1978 Volume 9 Issue 2 Pages 286-290
Recently, we experienced a case of hepatic injury in a patient who had undergone mitral valve replacement and was taking warfarin to prevent the thromboembolism.
After starting warfarin treatment, it took approximately two weeks for the hepatic injury to appear. And the increase in the ratio of the eosinophilic leucocytes was roughly parallel to the deterioration of the liver function and the lymphocytes' blastoid transformation was positive. These findings suggest hepatitis due to a delayed hypersensitivity to warfarin.
On the other hand, the clinical course (Fig. 1) seems to show the hepatic injury having a dose dependent factor to warfarin.
This discrepancy between the laboratory data and the clinical course is very interesting and fully suggestive, and the etiology of this hepatic injury must be further studied.
