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Cerebrospinal fluid levels of biotin in various neurological disorders
Author(s) -
Anagnostouli M.,
Livaniou E.,
Nyalala J. O.,
Evangelatos G.,
Zournas C.,
Ithakissios D. S.,
Papageorgiou C.
Publication year - 1999
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1999.tb07369.x
Subject(s) - cerebrospinal fluid , biotin , multiple sclerosis , medicine , lumbar puncture , biotin deficiency , gastroenterology , epilepsy , blood–brain barrier , endocrinology , pathology , immunology , chemistry , central nervous system , vitamin , biochemistry , psychiatry
Objectives – To analyse biotin concentrations in human cerebrospinal fluid (CSF) and serum from controls without evidence of nutritional or neurological disorders and patients with common neurological disorders. Patients and methods – Cerebrospinal fluid was obtained from patients by lumbar puncture, serum was prepared from freshly drawn whole blood and biotinidase in samples was inhibited before being analysed for biotin by radioligand assay. Results – Assay characteristics were within an acceptable range (intra‐and interassay coefficient of variations were 8.8 and 12.0 respectively, recovery: 91–114% and sensitive, lowest standard concentration 15 ng/l). Significantly lower values for biotin were found in patients with multiple sclerosis (both CSF and serum) in comparison to the controls. Significantly reduced values for cerebrospinal fluid biotin were found in epileptics compared to controls, whereas, in serum the difference was approaching significance. No significant differences were observed in other groups of patients. Conclusion – There is a significant reduction in cerebrospinal fluid biotin in epileptics and patients with multiple sclerosis compared to controls. In epileptics this may be related to competition between biotin and anticonvulsants bearing carbamide ring for absorption. Reduction of biotin levels in patients with multiple sclerosis could be attributed to intestinal malabsorption caused by the underlying disease or a biotin‐binding immunoglobulin which may be involved in multiple sclerosis pathogenesis.