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We read with interest the paper by Costenbader et al on vitamin D intake and risks of systemic lupus erythaematosus (SLE) and rheumatoid arthritis (RA) in women.1
The authors conclude that their prospective study does not lend evidence that to the hypothesis that increasing vitamin D intake can protect against SLE or RA.
In this case, using semiquantitative questionnaires regarding the intake of food and the frequency of supplements to assess vitamin D status may not necessarily be a reliable way to indicate the actual absorption and serum levels. This is due to the fact that several other factors, including altered metabolic pathways and others, regulate the real availability. Therefore, the most reliable way to assess vitamin D status would be to evaluate serum levels.2 3
Recently, some authors disputed the findings of Merlino et al regarding an inverse association between vitamin D intake and the risk of RA and suggested that direct measurement in the serum is a more accurate system than is a questionnaire concerning diet, especially if sun exposure is not taken into account.4 5
Since lower serum vitamin D levels have also been associated with higher RA disease activity, we recently evaluated the serum 25(OH)D levels in female patients with RA from northern and southern Europe during winter and summer, and correlated these levels with the 28-joint Disease Activity Score (DAS28).6
Significant variations (increases) in 25(OH)D levels in the summer compared with winter were found in both populations. Interestingly, a significant, inverse correlation was found between 25(OH)D levels and DAS28 scores among patients from southern Europe in summer and among patients from northern Europe in winter.
Vitamin D may exert immunomodulatory effects, and hypovitaminosis D and increased prevalence of RA seem more common in northern European countries as compared with southern ones.7
However, vitamin D is classified as a secosteroid in which one of the rings has been broken, in this case by ultraviolet B light (sunlight), and the main source of vitamin D is de novo synthesis in the skin. It is noteworthy that although vitamin D is acquired through food, dietary intake alone is often insufficient, supplying only 20% of the body’s requirements.
Patients with SLE have multiple risk factors for vitamin D deficiency, including chronic steroid use, renal involvement, use of hydroxychloroquine, anti-vitamin D antibodies and the need to avoid sun exposure.8
One study showed that the serum vitamin D levels of 21 patients with SLE were lower than in healthy controls and another study involving 12 prednisolone-treated adolescents with SLE revealed that 7 were vitamin D deficient.9 10
We recently analysed the 25(OH)D serum levels of patients with SLE from northern Europe and compared them with those from southern Europe and correlated the data with other modulatory factors such as the intake of vitamin D, treatment with hydroxychloroquine and/or prednisolone, and clinical status.2 Interestingly, 25(OH)D was found to be significantly lower in all patients with SLE (vitamin D untreated), when compared to controls. Lastly, a significant, negative correlation was found between 25(OH)D serum levels and disease scores, obtained by the European consensus lupus activity measurement (ECLAM) and the SLE disease activity index (SLEDAI).
In summary, patients with RA and patients with SLE have multiple risk factors for vitamin D deficiency, and disease severity seems to be correlated to the lower 25-OH vitamin D serum levels. Therefore, caution is needed when assessing the possible correlations between food intake or vitamin D supplements and the risk of autoimmune diseases. The best indicator still remains serum levels of vitamin D.
Competing interests: None declared.
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