Gene/Protein Disease Symptom Drug Enzyme Compound
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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anorexia nervosa is associated with bone loss during adulthood, but may also delay skeletal growth and mineral accrual during growth. We asked the following questions. 1) Is anorexia nervosa associated with reduced bone size and reduced volumetric bone mineral density (vBMD)? 2) Is estrogen replacement therapy (ERT) or recovery from anorexia nervosa associated with normal bone size and vBMD? Using dual-energy x-ray absorptiometry, we measured bone size and vBMD of the third lumbar vertebra and femoral neck in a cross-sectional study of 161 female patients: 77 with untreated anorexia nervosa, 58 with anorexia nervosa receiving ERT, 26 recovered from anorexia nervosa, and 205 healthy age-matched controls. Results were expressed as the SD or z-score (mean +/- SEM). Deficits in vertebral body and femoral neck width in untreated women were -1.0 +/- 0.1 and -0.3 +/- 0.1 SD (P < 0.001 and P < 0.05, respectively). Deficits in bone width were less in the ERT-treated women than in untreated women at the vertebral body (-0.6 +/- 0.1 SD; P < 0.001), but not at the femoral neck (-0.4 +/- 0.2 SD; P < 0.05). There were no significant deficits in vertebral body and femoral neck width in recovered women (both -0.3 +/- 0.2 SD; P = NS). In untreated women, vertebral and femoral neck vBMD were -1.6 +/- 0.1 and -1.1 +/- 0.1 SD, respectively (both P < 0.001), less severely reduced in ERT-treated women (-1.2 +/- 0.2 and -0.6 +/- 0.2 SD, respectively; both P < 0.001), and least reduced in recovered women (-0.6 +/- 0.1 and -0.5 +/- 0.2 SD; P < 0.01 and P < 0.05, respectively). After adjusting for differences in fat and lean mass, vertebral body and femoral neck width were no longer reduced in untreated, ERT-treated, and recovered women. Adjustment for body composition had little effect on group difference in vBMD. Bone fragility in anorexia nervosa is due to reduced bone size and reduced vBMD. Although causality cannot be inferred in cross-sectional studies, the data are consistent with the view that malnutrition may contribute to reduced bone size, whereas estrogen deficiency may reduce vBMD. The use of ERT early in disease is a reasonable component of management if the chance of recovery appears remote.
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PMID:Bone size and volumetric density in women with anorexia nervosa receiving estrogen replacement therapy and in women recovered from anorexia nervosa. 1099 5

Skeletal development is heterogeneous. Throughout growth, bone size is more maturationally advanced than the mineral being accrued within its periosteal envelope; before puberty, appendicular growth is more rapid than axial growth; during puberty, appendicular growth slows and axial growth accelerates. We studied women with differing age of onset of anorexia nervosa to determine whether this temporal heterogeneity in growth predisposed to the development of deficits in bone size and volumetric bone mineral density (vBMD), which varied by site and severity depending on the age at which anorexia nervosa occurred. Bone size and vBMD of the third lumbar vertebra and femoral neck were measured using dual-energy X-ray absorptiometry in 210 women aged 21 years (range, 12-40 years) with anorexia nervosa. Results were expressed as age-specific SDs (mean +/- SEM). Bone width depended on the age of onset of anorexia nervosa; when the onset of anorexia nervosa occurred (1) before 15 years of age, deficits in vertebral body and femoral neck width did not differ (-0.77+/-0.27 SD and -0.55+/-0.17 SD, respectively); (2) between 15 and 19 years of age, deficits in vertebral body width (-0.95+/-0.16 SD) were three times the deficits in femoral neck width (-0.28+/-0.14 SD; p < 0.05 comparing the deficits), (3) after 19 years of age, deficits in the vertebral body width (-0.49+/-0.26 SD; p = 0.05) were half that in women with earlier onset of anorexia nervosa. No deficit in bone width was observed at the femoral neck. Deficits in vBMD at the vertebra and femoral neck were independent of the age of onset of anorexia nervosa but increased as the duration of anorexia nervosa increased, being about 0.5 SD lower at the vertebra than femoral neck. We infer that the maturational development of a region at the time of exposure to disease, and disease duration, determine the site, magnitude, and type of trait deficit in anorexia nervosa. Bone fragility due to reduced bone size and reduced vBMD in adulthood is partly established during growth.
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PMID:On exposure to anorexia nervosa, the temporal variation in axial and appendicular skeletal development predisposes to site-specific deficits in bone size and density: a cross-sectional study. 1109 8

To study the structural basis of bone fragility in men, we compared bone size and volumetric bone mineral density (vBMD) of the third lumbar vertebra and femoral neck in 95 men with spine fractures, 127 men with hip fractures, and 395 healthy controls using dual-energy X-ray absorptiometry (DXA). The results were expressed in absolute terms and age-specific SD scores (mean +/- SEM). In controls, vertebral body and femoral neck width increased across age, being 0.46 +/- 0.11 SD and 0.91 +/- 0.08 SD higher in elderly men than in young men, respectively (both,p < 0.001). Men with spine fractures had reduced vertebral body width (-0.45 +/- 0.10 SD;p < 0.01) but not femoral neck width (-0.15 +/- 0.10 SD, NS). Men with hip fractures had reduced femoral neck width (-0.45 +/- 0.11 SD; p < 0.01) and vertebral body width (-0.25 +/- 0.10 SD; p < 0.05). The deficits in bone volume (BV) exaggerated the deficits in bone mineral content (BMC) by 40% at the vertebrae in men with spine fractures and by 9% at the femoral neck in men with hip fractures. vBMD deficits were greater at the vertebrae in men with spine fractures than in men with hip fractures (-1.37 +/- 0.08 SD vs.-0.70 +/- 0.10 SD, respectively; p < 0.01) but were similar at the femoral neck (-0.93 +/- 0.10 SD and -0.76 +/- 0.11 SD, respectively, NS), despite the men with spine fracture being 10 years younger. Bone fragility leading to spine or hip fractures in men may be the result of fracture site-specific deficits in bone size and vBMD that have their origins in growth, aging, or both.
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PMID:Fracture site-specific deficits in bone size and volumetric density in men with spine or hip fractures. 1114 75