9 research outputs found

    Association of 25-Hydroxyvitamin D Deficiency in Pediatric Epileptic Patients

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    How to Cite This Article: Chaudhuri IR, Mridula KR, Rathnakishore Ch, Balaraju B, Bandaru VCS. Association of 25-Hydroxyvitamin D Deficiency in Pediatric Epileptic Patients. Iran J Child Neurol. Spring 2017; 11(2):48-56. Abstract Objective Epilepsy is a chronic neurological disorder requiring long-term therapy using antiepileptic medications. Reports have incriminated long-term antiepileptic drugs use in deficiency of vitamin D and bone diseases in all age groups. We aimed to investigate the association between serum 25-hydroxyvitamin D levels and pediatric epilepsy in Indian patients. Materials & Methods We prospectively recruited 100 pediatric epilepsy patients, on monotherapy for minimum one-year duration, and 50 age and sex matched controls. This study was carried out at Yashoda Hospital, India from 2011-2014. All cases and controls underwent tests for serum 25-hydroxyvitamin D, alkaline phosphatase, serum calcium and phosphorus levels. Results Patients with 25-hydroxyvitamin D deficiency were significantly higher among cases (45%) than controls (24%). Mean alkaline phosphatase was significantly higher in cases and mean serum calcium was significantly lower (8.3±1.5) in cases. Amongst antiepileptic drugs, carbamazepine and sodium valproate were significantly associated with 25-hydroxyvitamin D deficiency. Risk of vitamin D deficiency was highest with sodium valproate usage (odds:4.0;95%CI 1.4-11.6) followed by carbamazepine use (odds: 2.7; 95%CI 1.0-6.8). After adjustment using multiple logistic regression, antiepileptic drugs showed independent association with 25-hydroxyvitamin D deficiency (odds:2.2;95%CI 0.9-4.5). Conclusion 25-hydroxyvitamin D deficiency was significantly associated with use of carbamazepine and sodium valproate in pediatric epilepsy.References 1. Santhosh NS, Sinha S, Satishchandra P. Epilepsy: Indian perspective. Ann Indian Acad Neurol2014;17(Suppl 1):S3-11. 2. Sridharan R, Murthy BN. Prevalence and pattern of epilepsy in India. Epilepsia 1999;40:631-66. 3. RainaSK,RazdanS,NandaR.Prevalence of neurological disorders in children less than 10 years of age in RS Pura town of Jammu and Kashmir. J Pediatr Neurosci 2011; 6:103-05. 4. Misra A, Aggarwal A, Singh O, Sharma S. Effect of carbamazepine therapy on vitamin D and parathormone in epileptic children. Pediatr Neurol 2010 Nov;43:320- 24. 5. Lazzari AA, Dussault PM, Thakore-James M, Gagnon D, Baker E, Davis SA et al.Prevention of bone loss and vertebral fractures in patients with chronic epilepsy-antiepileptic drug and osteoporosis prevention trial. Epilepsia 2013;54:1997-2004.6. Menon B, Harinarayan CV. The effect of anti epileptic drug therapy on serum 25-hydroxyvitamin D and parameters of calcium and bone metabolism a longitudinal study. Seizure 2010;19:153-58. 7. Chaudhuri JR, Mridula KR, Alladi S, Anamika A, Umamahesh U, Balaraju B et al. Serum 25-hydroxyvitamin D deficiency in ischemic stroke and subtypes in Indian patients. J Stroke 2014;16:44-50. 8. Fisher RS, van Emde Boas W, Blume W, Elger C, Genton P, Lee P, et al. Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE). Epilepsia 2005;46:470-72. 9. Chaudhuri JR, Mridula KR, Anamika A, Boddu DB, Misra PK, Lingaiah A et al. Deficiency of 25-hydroxyvitamin d and dyslipidemia in Indian subjects. J Lipids 2013;2013:623420. 10. Gniatkowska-Nowakowska A. Fractures in epilepsy children. Seizure 2010;19:324-25. 11. Shellhaas RA, Barks AK, Joshi SM. Prevalence and risk factors for vitamin D insufficiency among children with epilepsy. Pediatr Neurol 2010;42:422-26. 12. Nettekoven S, Strohle A, Trunz B, Wolters M, Hoffmann S, Horn R, et al. Lichtinghagen R, Welkoborsky HJ, Tuxhorn I, Hahn A. Effects of antiepileptic drug therapy on vitamin D status and biochemical markers of bone turnover in children with epilepsy. Eur J Pediatr 2008;167:1369-77. 13. Rajantie J, Lamberg-Allardt C, Wilska M. Dose carbamazepine treatment lead to need of extera vitamin D in some mentally retarded children. Acta Pediatr Scand 1984;73:325-28. 14. Jekovec-Vrhovsek M, Kocijancic A, Prezelj J. Effect of vitamin D and calcium on bone mineral density in children with CP and epilepsy in full-term care. Dev Med Child Neurol 2000;42:403-05. 15. Pack AM. The Association between Antiepileptic Drugs and Bone Disease. Epilepsy Currents 2003; 3:91-95. 16. Babayigit A, Dirik E, Bober E, Cakmakci H. Adverse effects of antiepileptic drugs on bone mineral density. Pediatr Neurol 2006;35:177-81. 17. Pack AM. The impact of long-term antiepileptic drug use on bone health. Advanced Students 2005;5:S567-71.18. Voudris KA, Attilakos A, Katsarou E, Garoufi A, Dimou S, Skardoutsou A,et al. Early alteration in bone metabolism in epileptic children receiving carbamazepine monotherapy owing to the induction of hepatic drug-metabolizing enzymes. J Child Neurol 2005; 20: 513-16. 19. Malik R, Mohapatra JN, Kabi BC, Halder R. 5 Hydroxy Cholecalciferol Levels in Infants with Hypocalcemic Seizures J Nutr Food Sci 2014; 4:3 20. Razazizan N, Mirmoeini M, Daeichin S, Ghadiri K. Comparison of 25-hydroxy vitamin D, calcium and alkaline phosphatase levels in epileptic and non-epileptic children. Acta Neurol Taiwan 2013;22:112-16. 21. Krishnamoorthy G, Karande S, Ahire N, Mathew L, Kulkarni M. Bone Metabolism Alteration on Antiepileptic Drug Therapy. Indian J Pediatr 2009; 76 : 377-83. 22. Valsamis HA, Arora SK, Labban B, McFarlane SI.Antiepileptic drugs and bone metabolism. Nutr Metab (Lond) 2006;3:36 23. MintzerS, Boppana P, Toguri J, DeSantis A. Vitamin D levels and bone turnover in epilepsy patients taking carbamazepine or oxcarbamazepine. Epilepsia 2006;47:510-15. 24. Pack AM, Morrell MJ. Adverse effect of antiepileptic drug on bone structure: Epidemiology mechanisms and therapeutic indications.CNS Drugs 2001;15:633-42. 25. Yaghini O, Tonekaboni SH, Amir Shahkarami SM, Ahmad Abadi F, Shariat F, Abdollah Gorji F. Bone mineral density in ambulatory children with epilepsy. Indian J Pediatr 2015;82:225-29. 26. Verrotti A, Greco R, Morgese G, Chiarelli F. Increased bone turnover in epileptic patients treated with carbamazepine. Ann Neurol 2000;47: 385-88. 27. Ginige N,de Silva KSH, Wanigasinghe JK, Gunawardane NS, Munasinghe TMJ. Effects of long term anti epileptic drugs on serum vitamin D levels and bone profile in a cohort of Sri Lankan children. Int J Pediatr Endocrinol 2015,2015(Suppl 1):P66. 28. Hosseinpour F, Ellfolk M, Norlin M, Wikvall K. Phenobarbital suppresses vitamin D3 25-hydroxylase expression: a potential new mechanism for drug-induced osteomalacia. Biochem Biophys Res Commun 2007;357:603-07. 29. Heo K, Rhee Y, Lee HW, Lee SA, Shin DJ, Kim WJ, et al. The effect of topiramate monotherapy on bone mineral density and markers of bone and mineral metabolism in premenopausal women with epilepsy. Epilepsia 2011;52:1884-89. 30. Zhou C, Assem M, Tay JC, Watkins PB, Blumberg B, Schuetz EG, et al.Steroid and xenobiotic receptor and vitamin D receptor crosstalk mediates CYP24 expression and drug-induced osteomalacia. J Clin Invest 2006;116:1703-12. 31. Pascussi JM, Robert A, Nguyen M, Walrant-Debray O, Garabedian M, Martin P, et al.. Possible involvement of pregnane X receptor-enhanced CYP24 expression in drug-induced osteomalacia. J Clin Invest 2005;115:177- 86. 32. Holick MF. Stay tuned to PXR: an orphan actor that may not be D-structive only to bone. J Clin Invest 2005;115:32- 4. 33. Perucca E. Clinical implications of hepatic microsomal enzyme induction by antiepileptic drugs. Pharmacol Ther 1987;33:139-44. 34. Koch HU, Kraft D, von Herrath D, Schaefer K. Influence of diphenylhydantoin and phenobarbital on intestinal calcium transport in the rat. Epilepsia 1972;13:829-41. 35. Weinstein RS, Bryce GF, Sappington LJ, King DW, Gallagher BB. Decreased serum ionized calcium and normal vitamin D metabolite levels with anticonvulsant drug treatment. J Clin Endocrinol Metab 1984;58:1003-09. 36. Onodera K, Takahashi A, Sakurada S, Okano Y. Effects of phenytoin and/or vitamin K2 (menatetrenone) on bone mineral density in the tibia of growing rats. Life Sci 2002; 70: 1533-42. 37. Vernillo AT, Rifkin BR, Hauschka PV. Phenytoin affects osteoblastic secretion from osteoblastic rat osteosarcoma 17/2.8 cells in culture. Bone 1990;11:309-12. 38. Guo C, Ronen GM, Atkinson SA. Long-term valproate and lamotrigine treatment may be a marker for reduced growth and bone mass in children with epilepsy. Epilepsia 2001; 42:1141-47. 39. Nakken KO, Tauboll E. Bone loss associated with use of antiepileptic drugs. Expert Opin Drug Saf 2010;9:561-71. 40. Lee RH,Lyles KW, Colon-Emeric C. A review of the effect of anticonvulsant medications on bone mineral density and fracture risk. Am J Geriatr Pharmacother 2010; 8:34-46. 41. Teagarden DL, Meador KJ, Loring DW. Low vitamin D levels are common in patients with epilepsy. Epilepsy Res 2014;108:1352-56. 42. Wu FJ, Sheu SY, Lin HC. Osteoporosis is associated with antiepileptic drugs: a population-based study. Epileptic Disord 2014;16:333-42. 43. Cansu A, Yesilkaya E, Serdaroglu A, Hirfanoglu TL, Camurdan O, Gulbahar O, et al. Evaluation of bone turnover in epileptic children using oxcarbazepine. Pediatr Neurol 2008;39:266-71. 44. Bergqvist AG, Schall JI, Stallings VA. Vitamin D status in children with intractable epilepsy, and impact of the ketogenic diet. Epilepsia 2007;48:66-71. 45. Nicolaidou P, Georgouli H, Kotsalis H, Matsinos Y, Papadopoulou A, Fretzayas A, et al.Effects of anticonvulsant therapy on vitamin D status in children: Prospective monitoring study. J Child Neurol 2006;21:205-09. 46. Farhat G, Yamout B, Mikati MA, Demirjian S, Sawaya R, El-Hajj Fuleihan G. Effect of antiepileptic drugs on bone density in ambulatory patients. Neurol 2002;58:1348-53. 47. Harijan P, Khan A, Hussain N. Vitamin D deficiency in children with epilepsy: Do we need to detect and treat it? J Pediatr Neurosci 2013;8:5-10. 48. Mikati MA, Dib L, Yamout B, Sawaya R, Rahi AC, Fuleihan Gel-H. Two randomized vitamin D trials in ambulatory patients on anticonvulsants: Impact on bone. Neurol 2006; 67:2005-14. 49. Bianchini G, Mazzaferro S, Mancini U, Bianchi AR, Donato G, Massimetti C,et al.Calcium phosphorus changes in chronic anticonvulsant therapy: effects of administration of 25 hydroxy vitamin D3 on secondary hyperparathyroidism. Acta Vitaminol Enzymol 1983;5:229-34. 50. Drezner MK. Treatment of anticonvulsant drug – induced bone disease. Epilepsy Behav 2004;5:S41-7. 51. Howard JM. Anticonvulsant induced bone disease. Editorial. Arch Neurol 2004;58:1352-53

    Bilingualism delays the onset of behavioral but not aphasic forms of frontotemporal dementia

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    Bilingualism has been found to delay onset of dementia and this has been attributed to an advantage in executive control in bilinguals. However, the relationship between bilingualism and cognition is complex, with costs as well as benefits to language functions. To further explore the cognitive consequences of bilingualism, the study used Frontotemporal dementia (FTD) syndromes, to examine whether bilingualism modifies the age at onset of behavioural and language variants of Frontotemporal dementia (FTD) differently. Case records of 193 patients presenting with FTD (121 of them bilingual) were examined and the age at onset of the first symptoms were compared between monolinguals and bilinguals. A significant effect of bilingualism delaying the age at onset of dementia was found in behavioural variant FTD (5.7 years) but not in progressive nonfluent aphasia (0.7 years), semantic dementia (0.5 years), corticobasal syndrome (0.4 years), progressive supranuclear palsy (4.3 years) and FTD-motor neuron disease (3 years). On dividing all patients predominantly behavioral and predominantly aphasic groups, age at onset in the bilingual behavioural group (62.6) was over 6 years higher than in the monolingual patients (56.5, p=0.006), while there was no difference in the aphasic FTD group (60.9 vs. 60.6 years, p=0.851). The bilingual effect on age of bvFTD onset was shown independently of other potential confounding factors such as education, gender, occupation, and urban vs rural dwelling of subjects. To conclude, bilingualism delays the age at onset in the behavioral but not in the aphasic variants of FTD. The results are in line with similar findings based on research in stroke and with the current views of the interaction between bilingualism and cognition, pointing to advantages in executive functions and disadvantages in lexical tasks

    Deficiency of 25-Hydroxyvitamin D and Dyslipidemia in Indian Subjects

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    Background. Vitamin D deficiency is widespread throughout the world. Several reports have incriminated vitamin D deficiency as the cause of rickets, osteomalacia, and other chronic diseases. Recent studies have suggested a possible link between deficiency of 25-hydroxyvitamin D and dyslipidemia. Aim. To investigate the association between 25-hydroxyvitamin D deficiency and dyslipidemia in Indian subjects. Methodology. We recruited 150 asymptomatic consecutive subjects from patients' attendees at the Departments of Neurology and Medicine in Yashoda Hospital, Hyderabad, India. Study period was from October 2011 to March 2012. All subjects underwent 25-hydroxyvitamin D assay by chemiluminescent microparticle immunoassay, fasting blood sugar and lipid profile, calcium, phosphorus, alkaline phosphatase, and C-reactive protein (CRP). Results. Out of 150 subjects, men were 82 (54.6%), and mean age was 49.4 (±15.6) years. Among risk factors, hypertension was noted in 63/150 (42%), 25-hydroxyvitamin D deficiency in 59/150 (39.3%), diabetes in 45/150 (30%), dyslipidemia in 60 (40%), smoking in 35/150 (23.3%), and alcoholism in 27/150 (18%). Deficiency of 25-hydroxyvitamin D was significantly associated with dyslipidemia ( = 0.0001), mean serum glucose ( = 0.0002) mean CRP ( = 0.04), and mean alkaline phosphatase ( = 0.01). Multivariate analysis showed that 25-hydroxyvitamin D deficiency was independently associated with dyslipidemia (odds ratio: 1.9; 95% CI : 1.1-3.5). Conclusions. We found that deficiency of 25-hydroxyvitamin D was independently associated with dyslipidemia in Indian subjects

    Deficiency of 25-Hydroxyvitamin D and Dyslipidemia in Indian Subjects

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    Background. Vitamin D deficiency is widespread throughout the world. Several reports have incriminated vitamin D deficiency as the cause of rickets, osteomalacia, and other chronic diseases. Recent studies have suggested a possible link between deficiency of 25-hydroxyvitamin D and dyslipidemia. Aim. To investigate the association between 25-hydroxyvitamin D deficiency and dyslipidemia in Indian subjects. Methodology. We recruited 150 asymptomatic consecutive subjects from patients’ attendees at the Departments of Neurology and Medicine in Yashoda Hospital, Hyderabad, India. Study period was from October 2011 to March 2012. All subjects underwent 25-hydroxyvitamin D assay by chemiluminescent microparticle immunoassay, fasting blood sugar and lipid profile, calcium, phosphorus, alkaline phosphatase, and C-reactive protein (CRP). Results. Out of 150 subjects, men were 82 (54.6%), and mean age was 49.4 (±15.6) years. Among risk factors, hypertension was noted in 63/150 (42%), 25-hydroxyvitamin D deficiency in 59/150 (39.3%), diabetes in 45/150 (30%), dyslipidemia in 60 (40%), smoking in 35/150 (23.3%), and alcoholism in 27/150 (18%). Deficiency of 25-hydroxyvitamin D was significantly associated with dyslipidemia (P=0.0001), mean serum glucose (P=0.0002) mean CRP (P=0.04), and mean alkaline phosphatase (P=0.01). Multivariate analysis showed that 25-hydroxyvitamin D deficiency was independently associated with dyslipidemia (odds ratio: 1.9; 95% CI : 1.1–3.5). Conclusions. We found that deficiency of 25-hydroxyvitamin D was independently associated with dyslipidemia in Indian subjects

    Dementia in developing countries: Does education play the same role in India as in the West?

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    ABSTRACT Evidence suggests that education protects from dementia by enhancing cognitive reserve. However, this may be influenced by several socio-demographic factors. Rising numbers of dementia in India, high levels of illiteracy and heterogeneity in socio-demographic factors provide an opportunity to explore this relationship. Objective: To study the association between education and age at dementia onset, in relation to socio-demographic factors. Methods: Association between age at dementia onset and literacy was studied in relationship to potential confounding factors such as gender, bilingualism, place of dwelling, occupation, vascular risk factors, stroke, family history of dementia and dementia subtypes. Results: Case records of 648 dementia patients diagnosed in a specialist clinic in a University hospital in Hyderabad, India were examined. All patients were prospectively enrolled as part of an ongoing longitudinal project that aims to evaluate dementia subjects with detailed clinical, etiological, imaging, and follow-up studies. Of the 648 patients, 98 (15.1%) were illiterate. More than half of illiterate skilled workers were engaged in crafts and skilled agriculture unlike literates who were in trade or clerical jobs. Mean age at onset in illiterates was 60.1 years and in literates 64.5 years (p=0.0002). Factors independently associated with age at dementia onset were bilingualism, rural dwelling and stroke, but not education. Conclusion: Our study demonstrates that in India, rural dwelling, bilingualism, stroke and occupation modify the relationship between education and dementia

    Impact of bilingualism on cognitive outcome after stroke

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    Background and Purpose:  Bilingualism has been associated with slower cognitive aging and a later onset of dementia. In this study, we aimed to determine whether bilingualism also influences cognitive outcome after stroke.  Methods:  We examined 608 patients with ischemic stroke from a large stroke registry and studied the role of bilingualism in predicting poststroke cognitive impairment in the absence of dementia.  Results: A larger proportion of bilinguals had normal cognition compared with monolinguals (40.5% versus 19.6%; P<0.0001), whereas the reverse was noted in patients with cognitive impairment, including vascular dementia and vascular mild cognitive impairment (monolinguals 77.7% versus bilinguals 49.0%; P<0.0009). There were no differences in the frequency of aphasia (monolinguals 11.8% versus bilinguals 10.5%; P=0.354). Bilingualism was found to be an independent predictor of poststroke cognitive impairment.  Conclusions  Our results suggest that bilingualism leads to a better cognitive outcome after stroke, possibly by enhancing cognitive reserve

    The Indian consensus guidance on stroke prevention in atrial fibrillation: An emphasis on practical use of nonvitamin K oral anticoagulants

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    The last ten years have seen rapid strides in the evolution of nonvitamin K oral anticoagulants (NOACs) for stroke prevention in patients with atrial fibrillation (AF). For the preparation of this consensus, a comprehensive literature search was performed and data on available trials, subpopulation analyses, and case reports were analyzed. This Indian consensus document intends to provide guidance on selecting the right NOAC for the right patients by formulating expert opinions based on the available trials and Asian/Indian subpopulation analyses of these trials. A section has been dedicated to the current evidence of NOACs in the Asian population. Practical suggestions have been formulated in the following clinical situations: (i) Dose recommendations of the NOACs in different clinical scenarios; (ii) NOACs in patients with rheumatic heart disease (RHD); (iii) Monitoring anticoagulant effect of the NOACs; (iv) Overdose of NOACs; (v) Antidotes to NOACs; (vi) Treatment of hypertrophic cardiomyopathy (HCM) with AF using NOACs; (vii) NOACs dose in elderly, (viii) Switching between NOACs and vitamin K antagonists (VKA); (ix) Cardioversion or ablation in NOAC-treated patients; (x) Planned/emergency surgical interventions in patients currently on NOACs; (xi) Management of bleeding complications of NOACs; (xii) Management of acute coronary syndrome (ACS) in AF with NOACs; (xiii) Management of acute ischemic stroke while on NOACs
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