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Effect of carbamazepine on coumadin metabolism.

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Fig 2. Wilson? disease; inversion recowry N M R image showing
decreased signal intensity in the putamen (arrow) and thalamus
NMR changes had been present early in the course of the
successfully treated patient but had resolved with therapy.
This possibility, and the reversibility of CT changes [ 5 ] with
treatment of Wilson’s disease, suggest a prominent role for
edema. Further study will be required to establish the precise
pathological significance and reversibility of NMR abnormalities in Wilson’s disease.
Supported in part by Diasonics, NMR, Inc, and by US Public Health
Service Grant CA 32850 from the National Cancer Institutc.
Fig 3. Wilson’s disease; spin-echo image shoiAing an increase in
signal intenstty in the mzdbrain tegmentum.
5. Williams FB, Walshe JM: Wilson’s disease: an analysis of the
cranid computerized tomographic appearances found in 60 pdtients. Brain 104:735-752, 1981
Effect of Carbamazepine
on Coumadin Metabolism
E. Wayne Massey, MD
Departments of *Neurology and S R a d i o f o ~ ~
and SRadiohgic Imaging Laboratory
UniverJ zty of Califorma, San Francisco
San Francisco, CA 94143
1. Bydder GM, Steiner R, Young IR: Clinical NMR imaging of the
brain: 140 cases. AJNR 3:459-480, 1982
2. Crooks LE, Arakawa M, Hoenninger J, et al: Nuclear magnetic
resonance whole-body imager operating at 3.5 KGauss. Radiology 143:169-174, 1982
3. Kaufman L, Crooks LE, Margulis AR (eds): Nuclear Magnetic
Resonance Imaging in Medicine. New York, Igaku-Shoin, 1981
4. Lukes SA, Crooks LE, Aminoff MJ, et al: Nuclear magnetic resonance imaging in multiple sclerosis. Ann Neurol 13:592-601,
Appropriate warning is not indicated in the manufacturer’s
information sheet regarding the effect of carbamazepine
(Ciba-Giegy) on Coumadin (warfarin sodium) metabolism.
Hansen and colleagues [ I ] reported two patients who experienced reduction in serum Coumadin half-life because of concurrent carbamazepine administration, Kendall and Boivin
[2] reported another, and Penry and Newmark 131 mentioned the problem. Nevertheless, the antagonism seems to
be generally unknown. The postulated mechanism is microsomal enzyme induction [4].
W e have observed this interaction in three patients in our
stroke rehabilitation unit. In a patient already receiving
Coumadin for deep vein thrombosis, the initiation of carbamazepine for treatment of painful neuropathy markedly
altered prothrombin time. Similar problems were observed
in two other patients already receiving anticoagulants who
were placed on carbamazepine.
The carbamazepine effect would not b e apparent in a patient receiving the anticonvulsant who was placed o n anticoagulation therapy unless carbamazepine was discontinued
while the anticoagulant was maintained.
Diz.'ihz of Neurology
Duke Uniorrsitj~Medical Center
Durham, NC 27710
692 Annals of Neurology
Vol 1 5
No 6 J u n e 1083
1. Hansen IM, Siersbock-Nielson K, Skovsted L: CdCbamUeplne
induced acceleration of diphenylhvdantoin and warfirin metabolism in man. Clin Pharmacol T h r r 12:539-543, lO71
2. Kendall AG, Boivin M: Warfarin-carbamdzepine interaction. Ann
lniern Med 94:280, 1981
3. Penry JK, Newmark ME: T h e use of antiepileptic drugs. A n n
Intern Med 90:207-208, 1979
4. Richens A, Woodford FP (eds): Anticonvuisant Drugs anJ Enzyme Induction. Amsrerilam, Associated Scientific Publishers,
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effect, metabolico, carbamazepine, coumadin
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