{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,6]],"date-time":"2026-11-06T22:03:48Z","timestamp":1794002628963,"version":"4.8.0"},"reference-count":26,"publisher":"FapUNIFESP (SciELO)","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arq Bras Endocrinol Metab"],"published-print":{"date-parts":[[2007,4]]},"abstract":"<jats:p>In this comparative, cross-sectional study, we evaluated 55 patients with epilepsy on chronic use of antiepileptic drugs (AED); [(38 females and 17 males, 35 \u00b1 6 years (25 to 47)] and compared to 24 healthy subjects (17 females\/7 males). Laboratorial evaluation of bone and mineral metabolism including measurements of bone specific alkaline phosphatase (BALP) and carboxyterminal telopeptide of type I collagen (CTX-I) were performed. Bone mineral density (BMD) was measured by DXA. BALP and CTX-I levels did not differ significantly between the groups. CTX-I levels were significantly higher in patients who were exposed to phenobarbital (P&lt; 0.01) than those who were not. Patients presented BMD of both sites significantly lower than the controls (0.975 \u00b1 0.13 vs. 1.058 \u00b1 0.1 g\/cm\u00b2; p= 0.03; 0.930 \u00b1 0.1 vs. 0.988 \u00b1 0.12 g\/cm\u00b2; p= 0.02, respectively). Total hip BMD (0.890 \u00b1 0.10 vs. 0.970 \u00b1 0.08 g\/cm\u00b2; p&lt; 0.003) and femoral neck (0.830 \u00b1 0.09 vs. 0.890 \u00b1 0.09 g\/cm\u00b2; p&lt; 0.03) were significantly lower in patients who had been exposed to phenobarbital, in comparison to the non-phenobarbital users. In conclusion, patients on AED demonstrate reduced BMD. Among the AED, phenobarbital seems to be the main mediator of low BMD and increases in CTX-I.<\/jats:p>","DOI":"10.1590\/s0004-27302007000300016","type":"journal-article","created":{"date-parts":[[2007,11,16]],"date-time":"2007-11-16T03:15:56Z","timestamp":1195182956000},"page":"466-471","source":"Crossref","is-referenced-by-count":19,"title":["Bone density and bone turnover markers in patients with epilepsy on chronic antiepileptic drug therapy"],"prefix":"10.1590","volume":"51","author":[{"given":"Carolina A.M.","family":"Kulak","sequence":"first","affiliation":[{"name":"UFPR, Brasil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vict\u00f3ria Z.C.","family":"Borba","sequence":"additional","affiliation":[{"name":"UFPR, Brasil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carlos Eduardo","family":"Silvado","sequence":"additional","affiliation":[{"name":"UFPR"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luciano de","family":"Paola","sequence":"additional","affiliation":[{"name":"UFPR"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus J.","family":"Seibel","sequence":"additional","affiliation":[{"name":"University of Sydney"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John P.","family":"Bilezikian","sequence":"additional","affiliation":[{"name":"Columbia University, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C\u00e9sar L.","family":"Boguszewski","sequence":"additional","affiliation":[{"name":"UFPR, Brasil"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"530","reference":[{"key":"ref1","series-title":"Seizures and Epilepsy","first-page":"195","volume-title":"Epileptic syndromes","author":"Engel JJ","year":"1989"},{"key":"ref2","series-title":"Epilepsia","first-page":"1","volume-title":"Considera\u00e7\u00f5es gerais","author":"Guerreiro CAM","year":"2000","edition":"3"},{"key":"ref3","series-title":"Dynamics of 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