Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bone mineral density (BMD) in cystic fibrosis (CF) patients falls progressively below normal with advancing age, in part due to steroid administration, low levels of sex hormones, chronic inflammatory disease, physical inactivity, and chronic malabsorption of calcium and/or vitamin D. The purpose of this study was to compare the fractional absorption of (45)Ca and urinary excretion of calcium in CF subjects and normal controls following a high-calcium breakfast containing (45)Ca. Seven young men and 5 young women with CF with pancreatic insufficiency were studied on two separate occasions, with and without administration of pancreatic enzymes. Eleven healthy young adults with normal BMD measurements served as controls. Mean T-scores at the lumbar spine and femur were significantly lower in the CF subjects (p<0.002). Following baseline, fasting collections, timed serum and urine samples were obtained for 5 h after the meal. Fractional absorption (FA) of (45)Ca was estimated by the method of Marshall and Nordin. At baseline, CF subjects had lower mean serum 25-hydroxyvitamin D, calcium and albumin values (p<0.03 for each), slightly, but not significantly (p = 0.12), lower albumin-corrected calcium values, equivalent serum 1, 25-dihydroxyvitamin D values and a trend toward a higher mean serum parathyroid hormone (PTH) value (p = 0.10). Without pancreatic enzymes, CF subjects showed significantly impaired calcium absorption (5 h FA: 11.8 +/- 0.5 for controls vs 8.9 +/- 0.2 for CF subjects, p = 0.02) and excretion (4 h excretion: 0.20 +/- 0.08 mg Ca/mg creatinine for controls vs 0.16 +/- 0.09 mg Ca/mg for CF subjects, p = 0.025). Addition of pancreatic enzymes did not fully compensate for this deficiency. In addition, CF patients had higher serum PTH values after a high-calcium meal (p = 0.03), suggesting mild secondary hyperparathyroidism. Altered calcium homeostasis is likely to be a factor in the development of bone disease in CF patients.
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PMID:Altered calcium homeostasis in adults with cystic fibrosis. 1050 88

Several gastrointestinal and liver diseases impair the absorption of calcium, phosphate, and/or vitamin D, and are associated with an increased incidence of bone disease. Changes in bone mineral density (BMD) using dual-energy X-ray absorptiomety (DXA) have been best studied in the malabsorptive disorder, celiac disease. Celiac disease is an inflammatory condition of the small intestine triggered by ingesting gluten present in wheat, rye, or barley. Chronic inflammation leads to intestinal atrophy and nutrient malabsorption. The disease affects the proximal small bowel; the site where calcium is best absorbed. About 70% of adults with celiac disease have abnormally low BMD values. Treatment with a gluten-free diet increases BMD, but not to normal values. As celiac disease may not be detected until adult life, the failure to reach normal BMD on a gluten-free diet can be explained, at least in part, by the failure to reach peak bone mass. All individuals with malabsorptive disorders should be screened for secondary bone disease. The development of easier and less expensive methods to assess BMD will facilitate screening those at risk for bone disease.
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PMID:Bone mass and gastrointestinal disease. 1086 6

Small intestine bacterial overgrowth is a malabsorption syndrome and, therefore, it may contribute to the occurrence of metabolic bone disease. However, studies that evaluate the magnitude of this problem and the potential underlying mechanisms are still needed. Fourteen patients with bacterial overgrowth and 22 comparable healthy volunteers took part in this study. All patients were affected by conditions known to predispose to bacterial overgrowth. Diagnosis was based on the following criteria: increased breath hydrogen levels in the fasting state and/or increased breath hydrogen excretion after the ingestion of 50 g of glucose solution, improvement after a 10-day course of antibiotic therapy of severity of symptoms and of H2 excretion parameters. Measurement of bone mineral density by dual-energy x-ray absorptiometry at lumbar spine and femoral level and evaluation of nutritional status were performed. Physical activity, sunlight exposure, and cigarette smoking were also evaluated. Patients showed lumbar and femoral bone mineral density values significantly lower than control group; also the prevalence of bone loss at both lumbar and femoral levels was higher in patient group than in healthy volunteers. Body mass index was significantly lower in patients than in healthy volunteers. Lumbar and femoral bone mineral density were significantly correlated and both correlated with body mass index and with duration of symptoms. No correlation between BMD values and physical activity, sunlight exposure, and cigarette smoking was evident. Our results show that small intestine bacterial overgrowth is an important cofactor in the development of metabolic bone disease. The severity of bone loss is related to poor nutritional status and duration of malabsorption symptoms.
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PMID:Small intestine bacterial overgrowth and metabolic bone disease. 1134 52

Bone disease is a frequently reported complication in primary biliary cirrhosis (PBC), but its pathogenesis is poorly understood. Calcium malabsorption has been considered as an important contributing factor. Ursodeoxycholic acid (UDCA) is the treatment of choice in PBC, improving survival, but its effect on calcium absorption is unknown. In this study, we have measured fractional calcium absorption, using a single isotope method, in a group of female PBC patients (median age: 60 years, range: 46-78 years) and age-matched female controls (median age: 58 years, range: 36-74). Bone mineral density (BMD) in PBC patients was significantly lower than age-matched controls (g/cm(2) +/- SEM; lumbar spine: controls 1.139+/-0.028, PBC patients 1.004+/-0.026, p = 0.0028; femoral neck: controls 0.944+/-0.034, PBC patients 0.819+/-0.023, p = 0.0032). Twenty two PBC patients, who were not vitamin D-deficient, were off and on UDCA for approximately 1 month and approximately 8 weeks, respectively. Fractional calcium absorption in PBC patients prior to UDCA treatment (mean +/- SEM, 33.8+/-2.6%) was significantly lower than controls (52.0+/-2.4%, p<0.001). Following UDCA therapy, fractional calcium absorption increased significantly (Off UDCA: 33.1+/-2.6%, On UDCA: 36.6+/-2.5%, p<0.0058). Osteocalcin levels were significantly raised in the PBC group (mean +/- SEM, ng/ml, 41.4+/-2.02) compared to controls (31.1+/-2.64, p = 0.002). There were no differences in parathyroid hormone (PTH) or 25-hydroxyvitamin D levels between these two groups or following UDCA therapy. In conclusion, we found that PBC patients display low spinal and femoral neck BMD, reduced fractional calcium absorption, and elevated plasma osteocalcin. The calcium malabsorption is corrected partially by UDCA therapy. Long-term studies are required to determine whether this effect can be sustained, and whether a sustained increase in fractional calcium absorption can translate into a favorable change in bone strength in patients with PBC.
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PMID:Ursodeoxycholic acid enhances fractional calcium absorption in primary biliary cirrhosis. 1218 28

Small intestinal bacterial overgrowth (SIBO) is one of the causes of malabsorption syndromes. The prevalence of metabolic bone disease in patients with SIBO is unknown, but a recent prospective case-control study indicated significant contribution of SIBO to the development of metabolic bone disease. We review this and other reports in the literature and discuss the possible mechanisms causing metabolic bone disease in patients with SIBO.
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PMID:Small intestinal bacterial overgrowth: a possible risk factor for metabolic bone disease. 1279 46

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.
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PMID:Bone loss associated with gastrointestinal disease: prevalence and pathogenesis. 1286 93

Inflammatory bowel diseases, most frequently Crohn's disease, are frequently accompanied by decreased bone mineral content (30-70%). The osteopenia is not explained by the side effects of treatment or the secondary malabsorption. There must be a common pathological pathway in the background. The mineral content of bones is most easily measured by dual-ray absorptiometry. The measurement should be performed at the time of the diagnosis of bowel disease. It is useful to perform some routine laboratory examinations (serum calcium and phosphate, urinary calcium excretion level, etc.) and some special tests (serum osteocalcin and crosslaps) to exclude some other pathological pathways as well as to plan the anti-osteoporotic therapy. Appropriate calcium and vitamin-D supplementation is essential in prevention and therapy as well. Several drug-classes have proven useful in the therapy of severe osteoporosis associated with inflammatory bowel diseases such as bisphosphonates, hormone replacement therapy, selective estrogen receptor modulators and calcitonin. The authors provide an algorithm for the therapy of metabolic bone disease in inflammatory bowel disease.
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PMID:[Osteoporosis associated with inflammatory bowel diseases]. 1520 26

Impaired bone metabolism following urinary diversion through intestinal segments has always been a controversial subject of unclear clinical relevance. Whereas the perpetuated pathophysiological considerations seem conclusive in theory, the role of acidosis and malabsorption is less clear in animal experimentation and, even more so, in the clinical reality of modern continent diversion. In hardly any of the available contemporary case series was overt derangement of the acid-base balance, rickets or osteomalacia encountered. No consistent changes in osteotropic serum parameters could be found with normal calcium and phosphate in all patients. The assumption that colonic reservoirs have a higher risk of developing metabolic bone disease could not be confirmed by clinical data. As early correction of base excess is easy and probably a common policy in patients with intestinal urinary reservoirs, it will be virtually impossible to further study the natural history of bone metabolism after urinary diversion. While there is no need for a bone specific follow-up in asymptomatic adults with a normal acid-base balance, particular attention should be paid to children and to all patients with impaired renal function.
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PMID:Bladder, bowel and bones--skeletal changes after intestinal urinary diversion. 1531 38

A 78 year old woman had suffered ten spontaneous bone fractures, the first occurring when she was 57 years old. She is now wheel-chair bound. After 21 years, the underlying osteomalacia due to oligosymptomatic celiac disease with malabsorption was diagnosed. The treatment consists of a gluten free diet and substitution of calcium and vitamin D until there is a normalisation of calcium, vitamin D and alkaline phosphatase. Any spontaneous fracture deserves a careful search for metabolic bone disease. An elevation of alkaline phosphatase indicates osteomalacia rather than osteoporosis.
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PMID:[Ten fractures in 21 years]. 1592 67

Crohn's disease (CD) is associated with a number of secondary conditions including osteoporosis, which increases the risk of bone fracture. The cause of metabolic bone disease in this population is believed to be multifactorial and may include the disease itself and associated inflammation, high-dose corticosteroid use, weight loss and malabsorption, a lack of exercise and physical activity, and an underlying genetic predisposition to bone loss. Reduced bone mineral density has been reported in between 5% to 80% of CD sufferers, although it is generally believed that approximately 40% of patients suffer from osteopenia and 15% from osteoporosis. Recent studies suggest a small but significantly increased risk of fracture compared with healthy controls and, perhaps, sufferers of other gastrointestinal disorders such as ulcerative colitis. The role of physical activity and exercise in the prevention and treatment of CD-related bone loss has received little attention, despite the benefits of specific exercises being well documented in healthy populations. This article reviews the prevalence of and risk factors for low bone mass in CD patients and examines various treatments for osteoporosis in these patients, with a particular focus on physical activity.
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PMID:Bone loss in Crohn's disease: exercise as a potential countermeasure. 1630 74


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