Osteoporosis in patients with inflammatory bowel disease.

Bone mineral content in spinal trabecular and peripheral cortical bone was measured in 75 unselected patients with small and/or large intestinal inflammatory bowel disease. Osteoporosis, defined as a bone mineral content greater than 2 SD below the age and sex matched normal mean value was present in 23 patients (30.6%). Three amenorrhoeic females aged 34, 38, and 42 years had severe clinical osteoporosis and a further three patients had one or more vertebral crush fractures. Eighteen of the 23 patients with osteoporosis had small intestinal disease with one or more resections and the mean lifetime steroid dose in those with osteoporosis was significantly higher than in those with normal bone mineral content. Bone mineral content in spinal trabecular bone showed significant negative correlations with lifetime steroid dose and serum alkaline phosphatase and a significant positive correlation with serum albumin. Peripheral cortical bone mineral content was positively correlated with body weight, height and body mass index. We conclude that the prevalence of osteoporosis is increased in patients with inflammatory bowel disease, severe clinical osteoporosis developing in some relatively young patients. The pathogenesis of this bone loss is probably multifactorial; steroid therapy is likely to be an important contributory factor.     

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.     

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.     

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.     

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.     

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.     

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.     

All patients with inflammatory bowel disease should have bone density assessment: pro

Bone loss is a common problem for individuals with inflammatory bowel disease. Corticosteroids play an important role in the development of osteoporosis in these patients; however, active disease and longer disease duration also appear to increase the risk of osteoporosis. Given the current burden of osteoporosis, bone mineral density is recommended.     

Steroid-related osteonecrosis in inflammatory bowel disease

Osteonecrosis is a serious complication of steroid therapy characterized by death of all the cellular elements of bone. We describe a series of patients with steroid-induced osteonecrosis in inflammatory bowel disease. Seven of 161 patients (4.3%) treated with corticosteroids for inflammatory bowel disease over a 10-yr period developed osteonecrosis. The median age at the onset of inflammatory bowel disease was 20 yr and for osteonecrosis the median age was 28 yr. Patients had received steroids for a mean duration of 42 wk with a mean daily dose of 26 mg/day and a mean cumulative lifetime prednisone dose of 7 g. Osteonecrosis occurred within 6 mo of the last administration of steroid in all patients. It presented with joint pain in the hip or knee and was frequently mistaken for the arthralgia of steroid withdrawal or the arthropathy of inflammatory bowel disease. Multiple joints were involved in 6 of the 7 patients. Surgery for the joint disease was required in 4 of the 7 patients. The median duration of follow-up was 2 yr. Five of the 7 patients continued to have significant joint pain and disability that limited their activity. We conclude that inflammatory bowel disease predisposes to steroid-induced osteonecrosis. The age of patients is younger, and the dose and duration are considerably lower than that reported for steroid-induced osteonecrosis in other disease states. Bone scans or magnetic resonance imaging should be performed in patients with joint pain who are receiving or have recently received corticosteroid therapy. Early detection and treatment may prevent the crippling long-term complications of this 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.     

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.     

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.     

Screening for osteoporosis in patients with inflammatory bowel disease by using urinary N-telopeptides

BACKGROUND: Patients with inflammatory bowel disease are at increased risk of osteoporosis. DESIGN AND METHODS: We carried out a prospective study of bone mineral density and biochemical markers of bone metabolism like osteocalcin and urinary N-telopeptides in 72 patients with inflammatory bowel disease and evaluated if one of these markers detects osteoporosis. In addition, bone mineral density and N-telopeptides were analysed retrospectively in a second series of 93 patients with inflammatory bowel disease in order to assess predictive values found in the first patient group in an independent sample. RESULTS: Multiple linear regression showed that N-telopeptides (P < 0.0001) and total white blood cell count (P = 0.006) correlated negatively with the bone mineral density of the lumbar spine and only N-telopeptides (P = 0.005) correlated negatively with the bone mineral density of the femoral neck. Using receiver operator characteristic curves N-telopeptide concentrations of > 40 (30) nmol N-telopeptides/mmol creatinine were chosen as best cut-off values to exclude osteoporosis at the lumbar spine (femoral neck). Using these cut-off values a negative predictive value of 100% (100%) and a positive predictive value of 37.5% (27.9%) were found in the first group, and a negative predictive value of 95.2% (96%) and a positive predictive value of 15.6% (23.3%) in the second, independent group of patients. CONCLUSION: Our data suggest that N-telopeptide levels could be used as a tool for the screening of osteoporosis and for selecting those inflammatory bowel disease patients where bone mineral density measurement is indicated.     

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.     

Improved physical performance and increased lean tissue and fat mass in patients with ulcerative colitis four to six years after ileoanal anastomosis with a J-pouch

PURPOSE: This study was designed to examine the longterm changes in physical performance, body composition, and bone mineral density in patients with ulcerative colitis undergoing ileoanal anastomosis with J-pouch. Patients were also screened for abnormalities in blood biochemistry. METHODS: Maximal isometric strength (sum of pinching, hand grip, arm flexion, and knee extension), work capacity (ergometer test at 1.5 W/kg), pulmonary function, body composition (dual-energy x-ray absorptiometry scan), and fatigue level were assessed before surgery and four to six years later. RESULTS: Of 24 patients examined preoperatively, 12 females and 8 males were retested. At follow-up, their mean age ± standard deviation was 38 ± 9 years, weight was 76 ± 14 kg, and height was 173 ± 7 cm. Compared with preoperative assessments, muscular strength had increased 10.6 ± 17.2 percent (P = 0.015), work capacity 10.4 ± 13.3 percent (P = 0.003), total tissue mass 4.6 ± 5.4 kg (P = 0.001), lean tissue mass 2.3 ± 2.2 kg (P = 0.001), fat mass 2.2 ± 3.7 kg (P = 0.014), and bone mineral density 1.6 ± 2.4 percent (P = 0.008). Seventeen of 20 patients had biochemical abnormalities. CONCLUSIONS: After ileoanal anastomosis with J-pouch, muscular strength and work capacity improved concomitant with an increase in total tissue mass, lean tissue mass, fat mass, and bone mineral density. Biochemical abnormalities were common.     

Adenocarcinoma at the site of ileoanal anastomosis in Crohn's disease: report of a case

PURPOSE: Proctocolectomy with ileoanal anastomosis has gained acceptance for the treatment of patients with ulcerative colitis. However, there are some patients with Crohn's disease who received ileoanal anastomosis, because some Crohn's colitis is difficult to differentiate from ulcerative colitis. The risk of cancer development at the site of ileoanal anastomosis has not been emphasized in Crohn's disease. METHODS: A 12-year-old patient with Crohn's disease was treated by proctocolectomy with straight ileoanal anastomosis. Twenty-five years after the operation, the patient noticed the tumor that developed at the site of ileoanal anastomosis. RESULTS: This article presents a patient with Crohn's disease who developed invasive adenocarcinoma at the site of ileoanal anastomosis 25 years after proctocolectomy with ileoanal anastomosis. CONCLUSIONS: An ileoanal anastomosis does not eliminate the risk of cancer development, and surveillance after this operation seems advisable.     

Bone mineral density in asthmatic patients using low dose inhaled glucocorticosteroids.

Inhaled glucocorticosteroids are clearly beneficial in subjects with moderate or severe asthma since they are well tolerated, reduce symptoms, and improve quality of life. Some studies suggest that inhaled glucocorticosteroids can adversely affect bone mineral density. The aim of this study is to determine the effects of inhaled glucocorticosteroid therapy on bone mineral density in female patients. Forty-five asthmatic female patients (36 premenopousal and 9 postmenopausal) and forty-six healthy control subjects were included in the study. Bone mineral density was measured from lumbar spine (L1-4) and femur (neck, trochanter, and Ward's triangle) by dual energy X-Ray absorptiometry. Age, occupation, menopause and smoking status, alcohol consumption, body mass index, previous fractures, family history of fractures, menstrual history, ooferectomy, number of pregnancies, the duration of lactation, physical activity and calcium intake were questioned according to the European Vertebral Osteoporosis Study Group (EVOS) form. Cumulative inhaled glucocorticosteroid dose was calculated. T score of femoral neck and T score and bone mineral density of Ward's triangle were significantly lower in asthmatic patients compared to control group but no statistically significant correlation was found between the disease duration, inhaled steroid treatment duration, cumulative inhaled dose and annual inhaled steroid dose and bone mineral density measurement. These results suggest that in asthmatic patients using low dose inhaled corticosteroids bone mineral density is lower than in healthy controls but it is still unclear if asthma by itself is a risk factor for osteoporosis.     

Osteoporosis in patients with inflammatory bowel disease: risk factors, prevention, and treatment

Patients with inflammatory bowel disease (IBD) are at increased risk for osteoporotic fracture. Bone density testing and osteoporosis management are recommended for IBD patients at greater risk for fracture (ie, postmenopausal women, men aged . 60 years, and those with low body mass indices, glucocorticoid use, family history of osteoporosis, and malabsorption). Patient management includes modification of osteoporosis risk factors, such as calcium and vitamin D supplementation, hormone deficiency correction, and smoking cessation. When indicated, bisphosphonates, such as risedronate and alendronate, have been shown to increase bone mass and reduce fracture risk in patients with glucocorticoid-induced osteoporosis. Infliximab, an anti-tumor necrosis factor a antibody, increases bone mineral density, but this effect has not as yet translated into reduced fracture risk.     

Reduced bone density in patients with inflammatory bowel disease.

BACKGROUND: Reduced bone mineral density in patients with inflammatory bowel disease is thought to be due to disturbances in calcium homeostasis or the effects of corticosteroid treatment. AIMS: To assess the prevalence and mechanism of reduced bone mineral density in 79 patients with inflammatory bowel disease (44 with Crohn's disease, 35 with ulcerative colitis) who did not have significant risk factors for low bone densities. METHODS: Dual x ray absorptiometry was used to measure bone mineral density and serum and urinary markers of osteoblast (alkaline phosphatase, procollagen 1 carboxy terminal peptide and osteocalcin) and osteoclast (pyridinoline, deoxypyridinoline, and type 1 collagen carboxy terminal peptide) activities to assess bone turnover. RESULTS: There was a high prevalence of low bone mineral density (prevalence of T scores < -1.0 from 51%-77%; T scores < -2.5 (osteoporosis) from 17%-28%) with hips being more often affected than vertebrae (p < 0.001). Reduced bone mineral density did not relate to concurrent or past corticosteroid intake, or type, site, or severity of disease. Whereas calcium homeostasis was normal, bone markers showed increased bone resorption without a compensatory increase in bone formation. CONCLUSIONS: The greater prevalence of reduced hip bone mineral density, as opposed to vertebral, mineral density and the pattern of a selective increase in bone resorption contrasts with that found in other known causes of metabolic bone disease.