In: Crohn's disease25 Jul 2012
Bone mineral density (BMD) is reduced in patients with Crohn’s disease. The mechanism underlying the lower bone mineral density is not clearly understood; however, multiple etiologies are likely involved. These include disease activity, corticosteroid therapy, calcium and vitamin D deficiency, acute inflammatory cytokine action on osteoclast and osteoblast activity, sex hormone deficiency, smoking and overall poor nutrition.
Previous studies have demonstrated that between 17% and 68% of Crohn’s disease patients exhibit frank serum 25-hydroxyvitamin D3 (25-OHD) deficiency, defined as a value less than 25 nmol/L (10 ng/mL). Several studies have identified an association between bone mineral density and 25-OHD status, and reported that vitamin D supplementation improved bone mineral density in Crohn’s disease patients. In contrast, other studies have failed to show an association between 25-OHD deficiency and reduced bone mineral density.
25-OHD serves as the major precursor and most objective measure of the active hormone 1,25-dihydroxyvitamin D3 (1,25-OHD) undergoing 1-alpha hydroxylation in the kidney.
1,25-OHD increases calcium and phosphate absorption and reabsorption in the gastrointestinal tract and kidneys, respectively, thus maintaining normal mineralization of newly formed bone. A low serum concentration of 1,25-OHD delays osteoid deposition by osteoblasts, increases parathyroid hormone (PTH) release and activity and results in increased bone resorption. Prolonged vitamin D deficiency results in osteomalacia in adults. It’s time to pay less money – just get cheap viagra online *only here at the best online pharmacy.
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