The role of non-invasive camera technology for gait analysis in patients with vestibular disorders

Purpose of the study Current balance assessments performed in clinical settings do not provide objective measurements of gait. Further, objective gait analysis typically requires expensive, large and dedicated laboratory facilities. The aim of this pilot study was to develop and assess a low-cost, non-invasive camera technology for gait analysis, to assist the clinical assessment of patients with vestibular disorders. Materials and methods used This is a prospective, case-controlled study that was developed jointly by the local Neurotology Department and the Centre for Sports Engineering Research. Eligible participants were approached and recruited at the local Neurotology Clinic. The gait assessment included two repetitions of a straight 7-metre walk. The gait analysis system, comprised of a camera (P3215-V, Axis Communications, Sweden) and analysis software was installed in an appropriately sized clinic room. Parameters extruded were walking velocity, step velocity, step length, cadence and step count per meter. The effect sizes (ESB) were calculated using the MatLab and were considered large, medium or small if >0.8, 0.5 and 0.2 respectively. This study was granted ethical approval by the Coventry and Warwickshire Research Ethics Committee (15/WM/0448). Results Six patients with vestibular dysfunction (P group) and six age-matched healthy volunteers (V group) were recruited in this study. The average velocity of gait for P group was 1189.1 ± 69.0 mm·s-1 whereas for V group it was 1351.4 ± 179.2 mm·s-1, (ESB: -0.91). The mean step velocities were 1353.1 ± 591.8 mm·s-1 and 1434.0 ± 396.5 mm·s-1 for P and V groups respectively (ESB: -0.20). The average cadence was 2.3 ± 0.9 Hz and 2.0 ± 0.5 Hz for P and V groups respectively (ESB: 0.60). The mean step length was 620.5 ± 150.7 mm for the P group and 728.5 ± 86.0 mm for the V group (ESB = -1.26). The average step count per meter was 1.7 ± 0.3 and 1.4 ± 0.1 for P and V groups respectively (ESB = 3.38). Conclusion This pilot study used a low-cost, non-invasive camera technology to identify changes in gait characteristics. Further, gait measurements were obtained without the application of markers or sensors to patients (i.e. non-invasive), thus allowing current, clinical practice to be supplemented by objective measurement, with minimal procedural impact. Further work needs to be undertaken to refine the device and produce normative data. In the future, similar technologies could be used in the community setting, providing an excellent diagnostic and monitoring tool for balance patients

Association of 25-Hydroxyvitamin D Deficiency in Pediatric Epileptic Patients

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

UK bone conduction hearing device consensus workshop:narrative summary

Objectives : To identify United Kingdom (UK)-specific research priorities in the field of bone conduction hearing devices (BCHDs). Method : Narrative summary of the discussions and outcomes of a UK BCHD research workshop. The workshop was organized on 8 September 2016 under the auspices of the National Institute for Health Research (NIHR) Clinical Research Network (CRN) ENT Specialty group and Royal College of Surgeons (RCS) Clinical Research Initiative. Representatives from a wide range of patient and professional groups from the UK and abroad were invited to attend. Main outcome measures were research priorities and approaches in the field of BCHDs. Results : Key research questions in the field of BCHDs are as follows: (1) What are the existing national BCHD practices? (2) What are the patient information and support needs on BCHDs? (3) Which outcomes should be measured across clinical studies in the field of BCHDs? The workshop suggested the following approaches to address these priorities: (1) a service evaluation of current UK BCHD practice; development of a national registry of BCHDs; (2) qualitative research to understand patient information and support needs; development of patient decision support tools; (3) development of core outcome sets for BCHDs. Discussion : Building upon the framework of the recent UK Research Agenda for ENT, Hearing and Balance, patients and professionals defined key UK-specific research priorities and approaches in the field of BCHDs. This approach promotes engagement, buy-in, national collaboration and thereby value of future BCHD research

Hearing Rehabilitation of Patients with Chronic Otitis Media:A Discussion of Current State of Knowledge and Research Priorities

Although chronic otitis media is a major cause of conductive and mixed hearing loss, auditory rehabilitation is currently not optimal for this patient group. Planning for hearing rehabilitation must accompany strategies for infection control when surgically managing patients with chronic otitis media. Several barriers prevent adequate hearing restoration in such a heterogeneous patient population. A lack of standardized reporting of surgical interventions, hearing, and quality of life outcomes impedes meta-analyses of existing data and the generation of high-quality evidence, including cost-effectiveness data, through prospective studies. This, in turn, prevents the ability of clinicians to stratify patients based on prognostic indicators, which could guide the decision-making pathway. Strategies to improve reporting standards and methods have the potential to classify patients with chronic otitis media preoperatively, which could guide decision-making for hearing restoration with ossiculoplasty versus prosthetic hearing devices. Appropriately selected clinical guidelines would not only foster directed research but could enhance patient-centered and evidence-based decision-making regarding hearing rehabilitation in the surgical planning process

An assessment of the clinical acceptability of direct acoustic cochlear implantation for adults with advanced otosclerosis in the United Kingdom

Hypothesis: Assess the clinical acceptability of direct acoustic cochlear implantation for patients with advanced otosclerosis and the support for conducting a controlled trial of its effectiveness in the United Kingdom. Background: Emerging evidence supports the efficacy of direct acoustic cochlear implantation in patients with advanced otosclerosis whose needs cannot be managed using the combination of stapes surgery and hearing aids. A controlled trial would provide evidence for its effectiveness and cost-effectiveness to healthcare commissioners. Methods: An online survey of clinical professionals was constructed to characterise current standard of care for patients with advanced otosclerosis and to assess whether clinicians would be willing to refer patients into a trial to evaluate direct acoustic cochlear implantation. A consensus process was conducted to define inclusion criteria for the future trial. Results: No survey respondent considered direct acoustic cochlear implantation to be inappropriate with a majority indicating that they would refer patients into a future trial. The consensus was that there is a lack of available treatment options for those patients with bone conduction thresholds worse than 55 dB HL and who did not meet current criteria for cochlear implantation. Conclusions: The present study confirms that a controlled trial to evaluate the effectiveness of direct acoustic cochlear implantation would have the support of clinicians in the UK. A feasibility study would be required to determine whether patients who meet the inclusion criteria could be recruited in a timely manner and in sufficient numbers to conduct a formal evaluation of effectiveness

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

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

Success rates in restoring hearing loss in patients with chronic otitis media:A systematic review

Abstract Objective To assess the effectiveness of tympanoplasty in treating chronic otitis media‐related hearing loss, published literature was systematically reviewed to determine the clinical success rate of tympanoplasty at restoring hearing in chronic otitis media patients at a minimum follow‐up period of 12‐months. Data Sources PubMed, Embase and the Cochrane Library. Methods Two independent reviewers performed literature searches. Publications reporting long‐term (≥12‐month) hearing outcomes and complications data on adult and pediatric patients with chronic otitis media were included and assessed for risk of bias and strength of evidence. To assess how tympanoplasty influences long‐term hearing outcomes, data on pure tone audiometry (air‐bone gap) and complications were extracted and synthesized. Results Thirty‐nine studies met the inclusion criteria. Data from 3162 patients indicated that 14.0% of patients encountered postoperative complications. In adult patients, mean weighted air‐bone gap data show closure from 26.5 dB hearing level (HL) (preoperatively) to 16.1 dB HL (postoperatively). In studies that presented combined adult and pediatric data, the mean preoperative air‐bone gap of 26.7 dB HL was closed to 15.4 dB HL. In 1370 patients with synthesizable data, 70.7% of patients had a postoperative air‐bone gap ˂ 20 dB HL at long‐term follow‐up. Finally, subgroup analysis identified that mean improvement in ABG closure for patients with and without cholesteatoma was 10.0 dB HL and 12.4 dB HL, respectively. Conclusion In patients with chronic otitis media, tympanoplasty successfully closed the air‐bone gap to within 20 dB HL in 7/10 cases and had an overall complication rate of 14.0%. Level of Evidence 2a

The Burden of Revision Sinonasal Surgery in the UK – Data from the Chronic Rhinosinusitis Epidemiology Study (CRES); a cross sectional study

Objectives/Hypothesis The aim of this study was to investigate the surgical revision rate in patients with Chronic Rhinosinusitis (CRS) in the UK CRS Epidemiology Study (CRES). Previous evidence from national Sinonasal Audit showed that 1459 CRS patients demonstrated a surgical revision rate 19.1% at 5 years, with highest rates seen in those with polyps (20.6%). Setting Thirty secondary care centres around the UK. Participants A total of 221 controls and 1249 patients with CRS were recruited to the study including those with polyps (CRSwNPs), without polyps (CRSsNPs) and with allergic fungal rhinosinusitis (AFRS). Interventions Self-administered questionnaire. Primary outcome measure The need for previous sinonasal surgery. Results A total of 651 patients with CRSwNPs, 553 with CRSsNPs and 45 with AFRS were included. A total of 396 (57%) of patients with CRSwNPs/AFRS reported having undergone previous endoscopic nasal polypectomy (ENP), of which 182 of the 396 (46%) reported having received more than one operation. The mean number of previous surgeries per patient in the revision group was 3.3 (range 2 to 30) and a mean duration of time of 10 years since the last procedure. The average length of time since their first operation up to inclusion in the study was 15.5 years (range 0-74). Only 27.9% of all patients reporting a prior ENP had received concurrent endoscopic sinus surgery (ESS) (n=102). For comparison, surgical rates in patients with CRSsNPs were significantly lower; 13% of cases specifically reported ESS and of those only 30% reported multiple procedures (chi-squared p < 0.001). Conclusions This study demonstrated there is a high burden of both primary and revision surgery in patients with CRS, worst in those with AFRS and least in those with CRSsNPs. The burden of revision surgery appears unchanged in the decade since the Sinonasal Audit

Deficiency of 25-Hydroxyvitamin D and Dyslipidemia in Indian Subjects

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&apos; 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

Exploring the association between ingestion of foods with higher potential salicylate content and symptom exacerbation in chronic rhinosinusitis:Data from the National Chronic Rhinosinusitis Epidemiology Study

INTRODUCTION: Pharmacological salicylates are known to trigger respiratory exacerbations in patients with Non-Steroidal Exacerbated Respiratory Disease (N-ERD), a specific phenotype of Chronic Rhinosinusitis (CRS) and asthma. The impact of dietary sources of salicylates across subgroups of CRS is not well understood. The hypothesis is that in patients with nasal polyps present, there is likely to be a higher incidence of symptom exacerbation due to dietary salicylates regardless of any known response to pharmacological salicylate. METHODS: The Chronic Rhinosinusitis Epidemiology Study (CRES) was a questionnaire-based case-control study which sought to characterise the UK CRS population in terms of sociological, economic and medical factors. Using specific questions to examine participant responses relating to symptom exacerbation from food groups thought to be high in salicylate content, this analysis of the CRES database sought to compare an estimate of the prevalence of dietary sensitivity due to food with higher potential salicylate content across patients with CRS with (CRSwNPs) and without nasal polyposis (CRSsNPs) and with allergic fungal rhinosinusitis (AFRS). RESULTS: The CRSwNPs group were significantly more likely than controls to report symptom exacerbation due to ingestion of food groups with higher potential dietary salicylate content. The same trend was observed amongst CRSsNPs participants to a lesser degree. Reported response to the individual specific food groups wine, nuts, spicy foods, fruit and vegetables demonstrated that a statistically significant proportion of CRSwNPs and AFRS participants reported sensitivity to wine. CONCLUSIONS: This analysis suggests that there is an association between symptom exacerbation in response to food products with higher potential salicylate content, specifically wine, in CRS patients both with and without nasal polyposis when compared to controls, but especially in the CRSwNPs and AFRS phenotypes. Further studies are needed to detail if this relationship represents a causal relationship to dietary salicylate. The data present the possibility that a wider group of CRS patients may elicit salicylate sensitivity than those with known N-ERD