A controlled study of bone mineral density in patients with inflammatory bowel disease.

To assess the prevalence of and risk factors for low bone mineral density in inflammatory bowel disease (IBD), 152 IBD patients and 73 healthy controls were studied. Sixty seven patients had ulcerative colitis, 78 had Crohn's disease (52 of them (66.7%) had ileal disease), and seven had indeterminate colitis. Bone mineral density values (g/cm2) measured by dual energy x ray absorbtiometry at the spine (L2-L4), the femoral neck, Ward's triangle, and the trochanter were 1.177, 0.948, 0.850, and 0.838 in the patients and 1.228 (p = 0.034), 1.001 (p = 0.009), 0.889 (NS), and 0.888 (p = 0.012) in the control group, respectively. The type or extent of the disease or previous small bowel resection did not have any significant effect on the bone mineral density values. There was a weak, but statistically significant negative correlation between bone mineral density and the total lifetime corticosteroid dose (in the lumbar spine r = -0.164, p = 0.04, the femoral neck r = -0.185, p = 0.02, Ward's triangle r = -0.167, p = 0.04, and the trochanter r = -0.237, p = 0.003). The patients whose lifetime corticosteroid dose (prednisone/prednisolone) was more than 10 g had especially low bone mineral density (p < 0.05 compared with the groups with no or less than 5 g of corticosteroid). The patients who had never taken peroral corticosteroids did not have decreased bone mineral density. In conclusion, IBD patients have significantly lower bone mineral density values than healthy controls, but the difference is not so great as has been reported previously. Low bone mineral density values in these patients are related to high lifetime corticosteroid doses.     

Biochemical markers and bone densitometry in inflammatory bowel disease.

AIMS: Bone mineral density is reduced in patients with inflammatory bowel disease. The possible causes of this situation are delayed puberty, malabsorption, and corticosteroid use, among others. No published data exist regarding the use of biochemical markers and bone densitometry to assess osteopenia in these patients in Spain. METHODS: We studied 54 patients (24 men and 30 women), 22 with Crohn's disease and 32 with ulcerative colitis. Age, type of disease and average daily dose of prednisone-equivalent corticosteroids were evaluated. Lumbar bone mineral density was assessed quantitative digital radiography densitometry. The bone resorption marker urine D-pyridinoline and the bone formation marker serum osteocalcin were also assessed. RESULTS: Mean age was 36.61 +/- 13.37 years. Daily corticosteroid dose was correlated with D-pyridinoline (r = 0.413; p < 0.01), and D-pyridinoline was inversely correlated with osteocalcin (r = -0.304; p < 0.01). There was a negative correlation between bone mineral density and corticosteroid dose. There was no relationship between biochemical markers and bone densitometry findings in these patients. There were no differences in terms of bone densitometry findings or biochemical markers between the two types of inflammatory bowel disease. CONCLUSIONS: D-pyridinoline correlated inversely with osteocalcin. Daily corticosteroid dose correlated directly with D-pyridinoline, and inversely with bone mineral density.     

Changes in (markers of) bone metabolism during high dose corticosteroid pulse treatment in patients with rheumatoid arthritis.

OBJECTIVE: To examine the effect of high dose corticosteroid pulse treatment (three times 200 mg dexamethasone intravenously in eight days) on calcium and bone metabolism in 17 consecutive patients with active rheumatoid arthritis (RA). METHODS: Bone formation was quantified by measurement of serum alkaline phosphatase, osteocalcin, and carboxyterminal propeptide of type I procollagen (pro-I-CPP) concentrations. Bone resorption was measured by urinary excretion of calcium, hydroxyproline, (free and total) deoxypyridinoline (Dpyr), (free and total) pyridinoline (Pyr), and serum concentrations of the carboxyterminal cross linked telopeptide of type I collagen (I-CTP). Disease activity of RA was measured by erythrocyte sedimentation rate, C reactive protein, and Ritchie and Thompson joint scores. RESULTS: Disease activity was initially high, and decreased during corticosteroid pulse treatment and the following five weeks. Osteocalcin, alkaline phosphatase, and pro-I-CPP concentrations were initially within normal limits, while I-CTP, Dpyr, and Pyr were increased. Osteocalcin and pro-I-CPP concentrations decreased (p < 0.01) during corticosteroid pulse treatment, but rapidly returned to baseline after the treatment. No changes were observed in alkaline phosphatase and urinary excretion of calcium and hydroxyproline. Bone resorption measured by serum I-CTP and urinary excretion of Pyr and Dpyr was unchanged or decreased (p < 0.05-0.01), depending on the time of measurement and the parameter measured. CONCLUSIONS: In these patients with active RA, bone resorption was increased, while bone formation was within normal limits. During high dose corticosteroid pulse treatment, bone formation was only transiently decreased, while markers of bone resorption were unchanged or decreased. Because corticosteroid pulse treatment has only a short term negative effect on bone formation, and because it probably reduces bone resorption, at least partly as a result of the decreased disease activity, the effect of corticosteroid pulse treatment on bone may be assumed to be relatively mild.     

Risk Factors for Low Bone Mineral Density in Children and Adolescents with Inflammatory Bowel Disease

Objective To evaluate bone mineral density of the lumbar spine in children and adolescents with inflammatory bowel disease, and to identify the clinical risk factors associated with low bone mineral density. Methods Bone mineral density of the lumbar spine was evaluated using dual-energy X-ray absorptiometry (DXA) in 40 patients with inflammatory bowel disease. Patients were 11.8 (SD = 4.1) years old and most of them were male (52.5%). Multiple linear regression analysis was performed to identify potential associations between bone mineral density Z-score and age, height-for-age Z-score, BMI Z-score, cumulative corticosteroid dose in milligrams and in milligrams per kilogram, disease duration, number of relapses, and calcium intake according to the dietary reference intake. Results Low bone mineral density (Z-score bellow -2) was observed in 25% of patients. Patients with Crohn's disease and ulcerative colitis had equivalent prevalence of low bone mineral density. Multiple linear regression models demonstrated that height-for-age Z-score, BMI Z-score, and cumulative corticosteroid dose in mg had independent effects on BMD, respectively, beta = 0.492 (P = 0.000), beta = 0.460 (P = 0.001), beta = -0.014 (P = 0.000), and these effects remained significant after adjustments for disease duration, respectively, beta = 0.489 (P = 0.013), beta = 0.467 (P = 0.001), and beta = -0.005 (P = 0.015). The model accounted for 54.6% of the variability of the BMD Z-score (adjusted R (2) = 0.546). Conclusions The prevalence of low bone mineral density in children and adolescents with inflammatory bowel disease is considerably high and independent risk factors associated with bone mineral density are corticosteroid cumulative dose in milligrams, height-for-age Z-score, and BMI Z-score.     

Hormone replacement therapy prevents bone loss in patients with inflammatory bowel disease.

Patients with inflammatory bowel disease have an increased prevalence of osteoporosis, and suffer high rates of spinal bone loss. Hormone replacement therapy (HRT) is effective in the treatment and prevention of osteoporosis but has not been studied in patients with inflammatory bowel disease. A two year prospective study of HRT in inflammatory bowel disease was performed in 47 postmenopausal women aged 44 to 67 years with ulcerative colitis (25) or Crohn's disease (22). Patients had radial and spinal bone density measured annually by single photon absorptiometry and quantitative computed tomography respectively. The mean (95% confidence intervals) annual change in radial bone density was +1.42%/yr (+0.58 to +2.26; P < 0.005) and for spinal bone +2.60%/yr (+1.06 to +4.15; p < 0.005). There was no significant correlation between rates of change of bone density at the two sites, or between the rates of change and the initial bone density either in the radius or spine. Twelve patients were given prednisolone during the study, and their rates of change for spinal bone density were lower, but values were not statistically significantly different from those who did not receive corticosteroids. Changes in bone density for patients with ulcerative colitis and Crohn's disease were not significantly different. The change in bone density did not correlate with the patients' age or number of years after the menopause. It is concluded that HRT is effective in prevention of bone loss in postmenopausal women with inflammatory bowel disease.     

Can biochemical markers be used to screen patients with inflammatory bowel disease for osteoporosis?

Reduced bone mineral density has been reported in patients with inflammatory bowel disease and recent studies indicate that there is also an increase in the relative risk of fracture. Absolute risk of fracture is, however, generally low and thus measurement of bone mineral density as a screening procedure for all patients with inflammatory bowel disease may be inappropriate. In one study, urinary excretion of N-telopeptides, which reflects whole body bone resorption, was shown to be negatively related to bone mineral density, raising the possibility that this measurement could be used to select those in whom bone densitometry is required. However, the value of this approach in predicting fracture risk remains unproven and the relative contributions of clinical risk factors, biochemical markers of bone turnover and bone mineral density measurements to fracture risk in patients with inflammatory bowel disease require further study.     

Effect of a gluten free diet on osteopenia in adults with newly diagnosed coeliac disease.

BACKGROUND/AIMS: Calcium and vitamin D malabsorption in coeliac disease predispose to skeletal demineralisation. This study aimed to determine bone mineral density in patients studied in the first year after diagnosis of coeliac disease, and to detect changes in bone mineral density over the subsequent year. METHODS: Lumbar spine and femoral neck bone mineral density was measured in 21 adults with coeliac disease, diagnosed and started on a gluten free diet during the preceding year, with dual energy x ray absorptiometry and repeated after 12 months. RESULTS: Bone mineral density was significantly lower in patients than in paired controls (matched for age and sex), at lumbar spine (0.819 g/cm2 compared with 1.021 g/cm2, p < 0.001 Wilcoxon signed rank test) and femoral neck (0.663 g/cm2 compared with 0.794 g/cm2, p < 0.001). Repeat measurement after 12 months demonstrated that patients had a significant gain in bone mineral density at lumbar spine (16.6%/year), and femoral neck (15.5%/year, p < 0.002, Wilcoxon signed rank test at both sites), whereas no significant change in bone mineral density was detected in controls. CONCLUSIONS: Treatment of coeliac disease with a gluten free diet is associated with a significant increase in bone mineral density, although patients still had lower bone mineral density than controls.     

Mutifactorial analysis of risk factors for reduced bone mineral density in patients with Crohn＇s disease

AIM: To determine the prevalence of osteoporosis in a cohort of patients with Crohn's disease (CD) and to identify the relative significance of risk factors for osteoporosis. METHODS: Two hundred and fifty-eight unselected patients (92 M, 166 F) with CD were studied. Bone mineral density (BMD) was measured at the lumbar spine and hip by dual X-ray absorptiometry. Bone formation was assessed by measuring bone specific alkaline phosphatase (BSAP) and bone resorption by measuring urinary excretion of deoxypyridinoline (DPD) and N-telopeptide (NTX). RESULTS: Between 11.6%-13.6% patients were osteoporotic (T score < -2.5) at the lumbar spine and/or hip. NTX levels were significantly higher in the patients with osteoporosis (P < 0.05) but BSAP and DPD levels were not significantly different. Independent risk factors for osteoporosis at either the lumbar spine or hip were a low body mass index (P < 0.001), increasing corticosteroid use (P < 0.005), and male sex (P < 0.01). These factors combined accounted for 23% and 37% of the reduction in BMD at the lumbar spine and hip respectively. CONCLUSION: Our results confirm that osteoporosis is common in patients with CD and suggest that increased bone resorption is the mechanism responsible for the bone loss. However, less than half of the reduction in BMD can be attributed to risk factors such as corticosteroid use and low BMI and therefore remains unexplained.     

Osteoporosis in treated adult coeliac disease.

Forty five women and 10 men with coeliac disease diagnosed in adult life, who were already on a gluten free diet, had serial bone mineral density measurements at the lumbar spine and femoral neck over 12 months. Osteoporosis, defined as a bone mineral density (BMD) < or = 2 SD below the normal peak bone mass was found in 50% of male and 47% of female coeliac patients. Patients with a BMD < or = 2 SD below age and sex matched normal subjects, had a significantly lower body mass index (21.3 kg.m-2 compared with 25.2 kg.m-2, p < 0.02 Wilcoxon rank sum test) and lower average daily calcium intake (860 mg/day compared with 1054 mg/day, p < 0.05 Wilcoxon rank sum test) than patients with normal bone mineral density. In postmenopausal women with coeliac disease there was a strong correlation between the age at menopause and BMD at both the lumbar spine (r = 0.681, p < 0.01, Spearman's rank correlation) and femoral neck (r = 0.632, p < 0.01). No overall loss of bone was shown over the 12 months of follow up, and relative to the reference population there was a significant improvement in BMD at the lumbar spine in women (p < 0.025, paired t test) and at the femoral neck in men (p < 0.05, paired t test). There was a significant negative correlation between the annual percentage change in BMD at the lumbar spine and the duration of gluten free diet (r = -0.429, p<0.01, Spearman's rank correlation), with the largest gain in BMD in patients with most recently diagnosed coeliac disease. Osteoporosis was shown in 47% of patients with treated adult coeliac disease. Recognised risk factors for osteoporosis in the general population including low body mass index, dietary calcium intake, and early menopause are particularly important in coeliac disease. Treatment of coeliac disease with a gluten free diet probably protects against further bone loss, and in the early stages is associated with a gain in bone mineral density.     

Bone mineral density and nutritional status in children with chronic inflammatory bowel disease

Background—Osteoporosis has been reported inadult patients with inflammatory bowel disease.
Aims—To evaluate bone mineral density (BMD),nutritional status, and determinants of BMD in children withinflammatory bowel disease.
Patients—Fifty five patients (34 boys and 21 girls, age range 4-18) were studied; 22 had Crohn's disease and 33 ulcerative colitis.
Methods—Lumbar spine and total body BMD, and bodycomposition were assessed by dual energy x rayabsorptiometry (DXA). Results were expressed as standard deviationscores (SDS). Lean body mass was also assessed by bioelectricalimpedance analysis (BIA). Yearly measurements during two years wereperformed in 21patients.
Results—The mean SDS of lumbar spine BMD andtotal body BMD were significantly lower than normal (−0.75 and−0.95, both p<0.001). Height SDS and body mass index SDS were alsodecreased. The decrease in BMD SDS could not be explained by delay inbone maturation. The cumulative dose of prednisolone correlatednegatively with lumbar spine BMD SDS (r=−0.32, p<0.02).Body mass index SDS correlated positively with total body BMD SDS(r=0.36, p<0.02). Patients with Crohn's disease hadsignificantly lower lumbar spine and total body BMD SDS than patientswith ulcerative colitis, even after adjustment for cumulative dose ofprednisolone. In the longitudinal data cumulative dose of prednisolonebetween the measurements correlated negatively with the change inlumbar spine and total body BMD SDS. Lean tissue mass measured by DXAhad a strong correlation with lean body mass measured by BIA(r=0.98).
Conclusions—Children with inflammatory boweldisease have a decreased BMD. Children with Crohn's disease have ahigher risk of developing osteopaenia than children with ulcerativecolitis. Corticosteroid therapy and nutritional status areimportant determinants of BMD in these patients.

Keywords:bone mineral density; inflammatory bowel disease; children; nutritional status; corticosteroid treatment; bodycomposition

     

Decreased axial bone mineral density in perimenopausal women with rheumatoid arthritis--a population based study.

OBJECTIVES--Although periarticular osteoporosis is a well-recognised phenomenon in rheumatoid arthritis (RA), there is considerable controversy over whether RA is associated with more generalised osteoporosis. The aetiology of this bone loss is probably multifactorial, including both life-style risk factors and disease-related determinants. Population-based studies on bone mineral density (BMD) in RA have not previously been conducted, and the purpose of the present cross-sectional population-based study was to determine whether patients with RA are at an increased risk of having osteoporosis. Furthermore, the determinants of BMD in RA patients were investigated. METHODS--BMD at the spine and femoral neck was measured in 143 women with RA. The control group consisted of 1611 women with no disease or taking any drugs known to affect bone metabolism. The study population was a random stratified sample from the Kuopio Osteoporosis Study, which included all perimenopausal women aged 47-56 years residing in Kuopio Province, Eastern Finland in 1989 (n = 14,220). The mean age of the patients at the time of densitometry was 53.7 years. RESULTS--The mean (SD) spinal and femoral neck BMD was significantly lower in patients with RA compared with controls [spine: 1.067 (0.161) v 1.129 (0.157) g/cm2, p < 0.001; femoral neck: 0.851 (0.136) v 0.932 (0.123) g/cm2, p < 0.001]. Analysis of variance showed that at the spine the difference was significant only in patients having corticosteroid treatment, whereas at the femoral neck patients with non-steroid treatment also had significantly lower BMD. When confounding factors were corrected, no significant difference could be found between non-steroid and corticosteroid treated patients with RA, suggesting that the independent effect of corticosteroids on BMD is only minimal. Multiple regression analysis found age, weight and functional grade to be significant predictors of spinal BMD (R2 = 0.403, p < 0.001). In the femoral neck weight, cumulative corticosteroid dose and functional grade were significant predictors of BMD (R2 = 0.410, p < 0.001). CONCLUSIONS--RA is associated with generalised osteoporosis. The physical impairment and body weight are the major determinants of both spinal and femoral bone mass in RA patients. The cumulative corticosteroid dose was also a significant determinant of femoral neck BMD. However, the independent effect of corticosteroids is questionable because the use of corticosteroids may be an indicator of more severe disease.     

Femoral neck osteopenia in patients with inflammatory bowel disease

Objective: The mechanism of bone loss in patients with inflammatory bowel disease (IBD) is not completely understood. The aim of this study was to assess indices of bone turnover and bone mineral density (BMD) in the lumbar spine and femoral neck in IBD patients.
Methods: Sixty-three patients with Crohn's disease and 41 with ulcerative colitis were studied. Serum bone-specific alkaline phosphatase (B-ALP), osteocalcin, parathyroid hormone (PTH), 25 hydroxyvitamin D, interleukin-6 (IL-6), and urinary N-telopeptide cross linked type 1 collagen (NTX) were determined. BMD of the lumbar spine and femoral neck was determined by dual x-ray absorptiometry in 59 patients.
Results: In the femoral neck 42% of the patients had osteopenia (−2.5 SD < BMD T score < −1 SD) and another 41% had osteoporosis (BMD T score < −2.5). In the spine 34% of the patients had osteopenia and additional 42% had osteoporosis. BMD T scores were lower in the femoral neck compared to the spine. Reduced BMD was unrelated to gender, disease type, lifetime corticosteroid dose, but inversely correlated with disease duration ( r =−0.36 , p < 0.05 ). Serum IL-6 was higher in IBD patients compared to controls. A reduced level of osteocalcin, a marker of bone formation, was present in 7% of patients and an increase in NTX, a marker of bone resorption, in 25% of them. Osteoporotic IBD patients (spine or hip BMD T score < −2.5) had increased serum IL-6, osteocalcin and PTH level compared to nonosteoporotic patients.
Conclusions: There is a high prevalence of reduced BMD at the spine and femoral neck in IBD patients, which is more severe in the hip. Bone turnover in osteoporotic IBD patients is associated with an increase in osteocalcin, PTH and IL-6. IL-6 may play a role in the pathogenesis of bone loss in IBD.     

Bone mineral density evaluation in inflammatory bowel disease patients

BACKGROUND: Inflammatory bowel disease patients have shown greater reduction of the bone mineral density compared to healthy people. AIM: To evaluate the bone mineral density in a population of patients with inflammatory bowel disease. METHODS: Ninety patients from 20 to 50 years old, of the Inflammatory Bowel Disease Ambulatory of the Gastroenterology Service of the Clinics Hospital, Curitiba, PR, Brazil, were selected for the evaluation. From those, 76 completed all the stages of the evaluation. The densitometry was made from lumbar column and right femur with a dual-energy x-ray absorptiometry (Hologyc QDR 1000/W) device. RESULTS: The inflammatory bowel disease patients had a significant reduction of the bone mineral density in all the evaluated parts, femur neck, total femur and lumbar column. The analysed variables, disease activity index, usage of corticoids, the lack of physical activities, the index body mass and previous surgeries did not have influence in the results. CONCLUSION: Reduced bone mineral density was founded in inflammatory bowel disease patients of the Clinics Hospital, mainly in the Crohn's disease patients, as described in literature. None analyzed variables had significant correlation to the bone mineral density.     

Reversal of osteopenia with diet in adult coeliac disease.

To evaluate the effects of a gluten free diet on bone mineral density in untreated adult patients with coeliac disease, 63 patients (17-79 years, 35 women) were examined at diagnosis and after one year taking a gluten free diet. Bone mineral density was measured in the forearm using single photo absorptiometry and in the lumbar spine, femoral neck, and trochanter using dual energy x ray absorptiometry. The values for each patient were compared with those of 25 healthy controls, matched for sex, age, and menopausal state. Before being given a gluten free diet bone mineral density in the total group was reduced at all sites (p < 0.001). Age adjusted bone mineral density was inversely correlated with age. During the first year taking a gluten free diet bone mineral density increased at all sites (p < 0.01). This was seen in patients of all ages and in patients who were without symptoms of malabsorption (weight loss or diarrhoea) before treatment. Low bone mineral density in patients with untreated coeliac disease increases rapidly when treatment with a gluten free diet is followed. These findings emphasise the importance of early diagnosis and treatment in all patients with coeliac disease.     

Bone mineral density is reduced in patients with Crohn''s disease but not in patients with ulcerative colitis: a population based study.

BACKGROUND: Patients with inflammatory bowel disease are at risk of developing metabolic bone disease. AIMS: To compare bone mineral density in patients with Crohn's disease with patients with ulcerative colitis and healthy subjects, and to evaluate possible risk factors for bone loss in inflammatory bowel disease. PATIENTS: 60 patients with Crohn's disease, 60 with ulcerative colitis, and 60 healthy subjects were investigated. Each group consisted of 24 men and 36 women. METHODS: Lumbar spine, femoral neck, and total body bone mineral density were measured by dual x ray absorptiometry (DXA), and Z scores were obtained by comparison with age and sex matched normal values. RESULTS: Mean Z scores were significantly lower in patients with Crohn's disease compared with patients with ulcerative colitis and healthy subjects. Patients with ulcerative colitis had bone mineral densities similar to healthy subjects. Use of corticosteroids, body mass index (BMI), and sex were significant predictor variables for bone mineral density in Crohn's disease. In ulcerative colitis only body mass index and sex were of significant importance. Disease localisation and small bowel resections had no influence on bone mineral density in patients with Crohn's disease. CONCLUSIONS: Patients with Crohn's disease have reduced bone mineral density. Several factors are probably involved, but the reduction is associated with corticosteroid therapy. When studying skeletal effects of inflammatory bowel disease, patients with Crohn's disease and those with ulcerative colitis should be evaluated separately.     

Androgen deficiency and bone mineral density in men with rheumatoid arthritis

OBJECTIVE: To investigate the prevalence of osteopenia/osteoporosis in a group of men with rheumatoid arthritis (RA); and to analyze the relationship between sex hormone status and bone mineral density (BMD), taking into account disease activity, disease duration, and corticosteroid intake. METHODS: Clinical and demographic details were collected on 50 consecutive men with RA. BMD at the lumbar spine and femoral neck were measured, together with plasma concentrations of testosterone, sex hormone binding globulin, and luteinizing hormone. RESULTS: The median age of patients was 67 years, with median disease duration 20 years. Fourteen patients had never been treated with oral corticosteroids, the remaining 36 received a range of prednisone doses over prolonged periods. Plasma testosterone concentration was moderately reduced in 40% (< 10 nmol/l) and severely reduced in 6% of men (< 8 nmol/l), but androgen deficiency was not related to bone density or fractures. Spinal and femoral neck BMD was reduced in 38 and 71% of the men, respectively. Femoral neck BMD was related to age, weight, disability status, and specific disease activity scores. The only predictors of spinal BMD were pack-years of smoking and physician global assessment. CONCLUSION: Reduced BMD is common among men with RA. The predictors for spine and femoral neck BMD bear little direct relationship to blood testosterone concentrations despite the relatively high prevalence of low testosterone concentrations in this population. These findings are more consistent with the possibility that low testosterone concentrations in men with RA are a bystander effect of systemic inflammatory disease.     

Reduced bone mineral density in human immunodeficiency virus-infected patients and its association with increased central adiposity and postload hyperglycemia

Reduced bone mineral density (BMD) and abnormalities in fat redistribution, glucose homeostasis, and lipid metabolism are prevalent among HIV-infected patients on highly active antiretroviral therapy (HAART). The relationship between the metabolic and skeletal complications of HIV is unclear. Fifty-one HIV patients on HAART (aged 30-54 yr, 86% male) and 21 HIV-negative control subjects (aged 31-51 yr, 82% male) were examined with oral glucose tolerance testing, a fasting lipid profile, and dual x-ray absorptiometry, and markers of bone formation (serum osteocalcin) and resorption (urinary deoxypyridinoline). HIV-infected subjects had a higher prevalence of either osteopenia or osteoporosis (World Health Organization criteria) at the spine, hip, or forearm, compared with HIV-negative controls (63% vs. 32%, P = 0.02) and evidence of increased bone resorption (urine deoxypyridinoline, 14.7 +/- 6.5 vs. 10.9 +/- 2.5 nmol/mmol creatinine, P = 0.012). Among the HIV-infected patients, those with reduced bone mineral density (n = 32) were similar to the group with normal BMD (n = 19) in the use of protease inhibitors, duration of HAART therapy, or other demographic variables. Plasma glucose 2 h after a glucose load (odds ratio 1.02 per 1 mg/dl increase, 95% confidence interval 1.01-1.05, P = 0.009) and central adiposity (trunk fat/total fat) (odds ratio 1.09 per 1% ratio increase, 95% confidence interval 1.00-1.18, P = 0.012) were associated with reduced BMD. These associations remained significant in a multivariate model including age and body mass index. Bone resorption was associated with female gender (P < 0.001) and non-high-density lipoprotein cholesterol (P = 0.034) in a multivariate linear regression model controlling for age, body mass index, protease inhibitor use, duration of HAART, and extremity fat. Reduced BMD is prevalent in HIV-infected patients on HAART and is related to central adiposity and postload hyperglycemia. Bone resorption is independently associated with female gender and dyslipidemia. HIV-infected patients with metabolic abnormalities may represent a population that would benefit from bone density screening.     

Metabolic bone disease in IBD

A substantial number of patients with inflammatory bowel disease (IBD) will manifest extra-intestinal complications. Metabolic bone disease and arthropathies are among the most debilitating of these. Decreased bone mineral density and increased fracture risk may occur in relation to the underlying disease itself or result from vitamin, mineral, and hormonal deficiencies; medications used to treat the underlying disease; lifestyle; and perhaps other factors. In many cases, the factors remain unidentified. Options for the treating clinician include correction of these deficiencies, treatment of the underlying disease, and use of medication to promote bone formation and decrease bone resorption.     

Low bone mineral density in patients with inflammatory bowel disease

To assess the prevalence and risk factors for low bone mineral density in inflammatory bowel disease, we studied 61 consecutive patients, mean age 36±11 years. Twenty-seven had a Crohn's disease and 34 ulcerative colitis (including 13 with ileoanal anatomosis). Three patients, two women and one man (32, 70, and 45 years old, respectively) had vertebral crush fractures. Bone mineral density measured by dual energy x-ray absorptiometry at spine and femoral level was more than 2sd below normal values in 23% of the patients, all of them having received steroid therapy. Eighteen patients (29%) had never received steroid therapy; their bone mineral density was not different than those who had. Univariate analysis showed a positive correlation between bone mineral density and body weight or oral calcium intakes, and a negative correlation with steroid daily dose. After ileoanal anastomosis, bone mineral density was not different from other groups and showed a positive correlation with time elapsed since coloproctectomy. We concluded that bone mineral density is low in patients with inflammatory bowel disease and exposes them to the risk of bone fracture. Bone mineral density after ileoanal anastomosis may increase with time after surgery.     

老年门诊人群骨密度和糖脂代谢指标的相关性研究

目的 观察老年门诊人群骨密度和糖脂代谢指标的相关性.方法 老年门诊就诊的60岁及以上患者196例,采用骨密度超声分析仪（QUS）对其进行骨密度的测定,根据检测结果分为骨量正常组、骨量减少组和骨质疏松组.并对患者进行问卷调查,包括年龄、身高、体重、疾病史以及空腹血糖、糖化血红蛋白、血脂、血钙、血磷、骨转换指标测定,分析老年骨质疏松的影响因素及和糖脂代谢指标的相关性.结果 空腹血糖、糖化血红蛋白、Ⅰ型胶原羧基端肽β特殊序列、25-羟维生素D3与骨密度T值呈相关关系（P分别为0.000,0.004,0.015,0.018;相关系数分别为-0.320,-0.207,-0.173,0.169）,进一步的多因素分析显示,空腹血糖与老年骨量下降呈相关性（P=0.011,相对危险度1.709,95％可信区间1.133 ～ 2.579）.伴有糖尿病的骨质疏松患者Ⅰ型胶原羧基端肽β特殊序列高于非糖尿病组（P =0.029）,而骨痛症状却较少（P=0.013）.结论 空腹血糖是老年门诊人群骨密度下降的危险因素.高血糖患者较易患骨质疏松,其骨代谢改变特点是：骨形成下降、骨吸收增加.在治疗2型糖尿病的同时,对老年人早期进行骨密度测定有重大意义.