Lipoprotein(a) Concentration Increases during Treatment with Carbamazepine

• Published in: Epilepsia (Copenhagen) Vol. 44; no. 3; pp. 457 - 460
• Main Authors: Brämswig, Suzanne, Sudhop, Thomas, Luers, Claus, Von Bergmann, Klaus, Berthold, Heiner K.
• Format: Journal Article
• Language: English
• Published: Boston, MA, USA Blackwell Science Inc 01.03.2003; Blackwell
• Subjects: Adult; Anticonvulsants - adverse effects; Anticonvulsants - pharmacology; Anticonvulsants - therapeutic use; Anticonvulsants. Antiepileptics. Antiparkinson agents; Biological and medical sciences; Carbamazepine; Carbamazepine - adverse effects; Carbamazepine - pharmacology; Carbamazepine - therapeutic use; Cholesterol - blood; Cholesterol, LDL - blood; Coronary Artery Disease - blood; Coronary Artery Disease - etiology; Diabetes mellitus; Diabetic Neuropathies - drug therapy; Humans; Lipoprotein(a); Lipoprotein(a) - blood; Male; Medical sciences; Neuropathic pain management; Neuropharmacology; Pharmacology. Drug treatments; Prospective Studies; Risk Factors; Stimulation, Chemical; Supine Position; Triglycerides - blood; Human; Chemotherapy; Treatment; Adult; Anticonvulsant; Carbamazepine- Lipoprotein(a)-Humans-Neuropathic pain management- Diabetes mellitus; Tricyclic compound; ELISA assay; Carbamazepine; Dibenzazepine derivatives; Lipoprotein a
• ISSN: 0013-9580; 1528-1167
• DOI: 10.1046/j.1528-1157.2003.44802.x

Purpose: Treatment with carbamazepine (CBZ) is known to affect apolipoprotein B–containing lipoprotein concentrations in serum. However, little is known about the effects of anticonvulsant drugs (AEDs) on lipoprotein(a) [Lp(a)], although Lp(a) has been characterized as independent cardiovascular risk factor. We investigated prospectively the effect of CBZ on lipoprotein(a) concentration in normolipidemic healthy adults. Methods: Twenty male volunteers were included in the study. Lp(a) levels were determined before and 69 ± 19 days after CBZ administration by using an enzyme‐linked immunoassay. Results: CBZ (mean plasma concentration, 6.6 ± 0.6 μg/ml) caused a significant increase in Lp(a) concentrations, with a median change of +19.5% (95% CI: +8.2, +53.3; p < 0.001). Total cholesterol, low density lipoprotein (LDL) cholesterol, and triglycerides also increased significantly. Conclusions: Although the precise mechanism of action of CBZ on Lp(a) elevation remains uncertain, it might be related to its enzyme‐inducing properties. During treatment with CBZ, special focus should be given to elevated LDL cholesterol and Lp(a) concentrations with regard to increased risk for atherosclerotic vascular diseases.