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.     

Osteoporosis and Determinants of Bone Density in Patients with Crohn's Disease

Low bone mineral density (BMD) is common inpatients with Crohn's disease; however, the pathogenesisof bone loss and risk factors for osteoporosis are notestablished. Our aim was to evaluate the clinical, dietary, and nutritional determinants of BMD inCrohn's disease. A cross-sectional analysis of 117patients with Crohn's disease was undertaken. Allpatients underwent a clinical and dietary evaluation including assessment of nutritional state andlife-style. BMD was measured at the hip and lumbar spineby dual-energy x-ray absorptiometry; and z scoresobtained by comparison with age- and sex-matched normal values for the healthy UK population.Multiple regression analysis was used to assessassociations between BMD and potential risk factors,allowing for possible confounding variables. Thirteen(11%) patients had osteoporosis (z score<–2), with osteopenia (z score <–1,>–2) in a further 34 (29%). Patients withjejunal disease had significantly lower BMD at the spine(P = 0.03) and femoral neck (P = 0.02) than those with disease atother sites. Mean BMD was significantly lower at the hipof patients with previous bowel resection (diff in means= 0.53, 95% CI-0.97, –0.08, P = 0.02), but type of surgery was not significant. Active disease,menstrual history, diet, level of physical activity, andsmoking were not associated with low bone mass. At thelumbar spine, body weight (P < 0.0001), male sex (P < 0.0001), and currentprednisolone use (P < 0.02) were independentlypredictive of low bone mass. Body weight (P <0.0001), male sex (P < 0.0001), and cumulativesteroid dose (P = 0.02) were predictive at the femoralneck. The major determinants of BMD in Crohn's diseaseare body weight, current steroid use, and cumulativesteroid dose. Men with Crohn's disease are at greatest risk of osteoporosis, with jejunal involvementand previous bowel resection also contributing to thelow bone mineral density.     

Longitudinal study of cortical bone loss in patients with inflammatory bowel disease.

Bone mineral density of the radius was measured by single-photon absorptiometry in 50 patients with inflammatory bowel disease. Thirty-three had Crohn's disease and 17 ulcerative colitis; 25 were women. The mean age was 45 years (range, 18-70 years). Measurements were repeated in 39 of them after a mean follow-up period of 7.9 years (range, 7.1-8.2 years). In female patients the mean (95% confidence interval) annual change in radial bone mineral density was -0.74% (-1.34% to -0.14%) (P = 0.022), the greatest bone loss occurring in postmenopausal women (mean, -1.16% (-2.01% to -0.30%)). In male patients the mean annual rate of bone loss was -0.07% (-0.41% to 0.28%) (P = NS). Patients with abnormally low values at the first measurement remained osteopenic at the second measurement, whilst some others with normal values initially showed increased rates of bone loss and had a subnormal bone mineral density after the follow-up period. These results show increased rates of cortical bone loss in some patients with inflammatory bowel disease and emphasize the need to monitor bone mass in these patients so that prophylactic measures can be instituted.     

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.     

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.     

Bone mineral density in patients with recently diagnosed inflammatory bowel disease

BACKGROUND & AIMS: A high prevalence of osteoporosis is reported in inflammatory bowel disease (IBD), and its pathogenesis is not completely resolved. We investigated whether bone mineral density (BMD) in patients with IBD at diagnosis is lower than in population controls, and whether BMD differs between patients with Crohn's disease and those with ulcerative colitis. METHODS: In 68 patients and 68 age- and gender-matched population controls, BMD of total body, spine, and hip was assessed using dual-energy x-ray absorptiometry within 6 months after establishing the diagnosis. Determinants for low BMD were assessed. RESULTS: There were no significant differences in BMD (g/cm(2)) between patients and controls, and no significant differences in BMD between patients with either Crohn's disease or ulcerative colitis. Multivariate regression analysis showed that duration of complaints longer than 6 months before diagnosis (P = 0.041), age (P = 0.019), and body mass index less than 20 kg/m(2) (P = 0.006) significantly correlated with low BMD. CONCLUSIONS: BMD in patients with recently diagnosed IBD was not significantly decreased compared with population controls. Subsequent development of osteoporosis in patients with IBD seems to be a phenomenon related to the disease process and/or the treatment modalities of IBD.     

Skeletal morbidity in inflammatory bowel disease

Patients with Crohn's disease are at increased risk of developing disturbances in bone and mineral metabolism because of several factors, including the cytokine-mediated nature of the inflammatory bowel disease, the intestinal malabsorption resulting from disease activity or from extensive intestinal resection and the use of glucucorticoids to control disease activity. Inability to achieve peak bone mass when the disease starts in childhood, malnutrition, immobilization, low BMI, smoking and hypogonadism may also play a contributing role in the pathogenesis of bone loss. The relationship between long-term use of glucocorticoids for any disease indication and increased risk for osteoporosis and fractures is well established. However, the relationship between Crohn's disease and ulcerative colitis and bone loss remains controversial. Depending on the population studied the prevalence of osteoporosis has thus been variably reported to range from 12 to 42% in patients with inflammatory bowel disease (IBD). In IBD most studies demonstrate a negative correlation between bone mineral density (BMD) and glucocorticoid use, but not all authors agree on the relationship between long-term glucocorticoid use and continuing bone loss. Whereas prospective studies do suggest sustained bone loss at both trabecular and cortical sites in long-term glucocorticoid users with inflammatory bowel disease, a decrease in bone mass is also observed in patients with active Crohn's disease not using glucocorticoids, and bone loss is not universally observed in patients with Crohn's disease using orally or rectally administered glucocorticoids. Data on vertebral fractures are scarce and there is no agreement about the risk of non-vertebral fractures in patients with Crohn's disease, although it has been suggested that non-vertebral fracture risk may be increased by up to 60% in patients with IBD. A recent publication reports an increased risk of hip fractures in Crohn's disease related to current and cumulative corticosteroid use and use of opiates, although these fractures could not be related to the severity of osteoporosis. The issue of the magnitude of the problem of osteoporosis has become particularly relevant in Crohn's disease, since the ability of therapeutic interventions to beneficially influence skeletal morbidity has been clearly established in patients with osteoporosis, whether post-menopausal women, men or glucocorticoid users. The main question that arises is whether all patients with Crohn's disease should be treated with bone protective agents on the assumption that they all have the potential to develop osteoporosis or whether the use of these agents should be restricted to patients clearly at risk of osteoporosis and fractures, providing these can be identified. We recommend, based on the available literature and our own experience, that all patients with Crohn's disease should be screened for osteoporosis by means of a bone mineral density measurement in addition to full correction of any potential calcium and vitamin D deficiency, to allow timely therapeutic intervention of the patient at risk while sparing the vast majority unnecessary medical treatment.     

炎症性肠病并发低骨量/骨质疏松的危险因素分析

目的 对炎症性肠病(IBD)患者的骨密度状况进行评估,探讨其下降的危险因素.方法 通过对IBD患者血液学指标、身高、体重及腰椎骨密度进行测量,并与健康志愿者比较,分析IBD患者骨质疏松的危险因素.结果 共收集克罗恩病(CD)77例,溃疡性结肠炎(UC)43例,37例健康志愿者作为对照组.CD组、UC组及对照组的腰椎骨质的T值分别为-1.72±1.20、-1.26±1.12和-0.62±0.87,CD组的T值低于UC组(P=0.045)和对照组(P=0.000),UC组T值低于对照组(P=0.014).CD组、UC组及对照组的腰椎骨质疏松的发生率分别为23.3%、14.0%和0;CD组的腰椎骨质疏松发生率高于对照组,差异有统计学意义(P=0.003);UC组的腰椎骨质疏松发生率有高于对照组的趋势,但差异无统计学意义(P=0.053).多元回归分析显示,低体重(BMI≤18.4kg/m~2)是CD(OR=11.25,95%CI 3.198～39.580,P=0.000)和UC(OR=14.50,95%CI 1.058～88.200,P=0.045)患者骨质疏松的危险因素.年龄、病程、病变部位、CD活动指数(CDAI)、服用糖皮质激素、服用免疫抑制剂、血清25-羟基维生素D浓度等因素与骨质疏松的发生无相关性.结论 骨密度下降的发生在IBD患者中较为普遍,低体重是IBD患者骨质丢失的危险因素.     

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.     

Bones and Crohn's: risk factors associated with low bone mineral density in patients with Crohn's disease

Previous studies have confirmed that the prevalence of decreased bone mineral density is elevated in patients with inflammatory bowel disease. The objective of the current study was to determine the prevalence of osteopenia and osteoporosis in a cross-sectional outpatient population of 242 adult patients with Crohn's disease and to determine which clinical characteristics and serum and urine biochemical factors might be predictive of bone loss. Thirty-seven percent had normal bone density, 50.0% were osteopenic, and 12.9% were osteoporotic. Among the sites used to diagnose low bone mineral density, the femoral neck demonstrated the highest prevalence of osteopenia and the ultra-distal radius the highest prevalence of osteoporosis. However, low bone mineral density at one site was always predictive of low bone mineral density at the other. Corticosteroid use during the year before assessment was found to be consistently predictive of low bone mineral density in males but not in females. In contrast, low body mass index and high platelet counts were consistently predictive of low bone mineral density in females but not in males. Disease location, smoking, and age were not predictive of changes in bone mineral density.     

Gender, age, and body weight are the major predictive factors for bone mineral density in Crohn's disease: a case-control cross-sectional study of 113 patients

OBJECTIVE: We conducted this study to assess bone mineral density and to evaluate conceivable predictive factors for bone loss in patients with Crohn's disease. METHODS: One hundred-thirteen patients with Crohn's disease and 113 healthy subjects, individually matched for gender, age, and body weight were investigated. The group consisted of 68 women and 45 men. The median duration of Crohn's disease was 6 yr. Two-thirds of the patients had been subjected to intestinal resection. Seventy-seven percent had at some time been treated with corticosteroids. Bone mineral density in the lumbar spine, the hip, and the total body skeleton was measured by dual-energy X-ray absorptiometry (DEXA). RESULTS: In patients with Crohn's disease bone mineral density was not different from that of healthy controls except for a regional decrease in bone mineral density of the hip in female patients. The strongest predictors of bone mineral density were gender, age, and body weight. Corticosteroid use was only a weak predictor of diminished bone density. Duration of disease and intestinal resection had no predictive value for bone mineral density. CONCLUSIONS: Gender, age, and body weight are the major determinants of bone mineral density in patients with Crohn's disease. As in healthy individuals, the combined effect of these factors account for up to 50% of the variability in bone mineral density.     

Low serum and bone vitamin K status in patients with longstanding Crohn's disease: another pathogenetic factor of osteoporosis in Crohn's disease?

BACKGROUND: A high prevalence of osteoporosis is reported in Crohn's disease. The pathogenesis is not completely understood but is probably multifactorial. Longstanding Crohn's disease is associated with a deficiency of fat soluble vitamins, among them vitamin K. Vitamin K is a cofactor in the carboxylation of osteocalcin, a protein essential for calcium binding to bone. A high level of circulating uncarboxylated osteocalcin is a sensitive marker of vitamin K deficiency. AIMS: To determine serum and bone vitamin K status in patients with Crohn's disease and to elucidate its relationship with bone mineral density. METHODS: Bone mineral density was measured in 32 patients with longstanding Crohn's disease and small bowel involvement, currently in remission, and receiving less than 5 mg of prednisolone daily. Serum levels of vitamins D and K, triglycerides, and total immunoreactive osteocalcin, as well as uncarboxylated osteocalcin ("free" osteocalcin) were determined. The hydroxyapatite binding capacity of osteocalcin was calculated. Data were compared with an age and sex matched control population. RESULTS: Serum vitamin K levels of CD patients were significantly decreased compared with normal controls (p<0.01). "Free" osteocalcin was higher and hydroxyapatite binding capacity of circulating osteocalcin was lower than in matched controls (p<0.05 and p<0.001, respectively), indicating a low bone vitamin K status in Crohn's disease. In patients, an inverse correlation was found between "free" osteocalcin and lumbar spine bone mineral density (r=-0.375, p<0.05) and between "free" osteocalcin and the z score of the lumbar spine (r=-0.381, p<0.05). Multiple linear regression analysis showed that "free" osteocalcin was an independent risk factor for low bone mineral density of the lumbar spine whereas serum vitamin D was not. CONCLUSIONS: The finding that a poor vitamin K status is associated with low bone mineral density in longstanding Crohn's disease may have implications for the prevention and treatment of osteoporosis in this disorder.     

Osteoporosis and inflammatory bowel disease: prevalence and risk factors in Tunisian patients

OBJECTIVES: The study was aimed to evaluate osteoporosis prevalence in a group of Tunisian patients with inflammatory bowel disease (IBD), to determine its risk factors, and to describe its mechanisms. SUBJECTS AND METHODS: We included 67 IBD patients, 43 patients with Crohn's disease (CD) and 24 with ulcerative colitis (UC). Bone mineral density was measured at the lumbar spine and left femoral neck by dual-energy X-ray absorptiometry. We used T score to express bone loss (osteopenia: -2.5 SD 2 years and active disease tended to be associated with lumbar osteoporosis; the ORs were respectively 4.87 [0.92-25.80] (P=0.06), 4.21 [0.87-20.57] (P=0.06), and 2.33 [0.78-6.67] (P=0.13). No association was found with cumulated dose of steroids even when considering only CD. Patients with osteoporosis showed significant increased CrossLaps and interleukin-6 levels that indicate both high bone resorption and inflammatory activity. CONCLUSIONS: Osteoporosis is frequent in IBD patients, especially in CD patients. Female gender, malnutrition (body mass index <20 kg/m2), disease course (> 2 years) and active disease would be risk factors of bone mineral loss in IBD. Osteoporosis is associated with enhanced bone resorption, that seems be linked to excessive intestinal inflammation.     

Longitudinal Study of Cortical Bone Loss in Patients with Inflammatory Bowel Disease

Bone mineral density of the radius was measured by single-photon absorptiometry in 50 patients with inflammatory bowel disease. Thirty-three had Crohn's disease and 17 ulcerative colitis; 25 were women. The mean age was 45 years (range, 18–70 years). Measurements were repeated in 39 of them after a mean follow-up period of 7.9 years (range, 7.1–8.2 years). In female patients the mean (95% confidence interval) annual change in radial bone mineral density was -0.74% (-1.34% to -0.14%) (P = 0.022), the greatest bone loss occurring in postmenopausal women (mean, -1.16% (-2.01% to -0.30%)). In male patients the mean annual rate of bone loss was -0.07% (-0.41% to 0.28%) (P = NS). Patients with abnormally low values at the first measurement remained osteopenic at the second measurement, whilst some others with normal values initially showed increased rates of bone loss and had a subnormal bone mineral density after the follow-up period. These results show increased rates of cortical bone loss in some patients with inflammatory bowel disease and emphasize the need to monitor bone mass in these patients so that prophylactic measures can be instituted.     

Increased rate of spinal trabecular bone loss in patients with inflammatory bowel disease.

The rate of spinal trabecular bone loss during one year was measured in 54 patients with inflammatory bowel disease. The mean change in spinal bone mineral content was -5.1 mg/ml K2HPO4, representing 3% of the initial bone mineral content. The rate of bone loss showed a significant negative correlation with body mass index (r = -0.276, p less than 0.05) but no other significant correlations were found with other clinical or biochemical indices, including the total amount of prednisolone taken during the course of the study. Eleven patients had bone loss greater than 15 mg/ml/year; these included four non-steroid treated patients, two of whom had disease confined to the large bowel. The results indicate rapid rates of bone loss in some patients with inflammatory bowel disease over the course of one year. Although steroid therapy and malnutrition are likely to be contributory factors in some patients, other, as yet unidentified, risk factors also operate. The rapid bone loss observed in some patients emphasises the need for effective prophylactic regimes.     

Increase of bone mineral density with sodium fluoride in patients with Crohn's disease

BACKGROUND AND AIMS: Low bone density with an increased risk of vertebral fractures is a frequent complication in inflammatory bowel disease. Since the aetiology of osteopathia in these patients is different compared to postmenopausal or steroid-induced osteoporosis, no treatment strategy is established. Supplementation of calcium and vitamin D has been shown to prevent further bone loss, but no data are available showing the anabolic effect of sodium fluoride in Crohn's disease. METHODS: We carried out a one-year prospective clinical trial in 33 patients with chronic active Crohn's disease who were randomly assigned to receive either calcium (500 mg b.i.d.) and 1000 IU vitamin D3 only, or retarded-release sodium fluoride (25 mg t.i.d.) additionally. The diagnosis of Crohn's disease had been made at least two years ago, and all patients had received systemic high-dose steroid therapy during the previous year. Eleven of 15 patients who received calcium/vitamin D and 15 of 18 patients who additionally received sodium fluoride completed the study. The primary endpoint of the study was the increase of bone mineral density, measured by dual energy X-ray absorptiometry (DXA) after one year of treatment. Bone-specific alkaline phosphatase and osteocalcin were used as markers for bone turnover. RESULTS: In the calcium/vitamin D only group, bone density was not significantly changed after one year of treatment, whereas in the calcium/vitamin D/fluoride group, bone density of the lumbar spine increased from -1.39+/-0.3 (Z-score, mean +/- SEM) to -0.65+/-0.3 (P<0.05) after one year of treatment. Increase of bone density was positively correlated to the osteoblastic markers bone-specific alkaline phosphatase (r = 0.53) and osteocalcin (r = 0.43). CONCLUSIONS: Sodium fluoride in combination with vitamin D and calcium is an effective, well-tolerated and inexpensive treatment to increase lumbar bone density in patients with chronic active Crohn's disease and osteoporosis.     

Bone loss associated with gastrointestinal disease: prevalence and pathogenesis

Decreased bone mineral density is a frequent finding in gastrointestinal disease. Factors contributing to this are (1) malabsorption of vitamin D, calcium and possibly vitamin K and other nutrients; (2) treatment with glucocorticoids; (3) inflammatory cytokines in inflammatory bowel disease; and (4) hypogonadism induced by gastrointestinal disease. A low bone mineral density has been reported in (1) patients who have undergone gastrectomy (27-44% with Z-scores of < -1); (2) pernicious anaemia; (3) coeliac disease (8-22% with Z-scores of < -2); (4) Crohn's disease (mean 32-38% with Z-scores of < -1); and (5) ulcerative colitis (mean 23-25% with Z-scores of < -1). Reduced bone mineral density is thus prevalent in these individuals and is compounded by age related bone loss, leading to the development of severe bone disease in some patients.     

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.     

Treatment with infliximab is associated with increased markers of bone formation in patients with Crohn's disease

OBJECTIVE: Osteoporosis is a common complication of Crohn's disease (CD). Glucocorticoid use and detrimental effects of inflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha) can lead to osteoporosis. The aim of this study was to assess the ability of treatment with the TNF-alpha antagonist infliximab to increase bone formation as measured by surrogate markers of bone turnover in patients with active CD. METHODS: Sera from 38 prospectively enrolled CD patients were examined for levels of bone alkaline phosphatase (BAP), N-telopeptide of type I collagen (NTX), immunoreactive parathyroid hormone (iPTH), calcium, and pro-inflammatory cytokines at baseline and 4 weeks following infliximab infusion. Crohn's Disease Activity Index (CDAI), Inflammatory Bowel Disease Questionnaire (IBDQ), and glucocorticoid dose also were collected. RESULTS: In this cohort, CDAI and IBDQ scores were significantly improved at week 4 (P<0.001). Infliximab therapy was associated with an increase in BAP, a marker of bone formation (P=0.010), whereas NTX, a marker of bone resorption, was not increased (P=0.801). Among 22 patients who were taking glucocorticoids, mean glucocorticoid dose decreased 36% (P<0.001; -7.9 mg). CONCLUSIONS: Treatment with infliximab was associated with increased markers of bone formation (BAP) without increasing bone resorption (NTX). This effect may be due to a beneficial effect of TNF-alpha blockade on bone turnover, a beneficial effect on CD activity resulting in decreased glucocorticoid dose, or both. Studies of longer duration are needed to assess the effect of infliximab on bone mineral density.