Hostname: page-component-cd9895bd7-mkpzs Total loading time: 0 Render date: 2024-12-28T06:40:01.207Z Has data issue: false hasContentIssue false
  • English
  • Français

Megaloblastic Anaemia Occurring During Treatment of Epilepsy with Phenytoin Sodium, Primidone and Phenobarbitone

Published online by Cambridge University Press:  08 February 2018

Robin C. Benians  and
Richard A. Hunter
Robin C. Benians
Affiliation:
Claybury Hospital, Woodford Green, Essex
Richard A. Hunter
Affiliation:
National Hospital for Nervous Diseases, Queen Square, London
Get access Rights & Permissions [Opens in a new window]

Extract

It has now been established that megaloblastic anaemia may develop in patients receiving the anti-convulsant drugs phenytoin sodium (“Epanutin”) and primidone (“Mysoline”), given alone or in combination with phenobarbitone. Hobson et al. (1956) found 16 such cases described in the literature, and reported a case of their own in which megaloblastic anaemia developed in a patient addicted to a preparation (“Tuinal”) containing equal parts of amylobarbitone sodium (“Sodium amytal”) and quinalbarbitone sodium (“Seconal Sodium”), which are closely related chemically to primidone, sodium phenytoin and phenobarbitone. Characteristically the anaemia is not related to a deficiency of nor does it respond to treatment with vitamin B12, nor is there achlorhydria, thus distinguishing it from true Addisonian pernicious anaemia. The condition however responds promptly to the administration of folic acid by mouth.

Type
Original Articles
Information
Journal of Mental Science , Volume 103 , Issue 432 , July 1957 , pp. 606 - 609
Copyright
Copyright © Royal College of Psychiatrists, 1957 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Badenoch, J., Proc. roy. Soc. Med., 1954, 47, 426.Google Scholar
Berlyne, N., Levene, M., and McGlashan, A., Brit. Med. J., 1955, i, 1247.CrossRefGoogle Scholar
Chalmers, J. N. M., and Boheimer, K., Lancet, 1954, ii, 920.CrossRefGoogle Scholar
Fuld, H., and Moorhouse, E. H., Brit. Med. J., 1956, i, 1021.Google Scholar
Girdwood, R. H., Quart. J. Med., 1956, n.s. 25, 87.Google Scholar
Girdwood, R. H., and Lenman, J. A. R., Brit. Med. J., 1956, i, 146.CrossRefGoogle Scholar
Hawkins, C. F., and Meynell, M. J., Lancet, 1954, ii, 737.Google Scholar
Hobson, Q. J. G., Selwyn, J. G., and Mollin, D. L., Lancet, 1956, ii, 1079.Google Scholar
Mollin, D. L., and Ross, G. I. M., Proc. Roy. Soc. Med., 1954, 47, 428.Google Scholar
Rhind, E. G., and Varadi, S., Lancet, 1954, ii, 921.Google Scholar
Webster, J. M., Lancet, 1954, ii, 1017.Google Scholar
Submit a response

eLetters

No eLetters have been published for this article.