Literature DB >> 25867815

Abnormal Skeletal Strength and Microarchitecture in Women With Celiac Disease.

Emily M Stein1, Halley Rogers1, Alexa Leib1, Donald J McMahon1, Polly Young1, Kyle Nishiyama1, X Edward Guo1, Suzanne Lewis1, Peter H Green1, Elizabeth Shane1.   

Abstract

CONTEXT: Osteoporosis is often a presenting sign of celiac disease (CD). Whether skeletal fragility in CD is associated with microarchitectural abnormalities is not known.
OBJECTIVE: The objective of the study was to evaluate microarchitecture and biomechanical properties of bone in CD.
DESIGN: This was a case-control study.
SETTING: The study was conducted at a university hospital outpatient facility. PATIENTS: Patients included premenopausal women with newly diagnosed CD (n = 33) and healthy controls (n = 33). MAIN OUTCOME MEASURES: Areal bone mineral density by dual-energy x-ray absorptiometry was measured as was trabecular and cortical volumetric bone mineral density (vBMD) and microarchitecture by high-resolution peripheral computed tomography of the distal radius and tibia. Whole-bone stiffness estimated by finite element analysis. PTH, 25-hydroxyvitamin D, and bone turnover markers were also measured.
RESULTS: Groups had similar age, race, and body mass index. Both groups had sufficient 25-hydroxyvitamin D and normal calcium and PTH. Areal bone mineral density was lower in CD. By high-resolution peripheral computed tomography, CD had lower trabecular vBMD, fewer, more widely, and irregularly spaced trabeculae at both the radius and tibia (8%-33%). At the tibia, they also had lower total density (8%) and thinner cortices (10%). Whole-bone stiffness and failure load were lower (11%-21%) in CD at both sites. Biomechanical deficits were associated with trabecular abnormalities.
CONCLUSIONS: Women with CD had abnormal vBMD and microarchitecture at both the radius and tibia. Trabecular bone was preferentially affected. These deficits were associated with lower estimates of skeletal strength. These findings suggest a potential structural mechanism for skeletal fragility in CD and support further research into the pathogenesis of fracture in this population.

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Year:  2015        PMID: 25867815      PMCID: PMC4454795          DOI: 10.1210/jc.2015-1392

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


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