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)

A secondary hyperparathyroidism resulting from decreased intestinal calcium (Ca) absorption has been proposed as a contributory factor to glucocorticoid-induced osteoporosis. Inhaled steroids do not usually suppress adrenal gland function unless daily doses above 1,500 microgram are used. A recent study, however, has shown a reduced total body calcium in patients on regular beclomethasone treatment. In theory, osteopenia in these patients could be due to a direct effect of inhaled steroids on bone or due to an impaired intestinal calcium absorption. In this study, Ca absorption and parathyroid hormone (PTH) secretion were evaluated in three groups: 1) asthmatics on continuous oral and inhaled steroid treatment (11.3 +/- 4.4, range 5-33.5 mg.day-1 prednisone and 660 +/- 265, range 400-1,600 microgram.day-1 beclomethasone, respectively); 2) asthmatics on regular beclomethasone therapy (585 +/- 210, range 400-1,200 microgram.day-1); and 3) healthy subjects. The prevalence of vertebral fractures was evaluated by a spinal X-ray. No differences were found in either Ca absorption or PTH serum levels between asthmatics and healthy subjects (analysis of variance-ANOVA). Vertebral fractures were significantly more frequent in patients from group 1 (14 of 25) than in those from group 2 (2 or 25). We conclude that both prolonged oral steroid treatment and inhaled steroids, at doses lower than 1,600 microgram.day-1 do not cause Ca malabsorption, and that hyperparathyroidism does not contribute to osteoporosis in these patients.
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PMID:Intestinal calcium absorption and parathyroid hormone secretion in asthmatic patients on prolonged oral or inhaled steroid treatment. 185 73

Vitamin D has certain clearly defined effects on bone: vitamin D deficiency results in defective bone mineralization, whereas 1,25-dihydroxy-vitamin D3 (1,25-(OH)2D3) stimulates bone resorption. Studies of the use of 1,25-(OH)2D3 to prevent or treat osteoporosis have given conflicting results concerning bone remodeling. However, 1,25-(OH)2D3 or other vitamin D metabolites seem to play a role in the correction of calcium malabsorption, which is a common feature in osteoporosis.
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PMID:Is there a role for vitamin D in osteoporosis? 193 97

Abuse of alcohol is considered to be an important risk factor for fractures and osteoporosis. Alcohol abuse is associated with deleterious changes in bone structure detected by histomorphometry, and with a decrease in bone mineral density. These changes may also be produced by factors commonly associated with alcohol abuse, e.g., nutritional deficiencies, liver damage, and hypogonadism. Thus the etiology of alcohol-associated bone disease is multifactorial. Alcohol has, however, clear-cut direct effects on bone and mineral metabolism. Acute alcohol intoxication causes transitory hypoparathyroidism with resultant hypocalcemia and hypercalciuria. Prolonged moderate drinking elevates serum parathyroid hormone (PTH) levels, whereas chronic alcoholics are characterized by low serum levels of vitamin D metabolites with resultant malabsorption of calcium, hypocalcemia, and hypocalciuria. Independently of whether alcohol consumption is of short duration, social, or heavy and chronic, it seems to suppress the function of osteoblasts, as evidenced by low serum levels of osteocalcin. It has recently been reported, however, that alcohol can also have a beneficial effect on bone. Among postmenopausal women, moderate alcohol consumption correlates positively with central and peripheral bone mineral density, and with serum estradiol levels.
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PMID:Alcohol and bone. 193 4

Almost all segments of the gastrointestinal tract have been used as urinary tract substitutes. The specific nutritional and gastrointestinal complications depend on the particular portion of bowel that is removed from the alimentary tract. The use of stomach theoretically may predispose the patient to hypergastrinemia and peptic ulcer disease, hypocalcemia, and iron deficiency or megaloblastic anemia. Resection of a large amount of jejunum causes malabsorption. Limited use of colon segments usually is well tolerated, but loss of large parts of the colon directly decreases available absorptive area, resulting in diarrhea. Resection of the ileum and ileocecal valve can lead to several disease states. One is mixed secretory-osmotic diarrhea. Decreased ileal reabsorption of bile salts results in fat malabsorption and steatorrhea. The presentation of increased amounts of bile salts and fatty acids to the colon decreases water absorption and stimulates active chloride and water secretion, producing a cholera-like high-volume secretory diarrhea. The loss of the ileocecal valve and ileum segment accelerates intestinal transit time, which does not allow for complete digestion and absorption of food. Water and electrolytes remain associated with undigested food particles and may overwhelm the absorptive capacity of the colon, resulting in an osmotic diarrhea. A second problem is vitamin B12 deficiency. Surgical reduction of sites in the terminal ileum for active and exclusive uptake of vitamin B12 might lead to hypovitaminosis. If this is unrecognized, patients may develop irreversible neurologic injury. A third problem is cholelithiasis. Derangements in bile salt metabolism can occur when as little as 10 cm of ileum is resected, and the propensity to form gallstones is increased. Pigment gallstones appear to be the predominant stone associated with ileal resections. The fourth possible problem is urolithiasis, the etiology of which is multifactorial in patients with ileal resections. With decreased availability of bile salts, fat malabsorption occurs. Fatty acids bind with calcium and magnesium to form soaps, resulting in increased levels of free oxalate available for absorption. Moreover, fatty acids directly increase colonic permeability to oxalate.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutritional and gastrointestinal complications of the use of bowel segments in the lower urinary tract. 194 6

Absorption studies were performed in 17 patients with ulcerative colitis operated on with colectomy and an ileal two-limbed J-pouch anastomosis. The patients were studied 3 and greater than or equal to 18 months after closure of the temporary ileostomy. Increased stool mass (median, 609 g/24 h) was found in all patients and was unchanged with time. Moderate steatorrhoea was present in 29% of the patients 3 months postoperatively, but faecal fat excretion normalized with time. Calcium absorption was normal in all but one patient regardless of time after operation. An abnormal bacterial deconjugation, evaluated by a 14C-glycocholic acid breath test was present in 27% of the patients and increased significantly with time. Forty per cent of the patients had increased faecal bile acid excretion. B12 malabsorption was present in 29-35% of the patients. In conclusion, ileal J-pouch anastomosis for ulcerative colitis causes increased stool mass in all patients and produces moderate bile acid deconjugation and malabsorption in about one-third to half. Substitution therapy with vitamin B12 is necessary in about one-third of the patients. Intestinal adaptation as far as absorption is concerned is minimal after the first 3 postoperative months.
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PMID:Absorption studies after ileal J-pouch anastomosis for ulcerative colitis. A prospective study. 200

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

Intestinal Ca2+ malabsorption has been described in spontaneously hypertensive rats (SHRs), but the molecular basis for this defect is unknown. In this study, we measured intestinal alkaline phosphatase and vitamin D-dependent Ca(2+)-binding protein (calbindin-D9k), two proteins implicated in the active pathway of intestinal Ca2+ absorption. Both proteins were measured in the small intestines of SHRs and their normotensive controls, Wistar-Kyoto rats, before, during, and after development of hypertension (4, 9, 14, 18, and 28 wk of age). At all ages, alkaline phosphatase activity in duodenum (0-6 cm) was decreased by 30-57% (P less than 0.001) and by 47-75% in the 2nd intestinal segment (6-12 cm) (P less than 0.001-0.05). Calbindin-D9k was decreased similarly. The decreases of calbindin were statistically significant (P less than 0.001-0.05) in the duodena at 4, 14, 18, and 28 wk (9-30% decreases) and in the 2nd segment at 4, 14, and 18 wk (38-69% decreases; P less than 0.001-0.005). Decreased calbindin in SHRs was documented in animals from two suppliers. The deficiencies of calbindin-D9k and alkaline phosphatase could not be attributed to malnutrition or to a generalized brush-border defect as indicated by body weights and the intestinal marker enzyme sucrase. Although calbindin-D9k was decreased in young SHRs, the serum 1,25-dihydroxycholecalciferol [1,25(OH)2D3] was increased by 59 and 129% in 4- and 9-wk-old SHRs (P less than 0.001), respectively; by contrast, serum 1,25(OH)2D3 was unchanged or decreased in older SHRs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intestinal vitamin D-dependent calbindin-D9k and alkaline phosphatase in spontaneously hypertensive rats. 203 38

Ninety systemic sclerosis (SSc) patients, all females, none of them suffering from either renal failure or intestinal malabsorption, and 90 sex and age matched controls were investigated for bone mineral content (BMC) by dual photon-absorptiometry (Am 241, I 125) (Osteoden P, NIM) evaluated at two sites of the nondominant radius. BMC as well as bone density (BD) were found to be significantly lower in the patients than in the controls. No alteration of calcium metabolism was detected in the patients, neither were we able to find any relationship between osteopenia and the extent of the involvement of the skin or of any internal organ. We observed, however, that the percentage of the patients in menopause was significantly greater than that of the controls (p less than .001). Furthermore, menopause had occurred in the patients significantly earlier than in the controls (p less than .001). Therefore, earlier menopause can play a role in the induction of osteopenia in systemic sclerosis. Further prospective studies are needed to check the hormonal status of SSc patients.
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PMID:Osteopenia in systemic sclerosis. Evidence of a participating role of earlier menopause. 206 1

The vitamin D dependent intestinal calcium-binding protein (calbindin-D9K) was measured by an enzyme-linked immunoadsorbent assay in small intestinal biopsy specimens from 10 children (aged 15-126 months). The aim was to study the relationship between calcium-binding protein and age, bone age, and height. The patients were examined due to complaints of chronic diarrhea, but no evidence of malabsorption was found. The amount of calbindin-D9K per mg of soluble protein in the small intestinal biopsy specimens was higher than previously studied in normal adults. Calbindin-D9K correlated inversely with chronological age, bone age, and height of the children (p = -0.87, rho = -0.66, and rho = -0.66; p less than 0.05). A direct correlation was found between calbindin-D9K and intestinal alkaline phosphatase activity (p = 0.60; p less than 0.05). The decline in calbindin-D9K may indicate that the active vitamin D dependent intestinal calcium absorption decreases during childhood.
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PMID:Measurement of calbindin-D9K in small intestinal biopsy specimens of children. 207 23

Home parenteral nutrition has prevented malnutrition in patients who cannot maintain adequate nutrition by enteral feedings alone. The risk of bone and mineral abnormalities in these patients is significant for several reasons. Pre-existing skeletal disease can occur from factors known to affect the population at large as well as from malnutrition, malabsorption, and corticosteroid use related to the underlying disease process. Long-term use of infused nutrients and potential toxins can further alter bone turnover. Hypercalciuria is frequently present during HPN, yet its etiology is poorly defined. Parenteral nutrition admixture concentrations of calcium, phosphorus, protein, sodium, and dextrose may all play a role. Any development of acidosis can certainly aggravate hypercalciuria, which may be an indirect marker of abnormal bone turnover. Although increased protein intake can promote the development of acidosis-induced calciuresis, infused phosphorus and acetate can help reduce calcium excretion. Parenteral nutrition contamination by aluminum can cause a spectrum of osteomalacic bone disease similar to aluminum-associated changes seen in renal failure patients. Even with recent attempts to remove aluminum from the parenteral admixture, low-turnover bone disease can still occur. At present, HPN-related bone disease is a poorly understood entity because of its multifaceted nature. Patients receiving long-term parenteral nutrition should be considered to have an increased risk for the development of metabolic bone disease. Early monitoring for and treatment of bone disease should be considered in all patients receiving HPN.
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PMID:Long-term parenteral nutrition and metabolic bone disease. 211 69


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