To the best of our knowledge, there have only been two reports regarding vitamin D in CU
Thorp et al. reported that serum 25(OH)D concentration was reduced as compared to that in patients with allergic rhinitis
. However, it has been suggested that the prevalence of severe vitamin D deficiency was significantly higher in patients with allergic rhinitis than among the normal population
. Therefore, in the present study we compared CSU patients with the healthy subjects. Similarly to the previous study, serum 25(OH)D concentration in CSU patients decreased as compared with the healthy subjects.
Thorp et al. showed that the proportion of all subjects with vitamin D deficiency (defined as 25-OHD < 30 ng/ml) was not significantly different between the 2 groups: chronic urticaria, 48% (12/25) versus controls, 28% (7/25; p = 0.24)
. In our study the subjects were divided into three groups according to serum 25(OH)D concentration, to describe vitamin D status: deficiency (<20 ng/ml), insufficiency (between 21 and 29 ng/ml), critically low level (< 10 ng/ml) as defined by most experts
[10, 17]. In contrasts to the previous study the proportion of vitamin D deficiency proved significantly higher in CSU patients.
The reason for such discrepancy is unclear, although it may be related to various factors, including 1) differences in the control group (healthy versus allergic rhinitis subjects), 2) seasons during which blood was collected, 3) regions and/or countries, 4) lifestyle. It has been reported that serum 25(OH)D concentrations in the European countries are lower than in the United States
[10, 17, 18].
There were not significant differences in serum 25(OH)D concentrations in CSU patients with and without glucocorticoid therapy. We found no association between serum concentrations of 25-(OH)D and the glucocorticoids doses in CSU patients. This is in accordance with the previous studies indicating that serum 25(OH)D concentration is unaffected by treatment, even with high doses of glucocorticoids
. Taken together, it seems unlikely that the glucocorticoid treatment of our patients is responsible for lower serum concentrations of 25(OH)D.
Although our and Thorp et al. results point to some changes in vitamin D status, such as a decrease in serum 25(OH)D concentration
, conclusions regarding the reasons for reduced concentration as well as relevance of such results for a possible risk factor in CSU and/or the disease activity cannot yet be drawn. While some data suggest that 25(OH)D levels are associated with an increased activity/severity of the inflammatory diseases
, we found no relationship between serum concentrations of 25(OH)D and CRP - a marker of CSU activity
Lower 25(OH)D concentration may therefore appear as a mere secondary phenomenon, manifested as a response to different stimuli, including inflammation, and as such, may not contribute in any way to pathogenesis of the disease. As chronic urticaria may be associated with lower serum 25OHD concentration during the active period of the disease, it would be interesting to recognize whether such phenomenon is present shortly after the disease onset and after a long lasting remission, suggesting vitamin D deficiency as a possible risk factor for CSU.
Interestingly, it has been reported that vitamin D metabolites regulate the synthesis of matrix metalloproteinases (MMP)
 and vitamin D insufficiency is associated with the increased circulating levels of MMP9 and CRP
, suggesting a possible mechanism for tissue damage in chronic inflammatory conditions, including CHD and diabetes
. On the other hand, it is known that both MMP9 and CRP concentrations are elevated in CSU
. In our study we did not observe any significant association between concentrations of 25(OH)D and CRP. Associations between vitamin D status and MMP9 overproduction in CSU should be established.
The limitations of this study included small sample size and single assessment of 25 (OH)D concentration performed in summer. Because serum 25(OH)D concentrations are lower in winter, it should be interesting to compare the seasonal differences. Therefore, we cannot exclude that prevalence of 25(OH)D deficiency might be higher following the summer season.
The serum 25(OH)D concentrations vary extensively between studies and depend on different environmental factors. Serum 25(OH)D concentration ≥ 30 ng/ml is defined by most experts as optimal vitamin D status with respect to maintenance of mineral homeostasis. So far, immune-inflammatory consequences of vitamin D insufficiency/deficiency, assessed on the basis of 25(OH)D concentrations alone, are unclear
[17, 18, 24].
Current data demonstrate the importance of screening for vitamin D deficiency measured by serum concentration of 25(OH)D in CSU patients. In addition, such observations may have certain therapeutic implications. Interestingly, it has been demonstrated that in patients suffering from idiopathic chronic urticaria, isolated pruritus, and rash with low 25(OH)D level, the symptoms resolution is often possible with oral supplementation of vitamin D
We speculate that treatment of vitamin D deficiency would not only preserve mineral homeostasis but, due to possible immunomodulatory and anti-inflammatory effects of vitamin D, might have a beneficial impact on CSU activity. Vitamin D supplementation may provide an important and viable complement to the already existing CSU therapy. Higher doses of corticosteroids may be required in therapy of patients with the immune-inflammatory diseases and concomitant vitamin D insufficiency/deficiency
. In addition, the association was found between low serum 25(OH)D concentration and the cardiovascular mortality
Interestingly, it has been demonstrated that vitamin D insufficiency/deficiency promotes immune-inflammatory response and exogenous vitamin D is able to diminish activation of APR
It seems important to know whether the anti-inflammatory effects of exogenous vitamin D influence CSU activity.