Carbamazepine
1
Reactions 1264 - 8 Aug 2009 S Carbamazepine Hypertension leading to reversible posterior leukoencephalopathy syndrome: case report Hypertension leading to reversible posterior leukoencephalopathy syndrome (RPLS) occurred in a 21-year-old man during treatment with carbamazepine. The man was admitted and diagnosed with idiopathic trigeminal neuralgia. He started receiving oral carbamazepine 200 mg/day on hospital day 1, increased to 400 mg/day on day 3. He developed a sharp increase in his blood pressure, reaching 170/126mm Hg on day 5, and increasing thereafter. In an endocrine secretion test to differentiate secondary hypertension, an increase in sympathetic nervous system activity was confirmed. On day 8, he became less responsive to questions. His brain wave pattern contained theta waves in the 6–7 Hz range, but they were localised, with no left-right difference, and no clear epileptic spikes. On MRI on day 9, T2-weighted and FLAIR imaging showed high signal intensity lesions in the vicinity of the bilateral fronto-parieto-occipital subcortex. ADC image showed high intensity in the same area, and in the absence of any contrasting effect caused by gadolinium these were considered signs of oedema that was vascular in origin. Hypertension persisted and he developed impaired consciousness. In view of the MRI findings, RPLS was suspected. The man received nicardipine and methylprednisolone, changed to nicardipine and amlodipine on day 12. By day 15, his consciousness was more or less clear, but his blood pressure had not reduced sufficiently. Carbamazepine was stopped on day 15. After valsartan was started on day 16, his blood pressure gradually normalised, and was thereafter normal without hypotensive medication. On subsequent MRI, the bilateral fronto- parieto-occipital subcortex lesions had disappeared. Author comment: "[I]t is thought that the cause of the slight effect of [nicardipine] and amlodipine may be that the induction of CYP3A4 by [carbamazepine] causes rapid metabolism of drugs that are Ca antagonists. . .[I]n the present case RPLS was triggered by the sudden increase in blood pressure caused by [carbamazepine]." Furuta N, et al. Reversible posterior leukoencephalopathy syndrome associated with carbamazepine-induced hypertension. Rinsho Shinkeigaku 49: 191-193, No. 4, Apr 2009 [Japanese; summarised from an English translation] - Japan 801146714 1 Reactions 8 Aug 2009 No. 1264 0114-9954/10/1264-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved
Transcript of Carbamazepine
Reactions 1264 - 8 Aug 2009
SCarbamazepine
Hypertension leading to reversible posteriorleukoencephalopathy syndrome: case report
Hypertension leading to reversible posteriorleukoencephalopathy syndrome (RPLS) occurred in a21-year-old man during treatment with carbamazepine.
The man was admitted and diagnosed with idiopathictrigeminal neuralgia. He started receiving oralcarbamazepine 200 mg/day on hospital day 1, increased to400 mg/day on day 3. He developed a sharp increase in hisblood pressure, reaching 170/126mm Hg on day 5, andincreasing thereafter. In an endocrine secretion test todifferentiate secondary hypertension, an increase insympathetic nervous system activity was confirmed. Onday 8, he became less responsive to questions. His brainwave pattern contained theta waves in the 6–7 Hz range,but they were localised, with no left-right difference, andno clear epileptic spikes. On MRI on day 9, T2-weightedand FLAIR imaging showed high signal intensity lesions inthe vicinity of the bilateral fronto-parieto-occipitalsubcortex. ADC image showed high intensity in the samearea, and in the absence of any contrasting effect caused bygadolinium these were considered signs of oedema thatwas vascular in origin. Hypertension persisted and hedeveloped impaired consciousness. In view of the MRIfindings, RPLS was suspected.
The man received nicardipine and methylprednisolone,changed to nicardipine and amlodipine on day 12. Byday 15, his consciousness was more or less clear, but hisblood pressure had not reduced sufficiently.Carbamazepine was stopped on day 15. After valsartan wasstarted on day 16, his blood pressure gradually normalised,and was thereafter normal without hypotensivemedication. On subsequent MRI, the bilateral fronto-parieto-occipital subcortex lesions had disappeared.
Author comment: "[I]t is thought that the cause of theslight effect of [nicardipine] and amlodipine may be that theinduction of CYP3A4 by [carbamazepine] causes rapidmetabolism of drugs that are Ca antagonists. . .[I]n thepresent case RPLS was triggered by the sudden increase inblood pressure caused by [carbamazepine]."Furuta N, et al. Reversible posterior leukoencephalopathy syndrome associatedwith carbamazepine-induced hypertension. Rinsho Shinkeigaku 49: 191-193, No.4, Apr 2009 [Japanese; summarised from an English translation] -Japan 801146714
1
Reactions 8 Aug 2009 No. 12640114-9954/10/1264-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved
