The relation between skin disorders and vitamin D
Article first published online: 22 FEB 2012
© 2011 The Author. BJD © 2011 British Association of Dermatologists
British Journal of Dermatology
Volume 166, Issue 3, pages 471–472, March 2012
How to Cite
Wulf, H.C. (2012), The relation between skin disorders and vitamin D. British Journal of Dermatology, 166: 471–472. doi: 10.1111/j.1365-2133.2012.10838.x
- Issue published online: 22 FEB 2012
- Article first published online: 22 FEB 2012
ORIGINAL ARTICLE, p 505
Vitamin D deficiency has been related to a high number of health disorders including skin cancer, autoimmune skin disorders, photodermatoses, atopic dermatitis and psoriasis. Special attention has been given to UVB phototherapy, as UVB is needed to convert 7-dehydrocholesterol to previtamin D3 in the skin.
When assessing vitamin D [measured as 25-hydroxyvitamin D, 25(OH)D] in a given skin disease, attention is normally paid to the degree of insufficiency and the percentage of patients with serum 25(OH)D below 50 nmol L−1 (insufficiency).
The following confounding factors should be kept in mind. (i) At what time of the year was sampling performed? In northern Europe serum 25(OH)D falls by about 1 nmol L−1 per week, corresponding to a total decrease of 25–35 nmol L−1 during winter.1,2 (ii) Dietary supplementation habits.3 Most diets contain very little vitamin D. Oily fish contains high levels, and fish/seal liver contains very high levels. Certain food products are fortified with vitamin D, and supplementation is becoming increasingly frequent. (iii) 25(OH)D analysis method. The gold standard, high-pressure liquid chromatography–mass spectrometry (HPLC-MS), is expensive to perform, and other methods are most commonly used. The percentage of the study population that is 25(OH)D deficient/insufficient is very dependent on the analysis methodology.4,5 Snellman et al.4 analysed serum 25(OH)D by three methods and found 8% insufficiency using HPLC-MS, 22% insufficiency using a radioimmunoassay and 43% using a chemiluminescent immunoassay.
As long as the methodology is not standardized it will be difficult to discuss insufficiency and make comparisons between studies.6 A study comparing different patient categories is therefore preferable, and the percentage insufficiency should be considered with great care.
The effect of UVB on vitamin D formation is very individual,7 due to different vitamin D levels at the initiation of UVB treatment,8 and possibly because of genetic factors.9,10 UVA does not contribute to vitamin D formation. The same UVB dose will increase serum 25(OH)D much more when serum 25(OH)D is low than when it is high,8 and exposure of more than about 25% of the body area does not seem to contribute additionally to increasing serum 25(OH)D formation.11
It must also be remembered that UVB doses administered in a treatment cabin will be given to all bare skin, whereas UVB from outdoor sunlight will depend on clothing and body orientation towards the sun. Therefore outdoor and cabin exposure will result in very different 25(OH)D formation, even when trying to achieve comparable UVB doses.
Sunscreen use is another factor that deserves attention as it absorbs UVB. However, in the way sunscreens are usually used, serum 25(OH)D does not seem to be affected.12 We should thus continue to use sunscreens.
In the study by Gisondi et al.13 in this issue of BJD it is interestingly found that a cohort of patients with untreated psoriasis has lower vitamin D levels than healthy control patients. That is quite surprising, as dermatologists anticipate that patients with psoriasis expose themselves to more sun than controls to improve their psoriasis, which should result in a higher vitamin D level. Some of the blood samples were drawn in winter, but that should not invalidate the results, as a high summer level will also be traceable as a high winter level.1
We may thus ask ourselves if patients with psoriasis expose themselves less to the sun in everyday situations when most 25(OH)D is formed, but possibly with higher erythemogenic doses over fewer days, which will not result in as effective vitamin D formation.1 The patients with psoriasis had a little higher body mass index, indicating that they may have a less healthy diet with lower vitamin D content than healthy controls, which might to some extent explain the lower vitamin D.
Psoriasis as such does not seem to affect the vitamin D level, as no relation was found with Psoriasis Area and Severity Index (PASI). A relation to PASI would have been expected if less/more vitamin D were formed in psoriasis plaques.
It is thus clear that much more evidence is needed to understand the relations between vitamin D and skin disorders.
Conflicts of interest