+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Preliminarily Analysis of Carbamazepine (CBZ) C 0 in Patients Visited Isfahan Epileptic Clinics

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.



          Carbamazepine (CBZ) is mostly considered as the first line of effective treatment against simple or complex partial seizure and primary-secondary generalization. To prevent side-effects related to higher amount of CBZ minimum concentration (C 0) in body fluid or seizure attacks associated to lower amount of CBZ-C 0, the suggested minimum therapeutic concentrations range from 4 to 12 ng/ml (according to previous publications). The aim of this preliminarily study was to investigate the scope of discrepancy associated to the C 0of CBZ in patients visited Isfahan Epileptic Clinic.


          A cross-sectional study of 22 patients located in neurology ward of Isfahan Neurosciences Research Centre (INRC) was carried out between April 1, 2012 and December 31, 2012. Female ( n = 9) and male subjects ( n = 13) with a mean age of 27.4 years (range; 16-38 years) were studied. Pharmacological (CBZ-C 0) and demographical variables were recorded and processed in excel.


          The results of CBZ-C 0 showed wide inter-individual variability. The mean value of CBZ-C 0 was 7.2 ng/ml. In 10 out of 22 patients, CBZ-C 0 were lower than the suggested therapeutic window (4-12 ng/ml). CBZ-C 0 in nine patients was non-detectable and in one patient was 0.5 ng/ml (45% < 4 ng/ml). In 55% of the patients, CBZ-C 0 ranged from 4.8 to 12 ng/ml.


          A schedule therapeutic drug monitoring based on measurement of CBZ-C 0for individual patient could be a practical marker to achieve therapeutic objectives. Further study related to correlating of CBZC 0to clinical events in Iranian Epileptic population seems to be valuable.

          Related collections

          Most cited references 28

          • Record: found
          • Abstract: found
          • Article: not found

          Comparison of the four anhydrous polymorphs of carbamazepine and the crystal structure of form I.

          For decades, carbamazepine (CBZ) has served as a model compound for groups engaged in the study of crystal polymorphism. Despite considerable effort, crystal structures for only three of its four anhydrous forms have previously been determined. Herein, we report the first single crystal X-ray structure of the high temperature modification of CBZ (form I). Form I crystallizes in a triclinic cell (P-1) having four inequivalent molecules with the following lattice parameters: a = 5.1705(6), b = 20.574(2), c = 22.245(2) A, alpha = 84.12(4), beta = 88.01(4), and gamma = 85.19(4) degrees. Furthermore, we compare the physical properties of the four anhydrous polymorphs of CBZ, including the first comprehensive characterization of form IV. Substantial differences are seen among these forms by powder X-ray diffraction, infrared spectroscopy, thermomicroscopy, and differential scanning calorimetry. These data are correlated to their respective crystal structures for the first time. We have found that all polymorphs possess identical strong hydrogen bonding patterns, similar molecular conformations, and stabilities that are within 0.7 kcal/mol of each other. Copyright 2003 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 92:2260-2271, 2003
            • Record: found
            • Abstract: found
            • Article: not found

            Molecular model of anticonvulsant drug binding to the voltage-gated sodium channel inner pore.

            The tricyclic anticonvulsant drugs phenytoin, carbamazepine, and lamotrigine block neuronal voltage-gated Na(+) channels, and their binding sites to domain IV-S6 in the channel's inner pore overlap with those of local anesthetic drugs. These anticonvulsants are neutral, in contrast to the mostly positively charged local anesthetics, but their open/inactivated-state blocking affinities are similar. Using a model of the open pore of the Na(+) channel that we developed by homology with the crystal structures of potassium channels, we have docked these three anticonvulsants with residues identified by mutagenesis as important for their binding energy. The three drugs show a common pharmacophore, including an aromatic ring that has an aromatic-aromatic interaction with Tyr-1771 of Na(V)1.2 and a polar amide or imide that interacts with the aromatic ring of Phe-1764 by a low-energy amino-aromatic hydrogen bond. The second aromatic ring is nearly at a right angle to the pharmacophore and fills the pore lumen, probably interacting with the other S6 segments and physically occluding the inner pore to block Na(+) permeation. Hydrophobic interactions with this second aromatic ring may contribute an important component to binding for anticonvulsants, which compensates energetically for the absence of positive charge in their structures. Voltage dependence of block, their important therapeutic property, results from their interaction with Phe-1764, which connects them to the voltage sensors. Their use dependence is modest and this results from being neutral, with a fast drug off-rate after repolarization, allowing a normal action potential rate in the presence of the drugs.
              • Record: found
              • Abstract: found
              • Article: not found

              Antiepileptic drug mechanisms of action.

              Established antiepileptic drugs (AEDs) decrease membrane excitability by interacting with neurotransmitter receptors or ion channels. AEDs developed before 1980 appear to act on sodium channels, gamma-aminobutyric acid type A (GABAA) receptors, or calcium channels. Benzodiazepines and barbiturates enhance GABAA receptor-mediated inhibition. Phenytoin (PHT), carbamazepine (CBZ), and possibly valproate (VPA) decrease high-frequency repetitive firing of action potentials by enhancing sodium-channel inactivation. Ethosuximide (ESM) and VPA reduce a low threshold (T-type) calcium-channel current. The mechanisms of action of the new AEDs are not fully established. Gabapentin (GBP) binds to a high-affinity site on neuronal membranes in a restricted regional distribution of the central nervous system. This binding site may be related to a possible active transport process of GBP into neurons; however, this has not been proven, and the mechanism of action of GBP remains uncertain. Lamotrigine (LTG) decreases sustained high-frequency repetitive firing of voltage-dependent sodium action potentials that may result in a preferential decreased release of presynaptic glutamate. The mechanism of action of oxcarbazepine (OCBZ) is not known; however, its similarity in structure and clinical efficacy to CBZ suggests that its mechanism of action may involve inhibition of sustained high-frequency repetitive firing of voltage-dependent sodium action potentials. Vigabatrin (VGB) irreversibly inhibits GABA transaminase, the enzyme that degrades GABA, thereby producing greater available pools of presynaptic GABA for release in central synapses. Increased activity of GABA at postsynaptic receptors may underline the clinical efficacy of VGB.

                Author and article information

                Int J Prev Med
                Int J Prev Med
                International Journal of Preventive Medicine
                Medknow Publications & Media Pvt Ltd (India )
                May 2013
                : 4
                : Suppl 2 , 8th Iranian Neurology Congress
                : S343-S346
                Isfahan Neurosciences Research Centre, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
                [1 ]Department of Neurology, Isfahan Neurosciences Research Centre, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
                Author notes
                Correspondence to: Dr. Zahra Tolou Ghamari, Isfahan Neurosciences Research Centre, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. E-mail: toloeghamari@
                Copyright: © International Journal of Preventive Medicine

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Brief Communication

                Health & Social care

                iranian, epilepsy, carbamazepine, c0


                Comment on this article