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May Long Term Oxcarbazepine Treatment Be Lead to Secondary Hyperparathyroidism?
O. Babacan,A. Karaoglu,S. Vurucu,E. Yesilkaya,O. Yesilyurt,T. Cayci,M. Gulgun,B. Unay,R. Akın,O. Ozcan 대한신경과학회 2012 Journal of Clinical Neurology Vol.8 No.1
Background and Purpose The adverse effects of newer antiepileptic drugs are not well-known. This study assessed the impact of oxcarbazepine (OXC) treatment on bone turnover. Methods Forty-four children with idiopathic focal (and/or secondarily generalized) epilepsy who had been treated with OXC for more than 1 year were compared with 33 healthy, age- and sexmatched children. Serum calcium, phosphorus, alkaline phosphatase, parathyroid hormone, osteocalcin, calcitonin, and 25-hydroxyvitamin D, and bone mineral density were measured to evaluate and compare bone mineralization between the two groups. Results The serum levels of calcium, osteocalcin, 25-hydroxyvitamin D, and bone mineral density did not differ significantly between the study and control groups. However, serum levels of parathyroid hormone, alkaline phosphatase, phosphorus, and calcitonin differed significantly between the two groups. Conclusions These findings suggest that OXC treatment leads to secondary hyperparathyroidism with high-turnover bone disease and/or impaired intestinal calcium absorption.
Turgut, L.,Hayirl, Armagan,Celebi, S.,Yoruk, M.A.,Gul, M.,Karaoglu, M.,Macit, M. Asian Australasian Association of Animal Productio 2006 Animal Bioscience Vol.19 No.8
This experiment was designed to examine the effects of supplemental vitamin D on laying performance, metabolic profile and egg quality of hens fed diets containing different fat sources and levels. Lohman strains (n = 480) were assigned to one of 10 diets: basal diet (BD), BD plus 2.5 and 5.0% sunflower oil (SO) or tallow (T) at vitamin D provided $1{\times}$ and $3{\times}$ of the current recommendation. The experiment lasted from week 30 to 44 of age. Each diet was tested in 12 replicate cages of 4 hens. Production, metabolism, and egg quality data were subjected to three-way ANOVA. Both fats decreased feed intake (FI) as compared to BD. Increasing SO and T levels linearly decreased and quadratically increased FI, respectively. The dietary factors did not affect egg production (EP) and egg weight. Vitamin D supplementation increased and decreased EP when diets contained SO and T, respectively. Feed conversion efficiency (FCE) for hens fed SO was lower than for hens fed T. However, increasing T level improved FCE, whereas increasing SO level worsened FCR. Vitamin D supplementation increased serum vitamin D and glucose concentrations. Vitamin D supplementation also caused a decrease and an increase in serum vitamin D concentration when diets contained SO and T, respectively. Serum glucose concentration for hens fed SO was lower than hens fed T. Increasing fat level linearly increased serum triglyceride and VLDL concentrations, regardless of the fat type. Increasing SO level linearly decreased serum cholesterol concentration. Vitamin D supplementation did not alter lipid metabolites. The dietary factors did not affect serum total protein, Ca, and P concentrations. As compared with BD, feeding SO decreased dry tibia and ash weights more than feeding T. Vitamin D supplementation tended to increase dry tibia weight and decrease tibia ash weight. Eggshell strength and thickness, yolk and albumen indexes, and Haugh unit were not responsive to the dietary factors. Eggshell strength quadratically increased with increasing T level. Yolk color for hens fed SO was lower than for hens fed T. The dietary factors did not affect most of yolk fatty acids. Increasing SO level quadratically decreased yolk $C_{18:2}$ concentration. Vitamin D supplementation increased and decreased yolk $C_{18:2}$ concentration when diets contained SO and T, respectively. In conclusion, increasing fat level improved laying performance without altering metabolic profile and egg quality. Vitamin D supplementation had minor alteration effects on laying performance, metabolic profile, and egg quality in response to fat feeding.