{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T19:05:17Z","timestamp":1792436717969,"version":"4.5.0"},"reference-count":41,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2007,10,9]],"date-time":"2007-10-09T00:00:00Z","timestamp":1191888000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Hematol"],"published-print":{"date-parts":[[2008,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Bone disease with osteoporosis and osteomalacia are common in sickle cell disease (SCD). Some patients have vitamin D deficiency and low bone mineral density (BMD). The role of vitamin D and calcium supplementation to restore bone health in SCD has not been well studied. In 14 adults with SCD, we measured 25(OH)D (25\u2010hydroxyvitamin D) and BMD at the femoral neck, lumbar spine, and distal third of the ulna plus radius, along with markers of bone resorption (CTx; C\u2010terminal component of pro\u2010collagen type I) and bone formation (osteocalcin) before and after 12 months of vitamin D<jats:sub>2<\/jats:sub> and calcium carbonate treatment. Pretreatment, all patients were vitamin D deficient with a mean 25(OH)D level of 10.7 \u00b1 4.7 ng\/ml, had low BMD at the lumbar spine (L\u2010spine), 0.87 \u00b1 0.11 g\/cm<jats:sup>2<\/jats:sup> (mean <jats:italic>Z<\/jats:italic>\u2010score of \u20132.6 3 \u00b1 0.71 SD and <jats:italic>T<\/jats:italic> score of \u20132.31 \u00b1 0.75 SD), femoral neck, 0.8 \u00b1 0.18 g\/cm<jats:sup>2<\/jats:sup> (mean <jats:italic>Z<\/jats:italic>\u2010score \u20131.36 \u00b1 0.84, <jats:italic>T<\/jats:italic>\u2010score \u20131.14 \u00b1 0.75), and the distal radius and ulna, 0.6 \u00b1 0.17 g\/cm<jats:sup>2<\/jats:sup> (mean <jats:italic>Z<\/jats:italic>\u2010score \u20131.18 \u00b1 0.79, <jats:italic>T<\/jats:italic>\u2010score \u20131.01 \u00b1 0.74) and had elevated CTx (0.87 \u00b1 0.5 ng\/ml) and osteocalcin levels (12.3 \u00b1 3.7 ng\/\u03bcl). After treatment, all patients corrected their 25(OH)D level (38.8 \u00b1 13.9 ng\/ml) (<jats:italic>P<\/jats:italic> &lt; 0.001) with a 3.6% \u00b1 3.9% increase in BMD at the L\u2010spine (<jats:italic>P<\/jats:italic> = 0.009), 4.6% \u00b1 8.5% increase at the femoral neck (<jats:italic>P<\/jats:italic> = 0.05) and 6.5% \u00b1 12.6% increase at the distal radius plus ulna (<jats:italic>P<\/jats:italic> = 0.09). CTx, osteocalcin, and PTH(i) levels were unchanged. Treatment of adult SCD with vitamin D and calcium can restore 25(OH)D levels to normal and improve BMD, but, markers of bone resorption remained unchanged. Screening for vitamin D deficiency and BMD in SCD patients seems warranted. Am. J. Hematol., 2008. \u00a9 2007 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ajh.21085","type":"journal-article","created":{"date-parts":[[2007,10,9]],"date-time":"2007-10-09T20:46:52Z","timestamp":1191962812000},"page":"271-274","source":"Crossref","is-referenced-by-count":56,"title":["Sickle cell bone disease: Response to vitamin D and calcium"],"prefix":"10.1002","volume":"83","author":[{"given":"Adeboye H.","family":"Adewoye","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tai 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