Biotin status of epileptics

Microbiologically determined plasma biotin levels in 404 epileptics under long-term treatment with anticonvulsants were markedly lower than in 112 controls (p less than 0.0005). Patients with partial epilepsy had lower biotin levels and higher average daily intake of AC than those with generalized e...

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Veröffentlicht in:Annals of the New York Academy of Sciences 1985-01, Vol.447 (1), p.297-313
Hauptverfasser: Krause, K.H, Bonjour, J.P, Berlit, P, Kochen, W
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container_title Annals of the New York Academy of Sciences
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creator Krause, K.H
Bonjour, J.P
Berlit, P
Kochen, W
description Microbiologically determined plasma biotin levels in 404 epileptics under long-term treatment with anticonvulsants were markedly lower than in 112 controls (p less than 0.0005). Patients with partial epilepsy had lower biotin levels and higher average daily intake of AC than those with generalized epilepsy. Epileptics treated with valproate sodium in monotherapy showed considerably higher biotin levels than epileptics with monotherapy of primidone (PRM), carbamazepine (CBZ), phenytoin (PHT) or phenobarbital (PB). The group of epileptics with high average daily dose of anticonvulsants had lower biotin levels than the group with low dose. In three patients with newly recognized epilepsy biotin levels were normal before starting anticonvulsant medication, increased during the first week and fell under the starting level in the following weeks. Four epileptics treated with PHT, PB, PRM or CBZ had an increased urinary excretion of organic acids, as found in patients with a deficiency of biotin-dependent carboxylases. In 37 epileptics undergoing long-term treatment plasma lactate concentrations were determined; they had a higher mean concentration than that found in controls. Our results suggest, that the lowering of biotin in epileptics is caused by intake of anticonvulsants and has a biochemical effect in these patients. It is discussed, whether this could be a factor in the mode of action of anticonvulsants.
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Patients with partial epilepsy had lower biotin levels and higher average daily intake of AC than those with generalized epilepsy. Epileptics treated with valproate sodium in monotherapy showed considerably higher biotin levels than epileptics with monotherapy of primidone (PRM), carbamazepine (CBZ), phenytoin (PHT) or phenobarbital (PB). The group of epileptics with high average daily dose of anticonvulsants had lower biotin levels than the group with low dose. In three patients with newly recognized epilepsy biotin levels were normal before starting anticonvulsant medication, increased during the first week and fell under the starting level in the following weeks. Four epileptics treated with PHT, PB, PRM or CBZ had an increased urinary excretion of organic acids, as found in patients with a deficiency of biotin-dependent carboxylases. In 37 epileptics undergoing long-term treatment plasma lactate concentrations were determined; they had a higher mean concentration than that found in controls. Our results suggest, that the lowering of biotin in epileptics is caused by intake of anticonvulsants and has a biochemical effect in these patients. It is discussed, whether this could be a factor in the mode of action of anticonvulsants.</description><subject>Adult</subject><subject>anticonvulsants</subject><subject>Anticonvulsants - pharmacology</subject><subject>biotin</subject><subject>Biotin - blood</subject><subject>biotin deficiency</subject><subject>Carbon-Carbon Ligases</subject><subject>Carboxy-Lyases - deficiency</subject><subject>epilepsy</subject><subject>Epilepsy - blood</subject><subject>Epilepsy - drug therapy</subject><subject>Female</subject><subject>Humans</subject><subject>interactions</subject><subject>Lactates - blood</subject><subject>Lactic Acid</subject><subject>Ligases - deficiency</subject><subject>Long-Term Care</subject><subject>Male</subject><subject>Methylmalonyl-CoA Decarboxylase</subject><subject>Middle Aged</subject><subject>Pyruvate Carboxylase Deficiency Disease</subject><issn>0077-8923</issn><issn>1749-6632</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1985</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kM1OwzAQhC0EKqXwBAhRceCW4LUd_3CDQgtSVQ5Q4LZyXAeltCTEqVTenkSpupc9fDO7miHkCmgMzdwsY1DCRFJyFoPRSVynoIVQ8faA9PfokPQpVSrShvFjchLCklJgWqge6XHDEp2YPjm_z4s6_xmG2tabMCyyoS_zlS_r3IVTcpTZVfBnuz0g8_Hj2-gpmr5Mnkd308hxJesIFPPGOEHT1DrnnV4A-ERpDZljCWhvmMqokYpR7cB5unBpyqnUVgsqwfMBue7ullXxu_GhxnUenF-t7I8vNgGVBGOMYo3wthO6qgih8hmWVb621R8CxbYZXGIbH9v42DaDu2Zw25gvdl826dov9tZdFQ2POp6H2m_32FbfKBVXCX7MJjhVDzKZjd_xs9FfdvrMFmi_qjzg_JVR4BSEEFRR_g9zzXdt</recordid><startdate>19850101</startdate><enddate>19850101</enddate><creator>Krause, K.H</creator><creator>Bonjour, J.P</creator><creator>Berlit, P</creator><creator>Kochen, W</creator><general>Blackwell Publishing Ltd</general><scope>FBQ</scope><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19850101</creationdate><title>Biotin status of epileptics</title><author>Krause, K.H ; Bonjour, J.P ; Berlit, P ; Kochen, W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c376t-172e99c40bbaccec8d11e57881fc2518e927f0967208c1ce0dcbb3068a84061e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1985</creationdate><topic>Adult</topic><topic>anticonvulsants</topic><topic>Anticonvulsants - pharmacology</topic><topic>biotin</topic><topic>Biotin - blood</topic><topic>biotin deficiency</topic><topic>Carbon-Carbon Ligases</topic><topic>Carboxy-Lyases - deficiency</topic><topic>epilepsy</topic><topic>Epilepsy - blood</topic><topic>Epilepsy - drug therapy</topic><topic>Female</topic><topic>Humans</topic><topic>interactions</topic><topic>Lactates - blood</topic><topic>Lactic Acid</topic><topic>Ligases - deficiency</topic><topic>Long-Term Care</topic><topic>Male</topic><topic>Methylmalonyl-CoA Decarboxylase</topic><topic>Middle Aged</topic><topic>Pyruvate Carboxylase Deficiency Disease</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Krause, K.H</creatorcontrib><creatorcontrib>Bonjour, J.P</creatorcontrib><creatorcontrib>Berlit, P</creatorcontrib><creatorcontrib>Kochen, W</creatorcontrib><collection>AGRIS</collection><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of the New York Academy of Sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Krause, K.H</au><au>Bonjour, J.P</au><au>Berlit, P</au><au>Kochen, W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Biotin status of epileptics</atitle><jtitle>Annals of the New York Academy of Sciences</jtitle><addtitle>Ann N Y Acad Sci</addtitle><date>1985-01-01</date><risdate>1985</risdate><volume>447</volume><issue>1</issue><spage>297</spage><epage>313</epage><pages>297-313</pages><issn>0077-8923</issn><eissn>1749-6632</eissn><abstract>Microbiologically determined plasma biotin levels in 404 epileptics under long-term treatment with anticonvulsants were markedly lower than in 112 controls (p less than 0.0005). 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source MEDLINE; Wiley Online Library Journals Frontfile Complete
subjects Adult
anticonvulsants
Anticonvulsants - pharmacology
biotin
Biotin - blood
biotin deficiency
Carbon-Carbon Ligases
Carboxy-Lyases - deficiency
epilepsy
Epilepsy - blood
Epilepsy - drug therapy
Female
Humans
interactions
Lactates - blood
Lactic Acid
Ligases - deficiency
Long-Term Care
Male
Methylmalonyl-CoA Decarboxylase
Middle Aged
Pyruvate Carboxylase Deficiency Disease
title Biotin status of epileptics
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