Literature DB >> 20662833

Vitamin D deficiency in patients with cutaneous lupus erythematosus is prevalent throughout the year.

G Heine1, A Lahl, C Müller, M Worm.   

Abstract

BACKGROUND: Vitamin D mediates immunomodulatory functions and its deficiency has been associated with an increased prevalence of immunological diseases including systemic lupus erythematosus (SLE). Chronic discoid or subacute cutaneous lupus erythematosus (CLE) are ultraviolet (UV)-triggered skin diseases. As vitamin D is mostly UV-derived and not from nutrition, its deficiency is frequent especially during the UV-deprived winter months.
OBJECTIVE: To compare the vitamin D status of patients with CLE with patients with type I allergy and healthy individuals during the summer or winter months.
METHODS: The vitamin D status of patients with CLE (n = 41) was compared with patients with type I allergy (n = 24), healthy individuals (n = 25) and a reference pool (n = 1951) by means of concentrations of circulating storage metabolite 25-hydroxyvitamin D in the summer and winter.
RESULTS: Serum 25-hydroxyvitamin D concentrations were lower during the winter in the reference population, and type I allergic and healthy individuals (29.2–35.5 nmol L)1) compared with the summer months (56.3–89.8 nmol L)1) and paralleled by the prevalence of vitamin D deficiency (serum 25-hydroxyvitamin D< 50 nmol L)1; winter: 70.8–73.4%, summer: 34.9–39.4%). In contrast, vitamin D deficiency in patients with CLE was prevalent throughout the year (summer: 85.7%,winter: 97.1%). In patients with CLE with concomitant prednisolone treatment, the 25-hydroxyvitamin D serum levels were comparable with (mean daily intake 877 IU) or without vitamin D supplementation during summer or winter (P = 0.75 and P = 0.14, respectively).
CONCLUSIONS: Our data identify vitamin D deficiency in patients with CLE throughout the year and indicate that monitoring and correcting the vitamin D status should be considered to prevent bone demineralization and fractures and to modulate beneficially immunological dysfunction.

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Year:  2010        PMID: 20662833     DOI: 10.1111/j.1365-2133.2010.09948.x

Source DB:  PubMed          Journal:  Br J Dermatol        ISSN: 0007-0963            Impact factor:   9.302


  8 in total

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