4.4 Article

Prevalence and correlates of vitamin D deficiency in adults after traumatic brain injury

期刊

CLINICAL ENDOCRINOLOGY
卷 85, 期 4, 页码 636-644

出版社

WILEY-BLACKWELL
DOI: 10.1111/cen.13045

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资金

  1. UK Medical Research Council [26659]
  2. Imperial College Healthcare Charity [7006/R21U]
  3. Guarantors of Brain
  4. Wellcome-GSK Imperial Translational Training Fellowship
  5. Wellcome Trust
  6. National Institute for Health Research (NIHR)
  7. National Institute for Health Research (NIHR) [NIHR-RP-011-048]
  8. UK Medical Research Council
  9. MRC [MR/K023926/1] Funding Source: UKRI
  10. Academy of Medical Sciences (AMS) [AMS-SGCL13-Gorgoraptis] Funding Source: researchfish
  11. Medical Research Council [MR/K023926/1] Funding Source: researchfish
  12. National Institute for Health Research [CL-2013-21-010, NIHR-RP-011-048] Funding Source: researchfish

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Objectives Traumatic brain injury (TBI) is a major cause of long-term disability with variable recovery. Preclinical studies suggest that vitamin D status influences the recovery after TBI. However, there is no published clinical data on links between vitamin D status and TBI outcomes. The aim was to determine the (i) prevalence of vitamin D deficiency/insufficiency, and associations of vitamin D status with (ii) demographic factors and TBI severity, and with (iii) cognitive function, symptoms and quality of life, in adults after TBI. Design Retrospective audit of patients seen between July 2009 and March 2015. Serum vitamin D (25-hydroxy-cholecalciferol) was categorized as deficient (<40 nmol/l), insufficient (4070 nmol/l) or replete (>70 nmol/l). Patients A total of 353 adults seen in tertiary hospital clinic (75.4% lighter skinned, 74.8% male, age median 35.1 year, range 26.6-48.3 year), 0.3-56.5 months after TBI (74.5% moderate-severe). Measurements Serum vitamin D concentrations; Adden-brooke's Cognitive Examination (ACE-R), Beck Depression Inventory-II (BDI-II), SF-36 Quality of Life, Pittsburgh Sleep Quality Index. Results In total, 46.5% of patients after TBI had vitamin D deficiency and 80.2% insufficiency/deficiency. Patients with vitamin D deficiency had lower ACE-R scores than those of vitamin D replete (mean effect size +/- SEM 4.5 +/- 2.1, P = 0.034), and higher BDI-II scores than those of vitamin D insufficient (4.5 +/- 1.6, P = 0.003), correcting for age, gender, time since TBI and TBI severity. There was no association between vitamin D status and markers of TBI severity, sleep or quality of life. Conclusion Vitamin D deficiency is common in patients after TBI and associated with impaired cognitive function and more severe depressive symptoms.

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