{"title":"托吡酯诱导锂毒性","authors":"Afaque H Khan","doi":"10.15406/JSRT.2018.04.00104","DOIUrl":null,"url":null,"abstract":"Numerous studies have described that mechanism of action of Topiramate has wide spectrum pharmacological properties. He has been used as mood stabilizers in bipolar and schizoaffective disorder, anorexia bulimia, epilepsy, migraine, essential tremors and cluster headache. It is also effective in treatment resistant bipolar disorder by augmentation of effects of lithium. It has been reported in recent literature that topiramate also use in binge eating disorder (BED) and for weight loss [1]. Topiramate reduces the frequency of the voltage sensitive sodium channels and play a key role in treatment of epilepsy. Topiramate potentiates the effects of inhibitory effects of Gama amino butyric acid-A in the brain. Topiramate has been also found, enhance the effects of Gaba stimulated chloride influx in cerebral which also increase frequency of activation of Gaba-A receptor in brain and exhibits an anticonvulsants action. Topiramate is also known to have inhibitory action on excitatory pathways of AMPA and glutamate receptors and contributes as an anticonvulsant agent. TPM also inhibits high voltage activated calcium channels and decrease their neurotransmitter release and inhibit calcium dependent second messenger system. TPM also has inhibitory action at carbonic anhydrate at proximal tubular level. TPM has been considered weak CAinhibitor and this property has no therapeutic values in treatment of epilepsy and other conditions. This action determines some of its side effects such as hyponatremia, metabolic acidosis and increase risk of nephrolithiasis [2].","PeriodicalId":91560,"journal":{"name":"Journal of stem cell research & therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2018-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Topiramate induced lithium toxicity\",\"authors\":\"Afaque H Khan\",\"doi\":\"10.15406/JSRT.2018.04.00104\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Numerous studies have described that mechanism of action of Topiramate has wide spectrum pharmacological properties. He has been used as mood stabilizers in bipolar and schizoaffective disorder, anorexia bulimia, epilepsy, migraine, essential tremors and cluster headache. It is also effective in treatment resistant bipolar disorder by augmentation of effects of lithium. It has been reported in recent literature that topiramate also use in binge eating disorder (BED) and for weight loss [1]. Topiramate reduces the frequency of the voltage sensitive sodium channels and play a key role in treatment of epilepsy. Topiramate potentiates the effects of inhibitory effects of Gama amino butyric acid-A in the brain. Topiramate has been also found, enhance the effects of Gaba stimulated chloride influx in cerebral which also increase frequency of activation of Gaba-A receptor in brain and exhibits an anticonvulsants action. Topiramate is also known to have inhibitory action on excitatory pathways of AMPA and glutamate receptors and contributes as an anticonvulsant agent. TPM also inhibits high voltage activated calcium channels and decrease their neurotransmitter release and inhibit calcium dependent second messenger system. TPM also has inhibitory action at carbonic anhydrate at proximal tubular level. TPM has been considered weak CAinhibitor and this property has no therapeutic values in treatment of epilepsy and other conditions. This action determines some of its side effects such as hyponatremia, metabolic acidosis and increase risk of nephrolithiasis [2].\",\"PeriodicalId\":91560,\"journal\":{\"name\":\"Journal of stem cell research & therapeutics\",\"volume\":\"1 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-02-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of stem cell research & therapeutics\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.15406/JSRT.2018.04.00104\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of stem cell research & therapeutics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15406/JSRT.2018.04.00104","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Numerous studies have described that mechanism of action of Topiramate has wide spectrum pharmacological properties. He has been used as mood stabilizers in bipolar and schizoaffective disorder, anorexia bulimia, epilepsy, migraine, essential tremors and cluster headache. It is also effective in treatment resistant bipolar disorder by augmentation of effects of lithium. It has been reported in recent literature that topiramate also use in binge eating disorder (BED) and for weight loss [1]. Topiramate reduces the frequency of the voltage sensitive sodium channels and play a key role in treatment of epilepsy. Topiramate potentiates the effects of inhibitory effects of Gama amino butyric acid-A in the brain. Topiramate has been also found, enhance the effects of Gaba stimulated chloride influx in cerebral which also increase frequency of activation of Gaba-A receptor in brain and exhibits an anticonvulsants action. Topiramate is also known to have inhibitory action on excitatory pathways of AMPA and glutamate receptors and contributes as an anticonvulsant agent. TPM also inhibits high voltage activated calcium channels and decrease their neurotransmitter release and inhibit calcium dependent second messenger system. TPM also has inhibitory action at carbonic anhydrate at proximal tubular level. TPM has been considered weak CAinhibitor and this property has no therapeutic values in treatment of epilepsy and other conditions. This action determines some of its side effects such as hyponatremia, metabolic acidosis and increase risk of nephrolithiasis [2].