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Vitamin D status and disease activity in systemic lupus erythematosus in Northern Ireland

Published online by Cambridge University Press:  30 November 2009

L. C. Breslin
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine BT52 1SA, UK
E. M. Duffy
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine BT52 1SA, UK
H. G. Mulholland
Affiliation:
Cancer Epidemiology & Prevention Research Group, Queen's University Belfast, Royal Victoria Hospital Site, Belfast BT12 6BJ, UK
S. A. Wright
Affiliation:
Musculoskeletal Education and Research Unit, Musgrave Park Hospital, Belfast BT9 7JB, UK
M. S. Barnes
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine BT52 1SA, UK
R. Hodd
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine BT52 1SA, UK
J. M. W. Wallace
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine BT52 1SA, UK
A. L. Bell
Affiliation:
Musculoskeletal Education and Research Unit, Musgrave Park Hospital, Belfast BT9 7JB, UK
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Abstract

Type
Abstract
Copyright
Copyright © The Author 2009

Systemic lupus erythematosus (SLE) is a complex autoimmune disease with no known cure and an unclear etiology. Patients often suffer from photosensitivity and for this reason are advised to stay out of direct sunlight and to wear a sun protection factor (SPF) of ≥15. Approximately 98% of vitamin D synthesis in the skin is blocked by a SPF of 15(Reference Holick1); therefore, individuals with SLE may be at greater risk of vitamin D deficiency. Vitamin D in its hormonally-active form has immunoregulatory properties and may impinge on the pathology of autoimmune diseases(Reference Cutolo and Osta2). The objectives of the present study were to assess vitamin D status in patients with SLE in comparison with age- and gender-matched controls and to compare dietary vitamin D intake and status with disease activity in SLE.

Patients with SLE were recruited between December 2005 and February 2006 as part of a larger study(Reference Wright, O'Prey and McHenry3). Control volunteers were recruited from University of Ulster staff. Vitamin D intakes were estimated from 4 d food diaries and vitamin D status was assessed by measuring plasma 25-hydroxyvitamin D (25(OH)D) using the OCTEIA 25(OH)D enzyme immunoassay (Immunodiagnostic Systems Ltd, Boldon, Tyne and Wear, UK). Disease activity was measured using the revised systemic lupus activity measure (SLAM-R)(Reference Bae, Koh and Chang4).

Mean dietary vitamin D intakes for the SLE (n 19) and control (n 19) groups were 2.8 (sd 2.6) μg and 2.2 (sd 1.3) μg respectively. Results from an independent t-test indicated individuals with SLE had significantly higher serum 25(OH)D (70.6 (sd 37.3) nmol/l) than controls (56.0 (sd 18.5) nmol/l; P=0.022) with 32% and 44% of SLE and controls with suboptimal levels (<50 nmol/l) respectively. Mean SLAM-R score for those with SLE was 9.1 (sd 3.8). Analysis revealed a significant negative correlation between dietary vitamin D intake and SLAM-R (r 0.657, P=0.006) and a significant positive correlation between vitamin D status and SLAM-R (r 0.539, P=0.017).

In conclusion, intake of vitamin D in both patients with SLE and controls was inadequate and inadequate intake was related to greater disease activity in the patients with SLE. The positive correlation reported between serum 25(OH)D and disease activity in SLE may be as a result of those patients with more active disease receiving steroidal treatment. Steroids are routinely administered in conjunction with vitamin D and Ca and the level of serum 25(OH)D in SLE would support vitamin D supplementation use. These results are preliminary findings and further investigation is required to elucidate the role of vitamin D in SLE.

References

1. Holick, MF (2004) Am J Clin Nutr 80, 16781688.Google Scholar
2. Cutolo, M & Osta, K (2008) Lupus 17, 610.CrossRefGoogle ScholarPubMed
3. Wright, SA, O'Prey, FM, McHenry, MT et al. (2008) Ann Rheum Dis 67, 841848.CrossRefGoogle Scholar
4. Bae, SC, Koh, HK, Chang, DK et al. (2001) Lupus 10, 405409.CrossRefGoogle ScholarPubMed
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