The frequency of vitamin D deficiency in adults with Crohn's disease.
ABSTRACT Vitamin D deficiency is a putative, pathogenic cofactor in the increase in osteopenia and osteoporosis seen in patients with Crohn's disease.
To determine the frequency of low serum 25-hydroxy-vitamin D3 (25-OHD) levels and the associated alterations in bone mineral density in a cohort of adults with Crohn's disease.
25-OHD levels were determined in 242 consecutive patients with Crohn's disease seen in two tertiary inflammatory bowel disease referral centres. Bone mineral density was assessed by dual energy x-ray absorptiometry.
Nineteen (8%) patients exhibited vitamin D deficiency (25-OHD less than 25 nmol/L) and 52 (22%) patients exhibited vitamin D insufficiency (25-OHD less than 40 nmol/L). Mean T-scores at the lumbar spine, femoral neck, total hip and ultradistal radius in the group with low 25-OHD did not differ from those of the normal 25-OHD group. Serum alkaline phosphatase and parathyroid hormone levels were higher in the low 25-OHD group than in the normal group. Decreased red blood cell (RBC) folate predicted low 25-OHD in male patients, while smoking, RBC folate and serum iron predicted low 25-OHD in female patients. The rate of low 25-OHD deficiency in the winter was significantly higher than that in the summer (11.9% versus 2.8%, respectively).
Vitamin D-deficient Crohn's disease patients exhibit biochemical evidence of metabolic bone disease, without detectable differences in bone mineral density. Sunlight exposure, nutrition and smoking status were predictors of vitamin D deficiency in this patient cohort.
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ABSTRACT: Background and aims Vitamin D deficiency has been observed in a wide range of medical conditions including Crohn's disease (CD). We aimed to assess whether CD patients have lower vitamin D levels than healthy controls, and to determine risk factors for vitamin D deficiency. Methods 25(OH)D was measured by chemiluminescent immunoassay in serum obtained from 101 CD patients and 41 controls. Demographics, sunlight exposure, dietary vitamin D intake, comorbidities and medication were recorded using validated questionnaires. In CD patients the Harvey–Bradshaw index, Montreal classification and surgical resections were also evaluated. 25(OH)D levels of > 75 nmol/L, between 50 and 75 nmol/L and < 50 nmol/L were considered as normal, suboptimal and deficient, respectively. Results Vitamin D levels were rather low but comparable among CD patients and controls (mean 25(OH)D 51.6 nmol/L(± 26.6) in CD, and 60.8 nmol/L(± 27.6) in controls. Multivariate regression analysis revealed BMI, sun protection behaviour, non-Caucasian ethnicity, no use of tanning beds, and no holidays in the last year as significantly associated with serum 25(OH)D levels in CD patients (R = 0.62). In the control group no statistically significant factors were identified that had an impact on 25(OH)D serum levels. Conclusions Vitamin D deficiency is common in CD patients, but also in healthy controls. Appropriate vitamin D screening should be advised in patients with CD. Moreover, the positive effect of sunlight on the vitamin D status should be discussed with CD patients, but this should be balanced against the potential risk of developing melanomas, especially in patients using thiopurines.Journal of Crohn s and Colitis 10/2014; 8(10). DOI:10.1016/j.crohns.2014.03.004 · 3.56 Impact Factor
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ABSTRACT: Vitamin D deficiency is common among patients with Crohn's disease. Serum 25-hydroxyvitamin D (25(OH)D) is the best measure of an individual's vitamin D status and current cut-off ranges for sufficiency are debatable. Several factors contribute to vitamin D deficiency in Crohn's disease. These include inadequate exposure to sunlight, inadequate dietary intake, impaired conversion of vitamin D to its active metabolite, increased catabolism, increased excretion and genetic variants in vitamin D hydroxylation and transport. The effects of low 25(OH)D on outcomes other than bone health are understudied in Crohn's disease. The aim of the present review is to discuss the potential roles of vitamin D and the possible levels required to achieve them. Emerging evidence suggests that vitamin D may have roles in innate and adaptive immunity, in the immune-pathogenesis of Crohn's disease, prevention of Crohn's disease-related hospitalisations and surgery, in reducing disease severity and in colon cancer prevention. The present literature appears to suggest that 25(OH)D concentrations of ≥75 nmol/l may be required for non-skeletal effects; however, further research on optimal levels is required.
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ABSTRACT: Vitamin D deficiency is commonly diagnosed among patients with inflammatory bowel disease (IBD). Patients with IBD are at risk of low bone density and increased fractures due to low vitamin D levels, long standing disease, and frequent steroid exposures; as a result, it is well established that vitamin D supplementation in this population is important. There is increasing support for the role of vitamin D in strengthening the innate immune system by acting as an immunomodulator and reducing inflammation in experimental and human IBD. The active form of vitamin D, 1,25(OH)D3, acts on T cells to promote T helper (Th)2/regulatory T responses over Th1/Th17 responses; suppresses dendritic cell inflammatory activity; induces antibacterial activity; and regulates cytokine production in favor of an anti-inflammatory response. Murine and human IBD studies support a therapeutic role of vitamin D in IBD. Risk factors for vitamin D deficiency in this population include decreased sunlight exposure, disease duration, smoking, and genetics. Vitamin D normalization is associated with reduced risk of relapse, reduced risk of IBD-related surgeries, and improvement in quality of life. Vitamin D is an inexpensive supplement which has been shown to improve IBD outcomes. However, further research is required to determine optimal serum vitamin D levels which will achieve beneficial immune effects, and stronger evidence is needed to support the role of vitamin D in inducing disease response and remission, as well as maintaining this improvement in patients' disease states.World Journal of Gastroenterology 05/2014; 20(17):4934-4947. DOI:10.3748/wjg.v20.i17.4934 · 2.43 Impact Factor
A. Hillary Steinhart