CiteULike: omalbam's bmd

Does thoracic or lumbar spine bone architecture predict vertebral failure strength more accurately than density?

EM Lochmüller — 2008-03-24T21:21:13-00:00

Osteoporosis International, Vol. 19, No. 4. (14 April 2008), pp. 537-545.

Abstract Summary Trabecular bone microstructure was studied in 6 mm bone biopsies taken from the 10th thoracic and 2nd lumbar vertebra of 165 human donors and shown to not differ significantly between these sites. Microstructural parameters at the locations examined provided only marginal additional information to quantitative computed tomography in predicting experimental failure strength. Introduction It is unknown whether trabecular microstructure differs between thoracic and lumbar vertebrae and whether it adds significant information in predicting the mechanical strength of vertebrae in combination with QCT-based bone density. Methods Six mm cylindrical biopsies taken at mid-vertebral level, anterior to the center of the thoracic vertebra (T) 10 and the lumbar vertebra (L) 2 were studied with micro-computed tomography (μCT) in 165 donors (age 52 to 99 years). The segment T11-L1 was examined with QCT and tested to failure using a testing machine. Results The correlation of microstructural properties was moderate between T10 and L2 (r ≤ 0.5). No significant differences were observed in the microstructural properties between the thoracic and lumbar spine, nor were sex differences at T10 or L2 observed. Cortical/subcortical density of T12 (r 2 = 48%) was more strongly correlated with vertebral failure stress than trabecular density (r 2 = 32%). BV/TV (of T10) improved the prediction by 52% (adjusted r 2) in a multiple regression model. Conclusion Microstructural properties of trabecular bone biopsies displayed a high degree of heterogeneity between vertebrae but did not differ significantly between the thoracic and lumbar spine. At the locations examined, bone microstructure only marginally improved the prediction of structural vertebral strength beyond QCT-based bone density.

Long-Term DHEA Replacement in Primary Adrenal Insufficiency: A Randomized, Controlled Trial

Eleanor Gurnell — 2008-02-09T17:47:52-00:00

J Clin Endocrinol Metab, Vol. 93, No. 2. (1 February 2008), pp. 400-409.

Context: Dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS) are the major circulating adrenal steroids and substrates for peripheral sex hormone biosynthesis. In Addison's disease, glucocorticoid and mineralocorticoid deficiencies require lifelong replacement, but the associated near-total failure of DHEA synthesis is not typically corrected. Objective and Design: In a double-blind trial, we randomized 106 subjects (44 males, 62 females) with Addison's disease to receive either 50 mg daily of micronized DHEA or placebo orally for 12 months to evaluate its longer-term effects on bone mineral density, body composition, and cognitive function together with well-being and fatigue. Results: Circulating DHEAS and androstenedione rose significantly in both sexes, with testosterone increasing to low normal levels only in females. DHEA reversed ongoing loss of bone mineral density at the femoral neck (P < 0.05) but not at other sites; DHEA enhanced total body (P = 0.02) and truncal (P = 0.017) lean mass significantly with no change in fat mass. At baseline, subscales of psychological well-being in questionnaires (Short Form-36, General Health Questionnaire-30), were significantly worse in Addison's patients vs. control populations (P < 0.001), and one subscale of SF-36 improved significantly (P = 0.004) after DHEA treatment. There was no significant benefit of DHEA treatment on fatigue or cognitive or sexual function. Supraphysiological DHEAS levels were achieved in some older females who experienced mild androgenic side effects. Conclusion: Although further long-term studies of DHEA therapy, with dosage adjustment, are desirable, our results support some beneficial effects of prolonged DHEA treatment in Addison's disease. 10.1210/jc.2007-1134

SHBG gene promoter polymorphisms in men are associated with serum sex hormone-binding globulin, androgen and androgen metabolite levels, and hip bone mineral density.

AL Eriksson — 2008-01-27T02:17:52-00:00

J Clin Endocrinol Metab, Vol. 91, No. 12. (December 2006), pp. 5029-5037.

CONTEXT: SHBG regulates free sex steroid levels, which in turn regulate skeletal homeostasis. Twin studies have demonstrated that genetic factors largely account for interindividual variation in SHBG levels. Glucuronidated androgen metabolites have been proposed as markers of androgenic activity. OBJECTIVE: Our objective was to investigate whether polymorphisms in the SHBG gene promoter [(TAAAA)(n) microsatellite and rs1799941 single-nucleotide polymorphism] are associated with serum levels of SHBG, sex steroids, or bone mineral density (BMD) in men. DESIGN AND STUDY SUBJECTS: We conducted a population-based study of two cohorts of Swedish men: elderly men (MrOS Sweden; n congruent with 3000; average age, 75.4 yr) and young adult men (GOOD study; n = 1068; average age, 18.9 yr). MAIN OUTCOME MEASURES: We measured serum levels of SHBG, testosterone, estradiol, dihydrotestosterone, 5alpha-androstane-3alpha,17beta-diol glucuronides, androsterone glucuronide, and BMD determined by dual-energy x-ray absorptiometry. RESULTS: In both cohorts, (TAAAA)(n) and rs1799941 genotypes were associated with serum levels of SHBG (P < 0.001), dihydrotestosterone (P < 0.05), and 5alpha-androstane-3alpha,17beta-diol glucuronides (P < 0.05). In the elderly men, they were also associated with testosterone and BMD at all hip bone sites. The genotype associated with high levels of SHBG was also associated with high BMD. Interestingly, male mice overexpressing human SHBG had increased cortical bone mineral content in the femur, suggesting that elevated SHBG levels may cause increased bone mass. CONCLUSIONS: Our findings demonstrate that polymorphisms in the SHBG promoter predict serum levels of SHBG, androgens, and glucuronidated androgen metabolites, and hip BMD in men.

DHEA in elderly women and DHEA or testosterone in elderly men.

KS Nair — 2007-10-21T23:39:35-00:00

N Engl J Med, Vol. 355, No. 16. (19 October 2006), pp. 1647-1659.

BACKGROUND: Dehydroepiandrosterone (DHEA) and testosterone are widely promoted as antiaging supplements, but the long-term benefits, as compared with potential harm, are unknown. METHODS: We performed a 2-year, placebo-controlled, randomized, double-blind study involving 87 elderly men with low levels of the sulfated form of DHEA and bioavailable testosterone and 57 elderly women with low levels of sulfated DHEA. Among the men, 29 received DHEA, 27 received testosterone, and 31 received placebo. Among the women, 27 received DHEA and 30 received placebo. Outcome measures included physical performance, body composition, bone mineral density (BMD), glucose tolerance, and quality of life. RESULTS: As compared with the change from baseline to 24 months in the placebo group, subjects who received DHEA for 2 years had an increase in plasma levels of sulfated DHEA by a median of 3.4 microg per milliliter (9.2 micromol per liter) in men and by 3.8 microg per milliliter (10.3 micromol per liter) in women. Among men who received testosterone, the level of bioavailable testosterone increased by a median of 30.4 ng per deciliter (1.1 nmol per liter), as compared with the change in the placebo group. A separate analysis of men and women showed no significant effect of DHEA on body-composition measurements. Neither hormone altered the peak volume of oxygen consumed per minute, muscle strength, or insulin sensitivity. Men who received testosterone had a slight increase in fat-free mass, and men in both treatment groups had an increase in BMD at the femoral neck. Women who received DHEA had an increase in BMD at the ultradistal radius. Neither treatment improved the quality of life or had major adverse effects. CONCLUSIONS: Neither DHEA nor low-dose testosterone replacement in elderly people has physiologically relevant beneficial effects on body composition, physical performance, insulin sensitivity, or quality of life. (ClinicalTrials.gov number, NCT00254371 [ClinicalTrials.gov].).

Serum 25-Hydroxyvitamin D and Bone Mineral Density in a Racially and Ethnically Diverse Group of Men

Marian Hannan — 2008-01-10T23:20:03-00:00

J Clin Endocrinol Metab, Vol. 93, No. 1. (1 January 2008), pp. 40-46.

Context: Although racial and ethnic differences in vitamin D status and bone mineral density (BMD) are recognized, less is known about how differences in vitamin D status impact BMD, especially among men. Objective: Our objective was to examine the relation between serum 25-hydroxyvitamin D [25(OH)D] and BMD by race and ethnic group. Design: We conducted a population-based, observational survey. Participants: Participants included 1114 Black, Hispanic, and White men, 3079 yr of age. Outcomes: We assessed 25(OH)D by a competitive protein binding assay and BMD by dual-energy x-ray absorptiometry. Results: Mean age +/- SD of the 331 Black, 362 Hispanic, and 421 White men was 48 +/- 12.8 yr. Mean 25(OH)D was lower among Black (25.0 +/- 14.7 ng/ml) and Hispanic (32.9 +/- 13.9 ng/ml) men compared with White men (37.4 +/- 14.0 ng/ml, P < 0.01). A higher percentage of both Black (44%) and Hispanic (23%) men had levels of 25(OH)D in the lowest quartile, compared with 11% of White men (P < 0.001). After adjusting for age, height, and weight, only White men showed significant positive correlation between 25(OH)D and BMD (range of correlations, 0.000.14). Serum 25(OH)D was not associated with BMD in Black or Hispanic men at any bone site. Results were similar when adjusted for age only. Conclusions: Our findings confirm substantial racial and ethnic group differences in BMD and serum 25(OH)D in men. Serum 25(OH)D and BMD are significantly related to one another in White men only. This may have implications for evaluation of bone health and supplementation in men with low levels of 25(OH)D. Further understanding of the biological mechanisms for these differences between race and ethnic groups is needed. 10.1210/jc.2007-1217