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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The analysis of respiratory hydrogen and methane was estimated as a useful index of intestinal fermentation of undigestible carbohydrate. A simultaneous and precious analysis of these gases as well as carbon dioxide was studied. A gas-impermeable multi-laminated film bag metalized by aluminum vapor was fitted to use as a storage bag; its impermeability was verified by measuring the residual rate of hydrogen after 3 months' storage. Hydrogen, methane and carbon dioxide of the breath gas even at 1 ppm could be determined simultaneously by using a gas-solid chromatography installed with a photoionization detector and active carbon column. To observe the genesis of hydrogen and methane after carbohydrate ingestion, pectin, a typical water-soluble dietary fiber, was fed to healthy volunteers. Increasing excretion of pulmonary hydrogen or methane showed the sign of intestinal fermentation as the results of carbohydrate malabsorption.
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PMID:Simultaneous determination of hydrogen, methane and carbon dioxide of breath using gas-solid chromatography. 162 82

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

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

Phosphorus is the sixth most abundant element in the body after oxygen, hydrogen, carbon, nitrogen, and calcium. It comprises about 1% of the total body weight of humans. Eighty-five percent of it is stored in the bone in the form of hydroxyapatite crystal; 14% is in the soft tissues in the form of energy-storing bonds with nucleotides (ATP, GTP), nucleic acids in chromosomes and ribosomes, 2,3-DPG in the red blood cells, and phospholipids in the cells' membranes. Less than 1% is in the extracellular fluids. Phosphate balance is maintained by multiple systems. The gut is responsible for the absorption of two thirds of the 4-30 mg/kg/day of phosphate intake. Absorption sites are all along the gut; in humans the most active site is the jejunum. The kidney filters 90% of the plasma phosphate and reabsorbs it in the tubuli. In states of hypophosphatemia the kidney can reabsorb the filtered phosphates very efficiently, reducing the amount excreted in the urine virtually to zero. The healthy kidney can excrete high loads of phosphate and rid the body of phosphate overload. Through the vitamin D-PTH axis the endocrine system regulates the phosphate balance by influencing the kidney, gut, and bone. Other hormones, including thyroid, insulin, glucagon, glucocorticosteroid, and thyrocalcitonin, play a lesser role in regulation of phosphate metabolism. Because of the complex control of phosphate homeostasis, various clinical conditions may lead to hypophosphatemia. These include nutritional repletion, gastrointestinal malabsorption, use of phosphate binders, starvation, diabetes mellitus, and increased urinary losses due to tubular dysfunction. The clinical picture of phosphate depletion is manifested in different organs and is due mainly to the fall in intracellular levels of ATP and decreased availability of oxygen to the tissues, secondary to 2,3-DPG depletion. The various manifestations of phosphate depletion are listed in Table 2. The treatment of hypophosphatemia consists of administering enteral or parenteral phosphate salts. An important aspect of dealing with the potentially serious effects of phosphate depletion is to prevent the depletion from happening in the first place. Hyperphosphatemia can occur in renal failure, hemolysis, tumor lysis syndrome, and rhabdomyolysis. The treatment of hyperphosphatemia usually consists of fluid administration (in the absence of kidney failure). In chronic hyperphosphatemia, phosphate binders such as aluminum and magnesium salts can reduce the phosphate load. The use of these phosphate binders is limited by their potential side effects.
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PMID:Consequences of phosphate imbalance. 306 Jan 61

We studied the effect of aluminum injections on bones of rats after intervals of 3, 6, and 9 weeks. To study reversibility, we allowed one group to recover for 3 weeks. Both weanling and adult rats were examined to determine the influence of age. The calcium, phosphate, creatinine, and parathyroid hormone levels were similar in aluminum-treated rats and controls. Aluminum could be seen by histochemical stain after 6 weeks, but at that time the bone was otherwise normal. By 9 weeks the bone formation (as measured by tetracycline labeling) in aluminum-treated rats was severely decreased on trabecular and endosteal surfaces. The periosteal surfaces showed normal formation. After 3 weeks of recovery, the bone formation rate in the young aluminum-treated rats was similar to that in the controls, although the serum and bone aluminum values had not significantly decreased. A higher percentage of aluminum was seen in the cement lines. In the adult rats, the bones had more stainable aluminum, and increased osteoid was noted along trabecular and periosteal surfaces. The doses of aluminum used in these rats greatly exceeded those that cause toxicity in humans; thus these findings may not directly apply to clinical practice. We conclude that aluminum administration can lead to decreased rates of bone formation in the rat, despite normal calcium level and renal function, and without decreased parathyroid hormone levels. The peritoneal route of administration could also have contributed to bone lesions by causing peritonitis, malabsorption, or both. Adult rats showed signs of early osteomalacia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Development and reversibility of aluminum-induced bone lesion in the rat. 379 13

An 18-month-old child, who had no evidence of liver disease, malabsorption, or chronic ingestion of coumarin compounds, was found to have plasma deficiencies of factors II, VII, IX and X. Assays for factor II and X by immunological techniques (antibody neutralization and immunoelectrophoresis) revealed normal or elevated antigenic activity of these factors, suggesting the presence of abnormal protein variants in the patient's plasma. On two-dimensional immunoelectrophoresis of the patient's plasma in calcium, a normal and an abnormal population of prothrombin were seen. The abnormal prothrombin had a mobility more anodal than that of normal prothrombin, but less anodal than that of acarboxyprothrombin. The abnormal prothrombin, in contrast to acarboxyprothrombin, adsorbed readily to both aluminum hydroxide and barium citrate, and could be identified by two-dimensional immunoelectrophoresis of a barium citrate eluate. We suspect that the abnormal variant represents a partially carboxylated prothrombin.
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PMID:Characterization of a variant prothrombin in a patient congenitally deficient in factors II, VII, IX and X. 737 10

A 60-year-old woman was evaluated for bone pain and incapacitating weakness. Initial laboratory studies showed a serum calcium level of 10.1 mg/dL, severe hypophosphatemia (1.1 mg/dL), and an elevated alkaline phosphatase level. X-ray films showed changes consistent with osteomalacia. Further studies revealed hypercalciuria (448 mg/24 hr) but absent urinary phosphorus. These data indicated phosphate malabsorption. Excessive use of an aluminum hydroxide-containing antacid was the cause of this patient's failure to absorb dietary phosphate. The features of this syndrome are reviewed to increase physicians' awareness of this illness, which occurs particularly in the elderly and is easily treated.
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PMID:Osteomalacia and weakness from excessive antacid ingestion. 743 92

Citrate is an inhibitor of the crystallization of stone-forming calcium salts. Hypocitraturia, frequently encountered in patients with nephrolithiasis, is therefore an important risk factor for stone formation. Potassium citrate provides physiological and physicochemical correction and inhibits new stone formation, not only in hypocitraturic calcium nephrolithiasis but also in uric acid nephrolithiasis. Inhibition of stone recurrence has now been validated by a randomized trial. Ongoing research has disclosed additional causes of hypocitraturia (sodium excess, low intestinal alkali absorption, but not primary citrate malabsorption). Moreover, new insights on potassium citrate action have been shown, notably that some of absorbed citrate escapes oxidation and contributes to the citraturic response, that ingestion with a meal does not sacrifice physiological or physicochemical action, that orange juice mimics but does not completely duplicate its actions, that potassium citrate may have a beneficial bone-sparing effect, that it may reduce stone fragments following ESWL, and that danger of aluminum toxicity is not great in subjects with functioning kidneys. Finally, the research on potassium citrate has led to two promising products, calcium citrate as an optimum calcium supplement and potassium-magnesium citrate which may be superior to potassium citrate in the management of stone disease.
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PMID:Citrate and renal calculi: an update. 778 99

Parenteral nutrition-associated metabolic bone disease in children is manifested primarily as osteopenia and, on occasion, fractures. The etiology is likely multifactorial, with calcium and phosphate deficiency playing a major role in the preterm infant and with the role of aluminum toxicity yet to be clearly defined in this population. Lack of normal values of bone histomorphometry in the premature infant as well as lack of normal data for biochemical markers of bone turnover in these patients contribute to the uncertainty. Other factors that may play a role in the pathogenesis include lack of periodic enteral feeding; underlying intestinal disease, including malabsorption and inflammation; the presence of neoplasms; and drug-induced alterations in calcium and bone metabolism. The true incidence and prevalence of parenteral nutrition-associated bone abnormalities in pediatric patients remain unknown.
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PMID:Metabolic bone disease of total parenteral nutrition. 943 1

Antacids containing aluminum and magnesium hydroxide are widely used nonprescription agents for treatment of gastritis and peptic ulcer disease. One of the side effects of these antacids is that they bind phosphate in the gut, resulting in its malabsorption. Short-term use, consistent with the directions on the manufacturer's label, is safe and effective for most patients. Heavy chronic use, even when within label, can cause serious skeletal impairment. This report concerns the case of a 39-year-old pharmacist who self-mediated for peptic ulcer disease with high doses of a potent antacid containing aluminum and magnesium hydroxide. The patient consumed over 18 kg of elemental aluminum and 15 kg of elemental magnesium over 8 years of antacid use. This treatment resulted in the clinical syndrome of severe osteomalacia due to profound phosphate depletion. Bone biopsy revealed stainable aluminum deposits along 27.6% of the total bone surface, which is a unique observation in a patient with normal renal function. Treatment included withdrawing the antacid and supplementation with phosphate, calcium, and vitamin D. She experienced marked subjective and objective improvement with this regimen. This included a striking increase in her bone mineral density occurring over the 2-year follow-up period. This case documents that long-term antacid therapy, even when used by patients with normal renal function and within the manufacturer's label recommendations, can lead to severe phosphate depletion, osteomalacia, and toxic accumulation of aluminum and magnesium. This clinical syndrome was readily treated by withdrawal of the antacid and with calcium and phosphate supplementation. Physicians recommending treatment with these compounds or learning of their patient's self-medication with them should inform the patient of the potential serious side effects these agents can cause when used chronically at maximally recommended doses.
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PMID:An interesting case of osteomalacia due to antacid use associated with stainable bone aluminum in a patient with normal renal function. 962 11


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