Vitamin D and Inflammatory Bowel Disease

Vitamin D deficiency has been recognized as an environmental risk factor for Crohn’s disease since the early 80s. Initially, this finding was correlated with metabolic bone disease. Low serum 25-hydroxyvitamin D levels have been repeatedly reported in inflammatory bowel diseases together with a relationship between vitamin D status and disease activity. Subsequently, low serum vitamin D levels have been reported in various immune-related diseases pointing to an immunoregulatory role. Indeed, vitamin D and its receptor (VDR) are known to interact with different players of the immune homeostasis by controlling cell proliferation, antigen receptor signalling, and intestinal barrier function. Moreover, 1,25-dihydroxyvitamin D is implicated in NOD2-mediated expression of defensin-β2, the latter known to play a crucial role in the pathogenesis of Crohn’s disease (IBD1 gene), and several genetic variants of the vitamin D receptor have been identified as Crohn’s disease candidate susceptibility genes. From animal models we have learned that deletion of the VDR gene was associated with a more severe disease. There is a growing body of evidence concerning the therapeutic role of vitamin D/synthetic vitamin D receptor agonists in clinical and experimental models of inflammatory bowel disease far beyond the role of calcium homeostasis and bone metabolism

Serology of Viral Infections and Tuberculosis Screening in an IBD Population Referred to a Tertiary Centre of Southern Italy

Background. With the introduction of more potent immunosuppressive agents in inflammatory bowel disease, prevention of opportunistic infections has become necessary by introducing screening programs. Prevalence of the most important infectious agents may vary in different geographical areas. The aim of our study was to assess the immune status for hepatitis B, varicella, mononucleosis, and cytomegalovirus infection together with the determination of the hepatitis C and tuberculosis status in Southern Italy. Methods. Prevalence of latent tuberculosis, together with serology of hepatitis B and C, Epstein-Barr virus, varicella zoster, and cytomegalovirus were collected by analysing retrospectively the clinical charts of IBD patients. Data were integrated with demographic and clinical features. Results. Data from 509 IBD patients divided in two age groups showed a prevalence of HBV infection in nonvaccinated patients of 9%. Seroprotection (HBsAb) in vaccinated IBD patients was lower (p 37 years of age. Conclusions. In younger patients, high susceptibility rates for primary herpesvirus infections should determine the choice of treatment. Loss of HBV seroprotection in already vaccinated patients should be considered for booster vaccination programs

Vitamin D and Inflammatory Bowel Disease

Vitamin D deficiency has been recognized as an environmental risk factor for Crohn’s disease since the early 80s. Initially, this finding was correlated with metabolic bone disease. Low serum 25-hydroxyvitamin D levels have been repeatedly reported in inflammatory bowel diseases together with a relationship between vitamin D status and disease activity. Subsequently, low serum vitamin D levels have been reported in various immune-related diseases pointing to an immunoregulatory role. Indeed, vitamin D and its receptor (VDR) are known to interact with different players of the immune homeostasis by controlling cell proliferation, antigen receptor signalling, and intestinal barrier function. Moreover, 1,25-dihydroxyvitamin D is implicated in NOD2-mediated expression of defensin-β2, the latter known to play a crucial role in the pathogenesis of Crohn’s disease (IBD1 gene), and several genetic variants of the vitamin D receptor have been identified as Crohn’s disease candidate susceptibility genes. From animal models we have learned that deletion of the VDR gene was associated with a more severe disease. There is a growing body of evidence concerning the therapeutic role of vitamin D/synthetic vitamin D receptor agonists in clinical and experimental models of inflammatory bowel disease far beyond the role of calcium homeostasis and bone metabolism

A <i>Strongyloides stercoralis</i> infection presenting as arthritis of sternoclavicular joint

A <i>Strongyloides stercoralis</i> infection presenting as arthritis of sternoclavicular join