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)

The synthesis of osteocalcin or bone gla protein by osteoblasts is markedly stimulated by 1,25-(OH)2D, a key hormone in the regulation of bone mineralization. The circulating levels of osteocalcin have been shown to reflect both the osteoid matrix production and the formation rate of mineralized bone in several metabolic bone diseases (osteoporosis, thyrotoxicosis, primary hyperparathyroidism) in which both mechanisms are tightly coupled because of the absence of mineralization defect. In this study, we measured in 12 patients (7 women, 5 men, 56 +/- 15 yr old) with untreated osteomalacia serum osteocalcin and vitamin D metabolites (25OHD and 1,25-(OH)2D). The results were correlated with biochemical and histomorphometric assessment of bone remodeling. Osteomalacia was due to vitamin D deficiency (5 cases), to vitamin D malabsorption (6 cases), and to hypophosphataemia in 1 case. When compared to control values, serum osteocalcin was increased in patients with osteomalacia (7.4 +/- 4 vs. 3.7 +/- 1.3 ng/mL; P less than 0.001) and was positively correlated with serum alkaline phosphatase (r = 0.65; P = 0.03) and negatively with 25 OHD (r = -0.61; P = 0.04). Serum osteocalcin was not correlated with 1,25-(OH)2D [r = -0.45; not significant (NS)] even after exclusion of the patient with hypophosphataemia. Serum osteocalcin was positively correlated with the osteoid volume and osteoid perimeter (r = 0.71 and 0.69 respectively; P less than 0.01) but not with any of the tetracycline-based parameter of bone mineralization at the tissue level (r ranging from -0.41 to +0.42, NS). Serum 25 OHD, but not 1,25-(OH)2D, was positively correlated with the mineralization rate (r = 0.59; P less than 0.05 and r = 0.54; NS). We conclude that in patients with osteomalacia, a condition which is characterized by an increased osteoid accumulation due to a decreased mineralization rate, the increased level of serum osteocalcin reflects the increased osteoid synthesis but not the mineralization defect. In this disease, serum osteocalcin is inversely correlated to the severity of vitamin D deficiency reflected by serum 25 OHD, but not to the serum levels of 1,25-(OH)2D.
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PMID:Serum osteocalcin is increased in patients with osteomalacia: correlations with biochemical and histomorphometric findings. 156 62

Osteomalacia is characterized by large osteoid seams and a preserved volume of bone trabeculae. The mineralization of newly formed bone requires adequate concentrations of calcium and phosphate: the Ca.P product has been regarded as a useful, empirical diagnostic test of osteomalacia. It decreases in patients with osteomalacia mainly because they have very low plasma phosphate levels. At present total body bone mineral and total body bone density can be directly measured by whole body absorptiometry, which indicates the lowest total mineral content of the skeleton which can increase quickly after adequate treatment. The main symptoms of osteomalacia are: bone pain; muscular weakness (commonly as pelvic girdle myopathy); Looser-Milkman pseudofractures or more often a pattern of generalized demineralization at X-ray. The main biochemical parameters in osteomalacia include: defective calcium absorption with hypocalcemia and hypocalciuria; defective intestinal phosphate absorption with hypophosphatemia; there is often increased renal phosphate clearance due to hypocalcemia and secondary hyperparathyroidism; elevated alkaline phosphatase and osteocalcin levels; high bone turnover confirmed by kinetic studies carried out with radiocalcium or 99mTc-MDP. An etiological classification of the osteomalacias includes: 1) nutritional osteomalacia: a) inadequate exposure to sunlight and/or insufficient vitamin D intake; b) defective intestinal absorption of vitamin D because of malabsorption syndromes (e.g. jejuno-ileal bypass for obesity).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The osteomalacias. 166 41

The action of 1 alpha-hydroxycholecalciferol (oxydevit) was estimated in 204 patients with renal osteodystrophy, osteoporosis of varying etiology, osteomalacia because of malabsorption, congenital rickets-like diseases. The drug was shown to be highly effective in the treatment of secondary hyperparathyroidism in uremia, steroidal and senile osteoporosis. The treatment involved replacement therapy.
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PMID:[Experience in treating metabolic osteopathies with 1 alpha-hydroxyvitamin D3 (oksidevit)]. 181 42

A 51 year old Yugoslavian patient was admitted to our hospital in reduced general condition with distinct hypocalcemia, osteomalacia, and with rectum stenosis. Our investigations led to the diagnosis of a malabsorption syndrome due to non-tropical sprue. The most likely cause of the rectum stenosis is an abuse of ergotamine-containing suppositories for several years. A gluten-free diet and the interruption of the use of the suppositories improved her general condition remarkably.
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PMID:[Non-tropical sprue and chronic inflammatory rectal stenosis in a patient with abuse of ergotamine-containing suppositories]. 190 44

The case of a 75-year-old woman with severe osteomalacia secondary to ingestion of large amounts of an aluminum-containing antacid is reported. Biochemical analysis revealed signs of phosphate malabsorption and increased levels of bone markers (S-alkaline phosphatase and U-hydroxyproline). A 99mTc-bone scan revealed multiple areas of increased uptake. The patient was normocalcaemic, with normal serum levels of intact parathyroid hormone and 25-hydroxyvitamin D. Serum 1,25-dihydroxyvitamin D was high normal. A transiliac bone biopsy from the patient showed severe osteomalacia. Symptoms, biochemical parameters, bone scan and bone morphology were all normalized 1 year after stoppage of antacid ingestion and treatment with vitamin D2. calcium phosphate and sodium fluoride because of severe osteopeni. The characteristics of this condition and the role of phosphate depletion and aluminum in the pathogenesis of bone lesions are discussed.
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PMID:Antacid-induced osteomalacia: a case report with a histomorphometric analysis. 200 45

The prevalence, type, and factors that may influence the development of bone disease in primary biliary cirrhosis, have been investigated in 20 consecutive patients, who, in addition to liver function tests and mineral and vitamin D metabolism studies, were submitted to a transiliac bone biopsy after tetracycline double-labeling for quantitative histomorphometric examination. Intestinal calcium absorption was also assessed in 16 patients. Seven patients (35%) had reduced bone volume and were considered osteoporotic. Three also had bone mineralization impairment, but did not have criteria for osteomalacia. Bone formation was depressed in 15 patients, and bone resorption was low or normal in 19 cases. Eroded surfaces were reduced in all osteoporotic patients. Duration of primary biliary cirrhosis was significantly longer in patients with osteoporosis (6.3 +/- 0.6 yr) than in those without osteoporosis (2.6 +/- 0.6, p = 0.004). Moreover, osteoporosis was more prevalent in postmenopausal women, and in those who had intestinal calcium malabsorption, which was present in 80% of osteoporotic patients but in only 18% of nonosteoporotic patients (p = 0.03). Osteoporosis and mineralization bone impairment were unrelated to the severity of cholestasis. 25-Hydroxyvitamin D was significantly lower in those patients with intestinal calcium malabsorption. The results of this study indicate that osteodystrophy in primary biliary cirrhosis is characterized mainly by "low-turnover" osteoporosis, which is related to the duration of the liver disease, postmenopausal condition, and calcium malabsorption.
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PMID:Factors influencing the development of metabolic bone disease in primary biliary cirrhosis. 222 Jul 29

A total of 2484 newly detected metabolic bone diseases during the past 17 years comprised 79.67% cases of osteoporoses and 20.33% of osteomalacia. The group of osteoporoses included 325 patients (16.43%) with the primary form of the disease, in 1654 patients (83.57%) a cause of decalcification of bones (secondary form) was found. With advancing time the number of secondary osteoporoses rises steadily, while the number of primary cases remains at the same level. In the aetiology of demineralization a major part was played by lactose intolerance, maldigestion and malabsorption, idiopathic, hypercalciuria, diabetes and steroids. The female: male ratio in primary osteoporoses was 4.71:1 and in secondary osteoporoses 2.35:1. Primary osteomalacia was recorded in 113 patients (22.38%) and secondary in 392 (77.62%). Here too with advancing time the number of secondary forms is increasing. The largest groups are hepatic and renal affections, smaller ones malabsorption and antiepileptic drugs. The female: male ratio in primary osteomalacia is 2.13:1 and in secondary osteomalacia 2.26:1. With the development of knowledge on the aetiopathogenesis of bone demineralizations we expect in future a further increase of secondary forms of the disease at the expanse of primary ones.
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PMID:[Secondary osteopenia]. 228 20

A patient with the painless onset of a cholecystocolonic fistula associated with virtually complete common bile duct obstruction due to stones provided a unique opportunity to assess the consequences of prolonged bile acid depletion on the digestion and absorption of nutrients. Over 2 years, the patient insidiously developed steatorrhea, osteomalacia with an atraumatic pelvic fracture, and congestive heart failure complicated by polymorphic ventricular tachycardia (torsade de pointes) all of which could be attributed to malabsorption of fat and fat-soluble vitamins.
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PMID:Cholecystocolonic fistula: malabsorptive consequences of lost bile acids. 232 84

We report on a 36-year-old female patient suffering from bilateral inguinal pain. The x-ray revealed significant osteoporosis of both proximal femurs with an impacted fatigue fracture of the right calcar and Looser zones at the left subtrochanteric femur. The intestinal biopsy proved coeliac disease, resulting in a secondary malabsorption. The authors conclude that osteomalacia in young patients could indicate coeliac-induced malabsorption.
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PMID:[Osteomalacia and fatigue fractures in celiac disease]. 234 37

D-lactate accumulates in some patients with malabsorption who continue oral intake of carbohydrate leading to a clinical syndrome of acidosis and encephalopathy. To assess the possibility that D-lactate contributes to acidosis and/or metabolic bone disease in patients with malabsorption receiving long-term parenteral nutrition yet maintaining oral intake, D-lactate levels in serum and urine were measured in 14 long-term parenteral nutrition subjects (average duration of support 74 months) and 27 control subjects. Significant elevations in both serum and urine D-lactate were found in only two parenteral nutrition subjects. Both subjects with elevated D-lactate levels had bone pain, x-ray evidence of fractures, and biopsy evidence of osteomalacia. These studies suggest that D-lactate accumulation may be a heretofore unappreciated metabolic abnormality associated with metabolic bone disease and acidosis in patients with malabsorption who are supported by long-term parenteral nutrition.
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PMID:D-lactate and metabolic bone disease in patients receiving long-term parenteral nutrition. 249 43


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