash, which usually disappears on discontinuation of the drug, and hematological depression (leukopenia, thrombocytopenia, and aplastic anemia). 

Carbamazepine has a moderate anticholinergic action that may cause symptoms of dry mouth and constipation. CNS effects include somnolence, ataxia, diplopia, loss of accommodation, dizziness, and headache, which are most prominent with overdosage. Erythroderma, photosensitivity, and skin rashes may also be seen, and, rarely, Stevens-Johnson syndrome or systemic lupus-like syndrome also occur. The drug also has other serious adverse effects, such as suppression of ventricular automaticity, and, rarely, blood dyscrasias (e.g.. agranulocytosis, leukopenia, thrombocytopenia, and aplastic anemia). Due to hepatic metabolism, hepatocellular and cholestatic jaundice may also be seen. 

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