Lately, RDW attracted attention because of its potential correlation with immunologic activity, which is interesting in chronic inflammatory diseases. In line with our baseline results, which show a significant higher RDW value in CD patients than in UC patients, one pilot study reported Temsirolimus price that RDW has the ability to differentiate between CD and UC [32]. Others proved that high RDW values

are significantly correlated to alternated CRP and ESR levels showing that it can detect inflammatory processes in the human body [33]. Interest in vitamin D increased after the identification of vitamin D receptors (VDRs) in most tissues and cells in the body and discovery of the importance of the active metabolite (calcitriol) as a potent immunomodulator [22, 34]. Recently, vitamin D deficiency was found to be associated with increased incidences of cardiovascular disease, CHIR-99021 clinical trial hypertension and cancer [35–38]. Poor vitamin D status has already been linked to auto-immune STI571 purchase diseases like diabetes type 1, multiple sclerosis and rheumatoid arthritis [39]. The association between IBD activity

and vitamin D has been described in animal studies by some authors but is rarely reported in human studies [34, 40, 41]. Concerning CD patients, a new hypothesis states that vitamin D deficiency is not only the consequence but also a cause of the inflammatory process leading to bone loss through a Th1-driven immune response [42]. This hypothesis is recently supported by findings of an essential function of VDR in the protection of the colonic mucosa by regulating intestinal homeostasis in response to enteric bacterial invasion and commensal bacterial colonization [43]. In addition, an improvement of bone status and a decrease in IBD activity after therapy with 1,25-dihydroxyvitamin

D was described in CD patients [44]. triclocarban Although significant progression has been made concerning the role of vitamin D and its receptor, the exact mechanism is not yet fully understood and could lead to a new breakthrough concerning the aetiology of IBD. The above-mentioned results on disease activity and vitamin D deficiency indicate that increased risk of osteoporosis in IBD patients may not be caused by vitamin D deficiency only. In our opinion, it is plausible that the inflammatory process itself (which may be causally connected with vitamin D status in the aetiology of IBD) might lead to a negative effect on bone status through pro-inflammatory immunologic responses or a direct action of interleukins on the osteoclast activity. This perspective is endorsed by Tilg et al.