Marrow fat and preadipocyte factor-1 levels decrease with recovery in women with anorexia nervosa

Women with anorexia nervosa (AN) have elevated marrow fat mass despite low visceral and subcutaneous fat depots, which is inversely associated with bone mineral density (BMD). Whether marrow fat mass remains persistently elevated or decreases with recovery from AN is currently unknown. In this study, we investigated changes in marrow fat in women who have recovered from AN (AN-R). We also studied the relationship between preadipocyte factor (Pref)-1—a member of the EGF-like family of proteins and regulator of adipocyte and osteoblast differentiation—and fat depots and BMD in AN-R compared with women with AN and healthy controls (HC). We studied 29 women: 14 with active or recovered AN (30.7 + 2.2 years [mean ± SEM]) and 15 normal-weight controls (27.8 ± 1.2 years). We measured marrow adipose tissue (MAT) of the L4 vertebra and femur by ¹H-magnetic resonance spectroscopy; BMD of the spine, hip, and total body by DXA; and serum Pref-1 and leptin levels. We found that MAT of the L4 vertebra was significantly lower in AN-R compared with AN (p = 0.03) and was comparable to levels in HC. Pref-1 levels were also significantly lower in AN-R compared with AN (p = 0.02) and comparable to levels in healthy controls. Although Pref-1 was positively associated with MAT of the L4 vertebra in AN (R = 0.94; p = 0.002), we found that it was inversely associated with MAT of the L4 vertebra in HC (R = −0.71; p = 0.004). Therefore, we have shown that MAT and Pref-1 levels decrease with recovery from AN. Our data suggest that Pref-1 may have differential effects in states of nutritional deprivation compared with nutritional sufficiency. © 2012 American Society for Bone and Mineral Research.     

Sequential Therapy With Recombinant Human IGF-1 Followed by Risedronate Increases Spine Bone Mineral Density in Women With Anorexia Nervosa: A Randomized,Placebo-Controlled Trial

Anorexia nervosa is complicated by low bone mineral density (BMD) and increased fracture risk associated with low bone formation and high bone resorption. The lumbar spine is most severely affected. Low bone formation is associated with relative insulin-like growth factor 1 (IGF-1) deficiency. Our objective was to determine whether bone anabolic therapy with recombinant human (rh) IGF-1 used off-label followed by antiresorptive therapy with risedronate would increase BMD more than risedronate or placebo in women with anorexia nervosa. We conducted a 12-month, randomized, placebo-controlled study of 90 ambulatory women with anorexia nervosa and low areal BMD (aBMD). Participants were randomized to three groups: 6 months of rhIGF-1 followed by 6 months of risedronate (“rhIGF-1/Risedronate”) (n = 33), 12 months of risedronate (“Risedronate”) (n = 33), or double placebo (“Placebo”) (n = 16). Outcome measures were lumbar spine (1° endpoint: postero-anterior [PA] spine), hip, and radius aBMD by dual-energy X-ray absorptiometry (DXA), and vertebral, tibial, and radial volumetric BMD (vBMD) and estimated strength by high-resolution peripheral quantitative computed tomography (HR-pCT) (for extremity measurements) and multi-detector computed tomography (for vertebral measurements). At baseline, mean age, body mass index (BMI), aBMD, and vBMD were similar among groups. At 12 months, mean PA lumbar spine aBMD was higher in the rhIGF-1/Risedronate (p = 0.03) group and trended toward being higher in the Risedronate group than Placebo. Mean lateral lumbar spine aBMD was higher, in the rhIGF-1/Risedronate than the Risedronate or Placebo groups (p < 0.05). Vertebral vBMD was higher, and estimated strength trended toward being higher, in the rhIGF-1/Risedronate than Placebo group (p < 0.05). Neither hip or radial aBMD or vBMD, nor radial or tibial estimated strength, differed among groups. rhIGF-1 was well tolerated. Therefore, sequential therapy with rhIGF-1 followed by risedronate increased lateral lumbar spine aBMD more than risedronate or placebo. Strategies that are anabolic and antiresorptive to bone may be effective at increasing BMD in women with anorexia nervosa. © 2021 American Society for Bone and Mineral Research (ASBMR).     

Reduced bone mineral in patients with eating disorders

Bone mineral measurements of the forearm and spine were made in 63 patients under treatment in the Eating Disorders Program of the University of Nebraska Medical Center, 26 with anorexia nervosa (AN), 11 with bulimia nervosa (BU) and 26 with features of both AN and BU (AN/BU). Comparison was made with a group of 211 normal women of similar age. Spinal bone mineral content (BMC) of L2-4 was 45.1 +/- 5.7 g in the normals, 38.0 +/- 7.5 in the AN's, 40.3 +/- 6.6 g in the AN/BU's and 44.4 +/- 6.9 g in the BU's. The AN and AN/BU averages were both significantly different from normal (p less than 0.0005), but the BU average was not. BMC was correlated with body weight in each group and weakly correlated with age in the patients under age 30 in the AN and AN/BU groups combined. Forearm bone mineral measurements in the AN's and AN/BU's were also significantly lower than normal, but the differences were not as great as for the spine. We conclude that bone mineral is reduced in these patients, severely in some of them, and that reduced body weight plays a role. Menstrual disturbances, inhibition of growth and development, and malnutrition remain open as causal factors. Potential for recovery from reduced bone mineral was not demonstrated in this study.     

Evaluation of urine deoxypyridinoline and bone mineral density in 861 Chinese during routine health examination.

The aim of this study was to investigate the interrelation among urine deoxypyridinoline (DPD), age, sex, and bone mineral density (BMD) and to clarify whether DPD can be used to screen for low bone mass (T-score <-1) of the lumbar spine and proximal femur in the Chinese population. We reviewed medical records over a 1-yr period of all subjects who completed an annual health examination. A total of 302 men (age: 48.20 +/- 10.86 yr) and 559 women (age: 46.45 +/- 11.16 yr) who lived in the Taipei area, had no major systemic disorders, and underwent urine DPD test and BMD examination of both the lumbar spine (L-BMD) and proximal femur (F-BMD) were recruited. The urine DPD was weakly correlated with middle age in men (r = 0.154, p < 0.01). There was no correlation between DPD and age in women. The DPD and L-BMD were weakly correlated in both middle-aged men (r = -0.165, p < 0.05) and women (r = -0.171, p < 0.01), and moderately correlated in elderly women (r = -0.315, p < 0.01). There was a higher correlation between DPD and F-BMD in men than in women, especially in the middle-aged groups (men: r = -0.258, p < 0.01; women: r = -0.170, p < 0.01). Women in the highest tertile of DPD had 2.40 times the risk (95% confidence interval: 1.49-3.85) of those in the lowest tertile after age adjustment. There was poor agreement or none between DPD and BMD measurements in patients with low bone mass at either site in either sex. Urine DPD tests to substitute for BMD measurements in routine health examination for Chinese is not recommended.     

Association between vitamin D and bone mineral density in Iranian postmenopausal women

The role of vitamin-D in determining bone mineral density (BMD), especially in less severe vitamin D deficiency, is still unclear. To investigate the possible association between 25-hydroxyvitamin D [25(OH)D] and BMD, 245 healthy free-living postmenopausal women, aged between 40 and 80, were randomly selected from participants of a population-based study. BMD was measured at the lumbar spine and hip by dual X-ray absorptiometry (Lunar DPXMD 7164). Serum 25(OH)D, parathyroid hormone (PTH), calcium, phosphorus, total and bone alkaline phosphatases, and urine deoxypyridinoline were measured. PTH was logarithmically transformed (LnPTH). Linear regression models were developed to determine the association between serum 25(OH)D and BMD at different sites. Means of age and duration of menopause were 57.7 +/- 7 and 9.4 +/- 6.8 years, respectively. Mean 25(OH)D was 73.0 +/- 62.3 nmol/l; 5.3% (n = 13) had 25(OH)D < 25 nmol/l and 37.6% (n = 92) had 25(OH)D between 25 and 50 nmol/l. Eleven percent of the women (n = 27) were osteoporotic in femoral neck and 25.3% of them (n = 62) were osteoporotic in lumbar spine sites. 25(OH)D correlated inversely with LnPTH (r = -0.25, P < 0.01). In the multivariate analyses, no association was found between 25(OH)D and BMD at any of the skeletal sites after adjusting for age, duration of menopause, body mass index, calcium, and LnPTH. However, BMD was associated inversely with LnPTH only in femoral neck but not in the other sites. This study did not show any association between 25(OH)D and BMD in free-living Iranian postmenopausal women.     

Diabetes is associated independently of body composition with BMD and bone volume in older white and black men and women: The Health, Aging, and Body Composition Study.

The association between type 2 diabetes, BMD, and bone volume was examined to determine the effect of lean and fat mass and fasting insulin in the Health, Aging, and Body Composition Study, which included white and black well-functioning men and women 70-79 years of age (N = 2979). Diabetes predicted higher hip, whole body, and volumetric spine BMD, and lower spine bone volume, independent of body composition and fasting insulin. INTRODUCTION: The purpose of this study was to determine if the association between type 2 diabetes and higher BMD observed in older white women is seen in elderly white men and blacks and to evaluate if higher BMD in diabetic individuals is accounted for by lean mass, fat mass, or fasting insulin differences. MATERIALS AND METHODS: In the Health, Aging, and Body Composition Study, which included white and black well-functioning men and women 70-79 years of age (N = 2979), 19% of participants had diabetes at baseline. Of those with diabetes, 57% were men, and 62% were black. Multivariate linear regression models examined independent effects of diabetes, lean mass, fat mass, visceral fat, and fasting insulin on BMD and bone volume while adjusting for relevant covariates. RESULTS AND CONCLUSIONS: Fasting insulin, visceral fat, and volumetric spine BMD, assessed by CT, and lean mass, fat mass, and total hip and whole body BMD, assessed by DXA, were higher (p < or = 0.05 for all) for those with diabetes. Hip BMD was higher in white men (0.99 +/- 0.14 versus 0.93 +/- 0.14 g/cm2, p < 0.001), black men (1.06 +/- 0.17 versus 1.00 +/- 0.15 g/cm2, p < 0.001), white women (0.83 +/- 0.13 versus 0.76 +/- 0.13 g/cm2, p < 0.001), and black women (0.90 +/- 0.15 versus 0.85 +/- 0.15 g/cm2, p < 0.001) with diabetes compared with those without diabetes, although the relationship was attenuated by body composition. In multiple regression models, diabetes was an independent predictor of higher hip, whole body, and volumetric spine BMD in all participants (p < or = 0.001), but lower spine volume (p = 0.01) and higher hip BMD for each race-gender group (p < or = 0.01). Type 2 diabetes was associated with a 4-5% higher total hip BMD in all race-gender groups of elderly adults, independent of body composition and fasting insulin levels.     

Osteoporosis and hip fracture in a young woman with anorexia nervosa

A 35-year-old woman with a 17-year history of anorexia nervosa (AN) sustained a pathologic fracture of the hip. Osteoporosis was confirmed by quantitative computed tomography of the lumbar spine and transiliac bone biopsy. Severe bone disease may exist in the anorexia nervosa syndrome and may to some extent be reversible on treatment of the underlying condition. AN could have profound effects on the peak bone mass achieved in the lifetime of the individual. Asymptomatic and symptomatic osteoporosis in young women may be based upon AN. Patients should be informed that osteoporosis can cause pathologic fractures as a sequela of self-imposed chronic malnutrition.     

The effect of anorexia nervosa on bone morphometry in young women

Changes in bone morphometry during chronic undernutrition were evaluated in 14 young women with anorexia nervosa (mean age +/- SEM = 25.5 +/- 4.4 yrs). Bone morphometry studies using the second metacarpal of the left hand showed significant depression for percent cortical area (p less than 0.05); cortical area (p less than 0.001) and combined cortical thickness (p less than 0.01) as compared to age, sex and race matched controls. A trend (p less than 0.10) was observed in study subjects for reductions in bone width and total area. Using percent cortical area (PCA) as the standard, subjects had mean cortical bone morphometry equivalent to 60-year-old women. Appendicular bone mass is significantly decreased in adults with anorexia nervosa. Anorexia nervosa should be considered in the differential diagnosis of osteopenia in young women, and serves as a model for studying the effects of chronic calorie and mineral malnutrition on bone remodeling at the time of attainment of peak bone mass.     

Marked increases in bone mineral density and biochemical markers of bone turnover in patients with anorexia nervosa gaining weight

Anorexia nervosa (AN) is a life-threatening eating disorder characterized by an inability to maintain a normal body weight and amenorrhoea, often associated with osteoporosis and increased risk of fragility fractures. Bone metabolism, including markers of bone turnover (serum total alkaline phosphatase, bone alkaline phosphatase [bone AP], osteocalcin [OC] and type I collagen C-telopeptide breakdown products [sCTX]) and bone mineral density (BMD) by dual energy X-ray absorptiometry (DXA) at the spine and at the hip, were evaluated in 55 consecutive women with AN undergoing a 3-month intensive nutritional rehabilitation program. The control group was constituted of 25 healthy young medical students. In AN patients body weight increased during the 3-month nutritional program from 37.8+/-5.1 (mean+/-SD) to 51.5+/-4.5 kg. The corresponding BMI rose to values >17.5 kg/m(2) in all patients. Mean BMD significantly rose by 2.6+/-3.5% and 1.1+/-3.6% at the hip and at the spine, respectively. The markers of bone formation, serum bone AP and osteocalcin, significantly rose by two-folds, while sCTX decreased by 16%. The changes in hip BMD were positively related (p<0.005) to changes in body weight and in bone AP (p<0.02) while the changes in spine BMD were positively related to changes in serum osteocalcin (p<0.05). In the 25 patients who attended the 12-month posttreatment control, mean body weight significantly decreased by 3.6+/-6.0 kg and this was not associated with any significant change in BMD values. In the patients in whom BMI fell again below 17.5 kg/m(2) hip BMD values decreased significantly. On the contrary, in the patients who maintained BMI >17.5 kg/m(2), BMD values continued to rise up to values over the 15-month observation of 4.8+/-6.2 and 7.1+/-12.1 at the spine and hip, respectively. In conclusion, we have demonstrated that substantial gains in weight in women with chronic AN are associated with remarkable increases in BMD at both the hip and the spine. If weight is maintained, the overall improvement approach 1 SD within 1 year. The changes in both weight and BMD are correlated with improvements in bone formation markers and diminutions in a marker of bone resorption.     

The effects of growth hormone replacement therapy on bone metabolism in adult-onset growth hormone deficiency: a 2-year open randomized controlled multicenter trial.

Adult hypopituitary patients with growth hormone deficiency (GHD) show a significant decrease in bone mass and an increased fracture rate. Replacement therapy with GH increases bone turnover. Most of the long-term data on bone mineral content (BMC) and bone mineral density (BMD) have been acquired in open, noncontrolled trials involving limited numbers of patients. To determine whether long-term GH therapy is beneficial for bone despite the increased bone turnover, 100 patients (59 men and 41 women), aged 25-65 years (mean, 49.7 years) with adult-onset GHD were randomized to treatment with GH (40 men and 28 women; mean dose, 0.18 IU/kg per week) or to a nontreated control group (19 men and 13 women) for 24 months. Despite a similar increase in parameters of bone turnover (osteocalcin [OC], procollagen type I carboxy-terminal propeptide [PICP], and pyridinolines ([PYD]) in male and female GH-treated patients compared with controls, the effects on BMC and BMD as evaluated by dual-energy X-ray absorptiometry were gender specific. A significant increase in spine BMC and BMD and total hip BMD and a decrease in BMD at the ultradistal radius over time was observed in male GH-treated patients compared with the evolution in controls (mean +/- SEM change at 24 months: +6.8 +/- 1.1% and p = 0.009, +5.1 +/- 0.8% and p = 0.005, +3.5 +/- 0.7% and p = 0.02, and -2.6 +/- 0.8% and p = 0.008, respectively). No significant treatment effects were observed in female patients. Despite the increase in the total remodeling space induced by GH treatment, prolonged GH therapy in adult-onset GHD has a positive effect on bone balance, maintaining bone mass in women, and even increasing it in men over a 2 year-period.     

Bone mass after long-term euthyroidism in former hyperthyroid women treated with (131)I influence of menopausal status.

The objective of this study was to assess bone mineral density (BMD) and bone markers in former hyperthyroid females after long-term euthyroidism (>4 yr) following (131)I therapy, as well as the potential influence of the timing of menopause. Twenty-six females ages 57 +/- 8 yr previously diagnosed with hyperthyroidism and treated with (131)I who were euthyroid for a minimum of the last 4 yr (10 +/- 5 yr) were studied. Eighteen patients (69%) were on levothyroxine (LT(4)) replacement therapy for 9 +/- 4 yr. BMD (g/cm(2) and Z-score) was measured by dual X-ray absorptiometry in the lumbar spine, femoral neck, and Ward's triangle. BMD (Z-score) was lower than the normal reference values for the Spanish population in all sites (lumbar spine: -0.65 +/- 1.13; femoral neck: -0.47 +/- 0.95; Ward's triangle: -0.37 +/- 0.88). No differences were found between BMD values according to the etiology of the hyperthyroidism or current LT(4) therapy. Current postmenopausal patients (n = 21) showed lower BMD than current premenopausal patients in the lumbar spine and femoral neck (p < 0.05). Those women who were postmenopausal at the time of the (131)I therapy (n = 15) also had lower lumbar spine BMD than premenopausal patients (p = 0.01), while no significant difference in BMD was seen according to the menopausal status when hyperthyroidism was diagnosed. Former hyperthyroid patients after long-term euthyroidism following (131)I therapy showed reduced BMD at the lumbar spine and proximal femur. Menopausal women showed a greater reduction in bone density. The menopausal status at the time of diagnosis did not seem to have long-term effects in bone density; nevertheless, an early therapeutic intervention in premenopause is suggested to reduce bone loss.     

Bone metabolism in anorexia nervosa: molecular pathways and current treatment modalities

Eating disorders are associated with a multitude of metabolic abnormalities which are known to adversely affect bone metabolism and structure. We aimed to comprehensively review the literature on the effects of eating disorders, particularly anorexia nervosa (AN), on bone metabolism, bone mineral density (BMD), and fracture incidence. Furthermore, we aimed to highlight the risk factors and potential management strategies for patients with eating disorders and low BMD. We searched the MEDLINE/OVID (1950–July 2011) and EMBASE (1980–July 2011) databases, focussing on in vitro and in vivo studies of the effects of eating disorders on bone metabolism, bone mineral density, and fracture incidence. Low levels of estrogen, testosterone, dehydroepiandrosterone, insulin-like growth factor-1 (IGF-1), and leptin, and high levels of cortisol, ghrelin, and peptide YY (PYY) are thought to contribute to the ‘uncoupling’ of bone turnover in patients with active AN, leading to increased bone resorption in comparison to bone formation. Over time, this results in a high prevalence and profound degree of site-specific BMD loss in women with AN, thereby increasing fracture risk. Weight recovery and increasing BMI positively correlate with levels of IGF-1 and leptin, normalisation in the levels of cortisol, as well as markers of bone formation and resorption in both adolescent and adult patients with AN. The only treatments which have shown promise in reversing the BMD loss associated with AN include: physiologic dose transdermal and oral estrogen, recombinant human IGF-1 alone or in combination with the oral contraceptive pill, and bisphosphonate therapy.     

Anorexia Nervosa: Slow Regain of Bone Mass

In a retrospective study of women aged 18–30 years, aimed at assessing factors associated with peak bone mass (PBM), 13 of 239 study cases reported having had anorexia nervosa. The mean total femoral and lumbar bone mineral density (BMD) values were not significantly lower in women who had had anorexia than in the pooled group (mean Z-scores of –0.60 and –0.48). Cases with less than 6 years since the anorexia had on average a present weight 5.7 kg less than their pre-morbid weights, while cases with more than 6 years since the eating disorder had an average weight 22.5 kg above their pre-morbid weights. The cases who had not regained their weight had BMD values significantly lower than the pooled material (mean Z-scores –1.15 and –0.9 in the lumbar spine and total femur respectively). Those who had regained their weight had BMD values as predicted from their present anthropometric data, while those who had not regained their weight had BMD values that were substantially below that predicted from their present weight. Anorexia nervosa seems to be associated with a low BMD which is even lower than that which can be predicted from the weight loss alone. This suggests that weight loss and other factors, such as menstrual dysfunction and estrogen deficiency, are independent and thus additive causes of bone loss in anorexia nervosa. Recovery of BMD seems slow, but the BMD may become as predicted from the anthropometric data after restoration of body weight and menses. The potential for recovery of BMD seems intact for several years after menarche. Received: 19 May 1998 / Accepted: 7 July 1999     

Smoking and bone loss among postmenopausal women.

We examined the effect of smoking on bone mineral density (BMD), rates of bone loss, and fractional whole-body retention of 47Ca in healthy postmenopausal women enrolled in a 2-year calcium supplementation trial. Bone density was measured by single- and dual-photon absorptiometry. BMD of the radius at the study baseline was inversely related to pack-years of exposure when controlled for body mass index and years since menopause (partial r = -0.18, p = 0.05, n = 125). The adjusted mean (+/- SD) annualized rate of bone change from the radius was greater among smokers than nonsmokers (-0.914 +/- 2.624%/year, n = 34, versus 0.004 +/- 2.568%/year, n = 278, respectively; p = 0.05). Similar trends were observed at the femoral neck, os calcis, and spine. Rates were were adjusted for caffeine intake, alcohol use, supplement type, and, at the spine only, menopausal status. At entry into the trial higher serum levels of alkaline phosphatase and lower levels of total and ionized calcium were found in smokers compared to nonsmokers. These differences did not persist with supplementation. In 44 women studied fractional 47Ca retention was lower in the 8 smokers than the 36 nonsmokers (16.6 versus 19.1%, respectively; p = 0.03). These results demonstrate an increased rate of bone loss at the radius after menopause and suggest that smoking is associated with decreased calcium absorption.     

Skeletal status and laboratory investigations in adolescent girls with anorexia nervosa

To our knowledge anorexia nervosa (AN) adversely influences bone density, but whether qualitative characteristics of bone are also affected is not known. For this reason we investigated prospectively the changes in skeletal status in a population of 18 adolescent girls with AN aged 11.5-18.1 years (mean 15.9+/-1.9 years) using both dual-photon X-ray absorptiometry (DXA) and quantitative ultrasound (QUS) measurements, bone turnover markers (osteocalcin, bone alkaline phosphatase - bALP, carboxy-terminal cross-linked telopeptide of type I collagen - ICTP), and laboratory investigations (serum total and ionised calcium, serum phosphate, urine calcium/creatinine ratio, luteinizing hormone - LH, follicle-stimulating hormone - FSH, estradiol). Measurements of bone mineral density at the spine (s-BMD) and total body (TB-BMD) and amplitude-dependent speed of sound (Ad-SOS) of the hand phalanges were performed at baseline, 7.8+/-2.4 and 19.4+/-5.6 months of follow-up. The mean values of TB-BMD, s-BMD and Ad-SOS measurements did not change during the period of observation. The mean Z-scores for TB-BMD and Ad-SOS were significantly lower after 19.4 months of observation vs. baseline (-1.06+/-1.00 vs. -0.67+/-0.98 vs. and -0.50+/-0.88 vs. 0.26+/-1.75, respectively). Z-scores for s-BMD decreased non-significantly (p=0.08). Among bone turnover markers, we observed a significant increase in bALP and a non-significant increase in osteocalcin serum concentrations which were below normal ranges for age, sex and Tanner stage at baseline. High baseline serum ICTP concentration decreased non-significantly, reaching normal ranges during the observation. We conclude that anorexia nervosa seriously affects skeletal status in adolescent girls. Bone turnover markers analysed together with densitometric parameters suggest that AN influences both bone formation and resorption processes. QUS measurements at hand phalanges may be an appropriate method in the evaluation of skeletal status in patients with AN.     

Red and White Blood Cell Counts Are Associated With Bone Marrow Adipose Tissue,Bone Mineral Density,and Bone Microarchitecture in Premenopausal Women

Bone marrow adipose tissue (BMAT) resides within the bone marrow microenvironment where its function remains poorly understood. BMAT is elevated in anorexia nervosa, a disease model of chronic starvation, despite depletion of other fat depots. In addition to BMAT, the marrow microenvironment also consists of osteoblast and hematopoietic progenitors. BMAT is inversely associated with bone mineral density (BMD) in multiple populations including women with anorexia nervosa, and regulates hematopoiesis in animal models. We hypothesized that BMAT would be associated with circulating populations of hematopoietic cells (red and white blood cells) in humans and performed a post hoc analysis of two studies—a cross-sectional study and a longitudinal study—to investigate this hypothesis. We studied 89 premenopausal women cross-sectionally (median age [interquartile range], 27 [24.5, 31.7] years), including 35 with anorexia nervosa. We investigated associations between red blood cell (RBC) and white blood cell (WBC) counts and BMAT assessed by ¹H-magnetic resonance spectroscopy, BMD assessed by DXA, and bone microarchitecture assessed by HR-pQCT. In addition, we analyzed longitudinal data in six premenopausal women with anorexia nervosa treated with transdermal estrogen for 6 months and measured changes in BMAT and blood cell counts during treatment. Cross-sectionally, BMAT was inversely associated with WBC and RBC counts. In contrast, BMD and parameters of bone microarchitecture were positively associated with WBC and RBC. In women with anorexia nervosa treated with transdermal estrogen for 6 months, decreases in BMAT were significantly associated with increases in both RBC and hematocrit (rho = −0.83, p = 0.04 for both). In conclusion, we show that BMAT is inversely associated with WBC and RBC in premenopausal women, and there is a potential association between longitudinal changes in BMAT and changes in RBC. These associations warrant further study and may provide further insight into the role and function of this understudied adipose depot. © 2020 American Society for Bone and Mineral Research.     

Age-related bone mineral density, bone loss rate, prevalence of osteoporosis, and reference database of women at multiple centers in China.

Our study surveyed age-related bone mineral density (BMD), bone loss rate, and prevalence of osteoporosis in women at multiple research centers in China. Survey results were used to establish a BMD reference database for the diagnosis of osteoporosis in Chinese women nationwide. We used dual-energy X-ray absorptiometry bone densitometers to measure BMD at posteroanterior (PA) lumbar spine (L1-L4; n=8142) and proximal femur (n=7290) in female subjects of age 20-89 yr from Beijing, Shanghai, Guangzhou, Chengdu, Nanjing, and Jiaxing. A cubic regression-fitting model was used to describe the change of BMD with age at various skeletal sites. Peak BMD occurred between 30 and 34 yr of age for femur neck and total femur, and between 40 and 44 yr for spine and trochanter measurement sites. Young adult (YA) BMD values (mean and standard deviation [SD], calculated as the average BMD in the age range of 20-39, were 1.116+/-0.12, 0.927+/-0.12, 0.756+/-0.11, and 0.963+/-0.13 g/cm2 at PA spine, femoral neck, trochanter, and total femur, respectively. The BMD of 85-yr-old women reflected a loss of 32% at the spine and 30-35% at femur measurement sites. The prevalence of osteoporosis, defined as a BMD of 相似文献   

Bone mineral metabolism after total gastrectomy

Gastric surgery is mostly needed for treatment of gastric malignancy. To investigate the effect of total gastrectomy on bone mineral density (BMD) and bone mineral metabolism we evaluated 18 patients after total gastrectomy. Mean interval since operation was 71 +/- 20 months. BMD results were compared with age- and gender-matched controls (n = 46) and also expressed as T and Z scores. Bone mineral density measured by dual-energy X-ray absorptiometry (DXA) was found to be significantly lower in patients after total gastrectomy compared with healthy controls in the lumbar spine (p = 0.017 for women, p = 0.002 for men), femoral neck (p = 0.004 for women, p = 0.001 for men), Ward's triangle (p = 0.031 for women, p = 0.003 for men), and greater trochanter (p = 0.001 for women, p = 0.001 for men). Z scores for lumbar spine, femoral neck, Ward's triangle, and greater trochanter were -0.83, -1.54, -1.02, and -1.19, respectively. Biochemical measurements correlated poorly with BMD and were found to be of lesser value in diagnosing reduced bone mass as well as in differential diagnosis of etiology of osteopenia. The results of our study show the deleterious effect of total gastrectomy on bone mineral status and suggest an increased fracture risk in these patients.     

Sclerostin levels and bone turnover markers in adolescents with anorexia nervosa and healthy adolescent girls

Sclerostin, product of the SOST gene, is an important determinant of bone formation and resorption. Adolescents with anorexia nervosa (AN) have low bone density and decreased levels of bone turnover markers. However, sclerostin has not been examined in AN as a potential mediator of impaired bone metabolism. Our study objectives were to (i) assess associations of sclerostin with surrogate bone turnover markers in girls with AN and controls and (ii) examine effects of transdermal estradiol on sclerostin in AN. 69 girls (44 with AN and 25 normal-weight controls) 13-18years old were studied at baseline. 22 AN girls were randomized to transdermal estradiol (plus cyclic medroxyprogesterone) or placebo in a double-blind study for 12months. Sclerostin correlated positively with P1NP and CTX in controls (r=0.67 and 0.53, p=0.0002 and 0.005, respectively) but not in AN despite comparable levels at baseline. Changes in sclerostin over twelve months did not differ in girls randomized to estradiol or placebo. The relationship between sclerostin and bone turnover markers is disrupted in adolescent girls with AN. Despite an increase in BMD with estradiol administration in AN, estrogen does not impact sclerostin levels in this group.     

Posterior-anterior and lateral dual-energy x-ray absorptiometry for the assessment of vertebral osteoporosis and bone loss among older men.

Lateral spine dual-energy x-ray absorptiometry (DXA) selectively measures the trabecular-rich vertebral bodies without the contributions of the cortical-rich posterior elements of the spine and is less affected by spinal degenerative disease than posterior-anterior DXA. We tested whether lateral DXA detects vertebral osteoporosis more often and is more sensitive to age-related bone loss than posterior-anterior DXA in 193 healthy, community-dwelling men aged 51-81 years (mean +/- SD; 67 +/- 8 years). All men had supine lateral, posterior-anterior, and proximal femur DXA scans on a Hologic QDR 2000 densitometer. A subset (n = 102) had repeat scans after 4 years to determine annualized rates of change in bone mineral density (BMD). Age was inversely and significantly associated with BMD in the midlateral (r = -0.27) and lateral (r = -0.24) but not posterior-anterior (r = 0.04) projections. Midlateral (-1.43 +/- 3.48% per year; p = 0.0001), lateral (-0.27 +/- 1.68% per year; p = 0.12), and hip (-0.19 +/- 1.02% per year; p = 0.06) BMD decreased, whereas posterior-anterior BMD increased (0.73 +/- 1.11% per year; p = 0.0001) during follow-up. When compared with normal values in 43 men aged 21-42 years, mean T scores were significantly lower with lateral (-1.47 +/- 1.32) and midlateral (-1.57 +/- 1.36) than posterior-anterior (-0.12 +/- 1.30; p < 0.0001) DXA. Only 2.6% of the older men were considered osteoporotic (T score < or = -2.5) at the posterior-anterior spine, whereas 11.0% were osteoporotic at the femoral neck, 22.5% at the lateral spine, and 24.6% were osteoporotic at the midlateral spine. We conclude that supine lateral DXA identifies considerably more men as osteoporotic and is more sensitive to age-related bone loss than posterior-anterior DXA. Spinal osteoporosis may represent a substantially greater health problem among older men than previously recognized.