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MEGALOBLASTIC ANÆMIA ASSOCIATED WITH ANTICONVULSANT DRUG THERAPY
Author(s) -
STOKES JOHN B.,
FORTUNE CYRIL
Publication year - 1958
Publication title -
australasian annals of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 0571-9283
DOI - 10.1111/imj.1958.7.2.118
Subject(s) - primidone , medicine , folic acid , phenytoin , vitamin , anticonvulsant , megaloblastic anemia , megaloblastic anaemia , pharmacology , pregnancy , phenobarbital , epilepsy , biology , psychiatry , genetics
Summary An epileptic boy of 16 years developed megaloblastic anæmia while being treated with primidone and phenytoin. There was an optimal hæmatological response to folic acid therapy. Laboratory investigations showed a normal serum concentration of vitamin B 12 and normal radioactive vitamin B 12 absorption. This is the thirty‐third reported case of megaloblastic anæmia associated with anticonvulsant therapy. Certain features common to the majority of these cases suggest that a folic acid deficiency or a derangement of folic acid metabolism is responsible for the megaloblastic anæmia. All 20 patients treated with folic acid responded optimally. Eight patients are reported to have responded to vitamin B 12 , one to liver extract and four to a combination of folic acid and vitamin B 12 . It is suggested that the anticonvulsant drugs have an antifolic acid action which is too mild to produce megaloblastic anæmia in the majority of epileptics unless one or more co‐factors operate. A suboptimal folic acid intake is postulated as the main co‐factor in at least five of the 20 cases in which there was a response to folic acid and perhaps also in some of the cases in which a response has been reported to vitamin B 12 . In one case repeated hæmorrhage, in another pregnancy and in a third case a possible latent steatorrhœa are postulated as additional co‐factors.

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