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

Previous studies have provided evidence that an anaerobic bacterium, which degrades dietary oxalate to CO2 and formate, is present in colonic contents of a number of herbivorous species, laboratory rodents and humans. The present study examines the possibility that these bacteria degrade significant amounts of oxalate and can influence colonic oxalate absorption. Guinea pigs adapted to a diet containing 2% sodium oxalate or fed a normal diet were challenged with 67, 135, 170 or 200 mg of sodium oxalate containing 0.5 microCi of [14C]oxalate, which was injected into the cecum. Adapted animals excreted approximately 2% of the 14C in the urine, regardless of the dose, whereas unadapted animals excreted significantly higher amounts in the urine at the two lower doses and died at the two higher doses. Conversely, antibiotic treatment of adapted guinea pigs reduced the ability of their cecal flora to degrade oxalate, and a correspondingly greater percentage of an injected oxalate load was excreted in the urine. Oxalate degradation rates in cecal fluid were depressed by the secondary bile salt deoxycholate, and in vitro studies with pure isolates of guinea pig and human strains of oxalate degraders confirmed that these bacteria were highly sensitive to low concentrations of deoxycholate. Results indicate that these bacteria may be important in preventing excess absorption of oxalate and raise the possibility that the hyperoxaluria associated with bile salt malabsorption of ileal disease in part may be due to suppression of these bacteria by the bile salts.
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PMID:Intestinal oxalate-degrading bacteria reduce oxalate absorption and toxicity in guinea pigs. 337 43

Hyperoxaluria occurs with many gastrointestinal disorders complicated by malabsorption. This hyperoxaluria is known to be the result of increased colonic absorption of dietary oxalate. Proposed mechanisms for this effect include alterations in fecal fatty acids, alterations in fecal bile acids, and acidification of colonic pH. Using an animal model of lactulose-induced chronic colonic acidification, we examined the effect of pH on oxalate absorption in vivo. Rats were fed a diet containing 6.77 mg oxalate per day with and without lactulose. Cecal pH of the animals receiving lactulose was significantly lower than controls (4.90 +/- 0.42 vs 7.17 +/- 0.38; p less than 0.001). Urinary excretion of oxalate was significantly greater in animals receiving the lactulose diet than in controls (0.975 +/- 0.144 vs 0.844 +/- 0.172 mg oxalate per day; p less than 0.001). These results demonstrate that acidification of the colon results in a significant increase in urinary oxalate excretion. Thus, acidification of the colon may be an important factor in the pathogenesis of enteric hyperoxaluria.
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PMID:Role of cecal pH in intestinal oxalate absorption in the rat. 341 Nov 98

An investigation of variables important to calcium stone formation in urine indicated significantly increased daily excretion of calcium and oxalate and decreased excretion of ascorbate and citrate by recurrent calcium stone formers. In addition, urine volume, sodium, mucopolysaccharide, and protein were also significantly increased. We compared the uptake of citrate and ascorbate from the gut into the blood in normal controls and stone formers. These studies indicated significantly depressed absorption of both these hydroxycarboxylic acids in recurrent calcium stone formers. We also found that concurrent administration of citrate inhibited ascorbate absorption and increased urinary oxalate excretion after an ascorbate load in normal subjects and stone formers. These findings suggest a mechanism that explains hyperoxaluria in stone patients on the basis of a malabsorption of citrate, ascorbate, and possibly other hydroxycarboxylic acids.
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PMID:Chemical factors important to calcium nephrolithiasis: evidence for impaired hydroxycarboxylic acid absorption causing hyperoxaluria. 380 7

The pattern of oxalate uptake in various segments of the bowel has been studied after 80% small bowel resection and antiperistaltic colon interposition in Rhesus monkeys. The levels of urinary oxalate excretion were significantly raised in the immediate postoperative period, with progressive reduction at six and 12 months. None of the animals developed renal calculi. The possible benefit of the colon interposition after massive small bowel resection, in the prevention of hyperoxaluria and urolithiasis is suggested. Improvement in the fat malabsorption, formation of insoluble calcium oxalate in the bowel lumen, leading to reduced net intestinal absorption of oxalates is the possible mechanism.
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PMID:Absorption and urinary excretion of oxalates following massive small bowel resection and colon interposition in rhesus monkeys. 651 51

During the last 10 years it has become apparent that hyperoxaluria often is present in malabsorptive states. This secondary hyperoxaluria could be explained by an increased uptake of dietary oxalate due to malabsorption of fatty acids and bile salts. Dietary prescriptions, including a low fat diet is advocated in the treatment of hyperoxaluria in Crohn's disease or after small bowel resection.
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PMID:Hyperoxaluria in malabsorptive states. 702 Feb 4

Changes in oxalate excretion (together with changes in urinary volume) constitute the most important factors in altering the probability of renal stone formation. However, investigations on oxalate metabolism have been sparse, perhaps because of the lack of an accurate method for measuring oxalate in biologic fluids. Available data clearly implicate increased urinary oxalate excretion as the etiological factor in stone formation in two groups of patients--those with primary hyperoxaluria and those with gastrointestinal malabsorption. Evidence for the existence of hyperoxaluria in the patient with the "garden" variety of calcium oxalate stones is less persuasive.
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PMID:Oxalate metabolism and renal calculi. 703 92

Renal failure secondary to oxalate interstitial nephritis developed in three patients with malabsorption and steatorrhea following a jejunoileal bypass, extensive small intestine resection and a partial gastrectomy. Hyperoxaluria was documented in two of the cases. The possibility that this complication can occur in patients after a jejunoileal bypass operation is now recognized. This report shows that it can also occur in patients with other bowel disorders that cause malabsorption and steatorrhea. Since the prognosis for patients with oxalate nephropathy is poor, renal function should be closely monitored in patients who are at risk because of these disorders. Therapy should be directed at correcting malabsorption, steatorrhea and hyperoxaluria. When the renal function of patients with a jejunoileal bypass continues to decline despite intensive medical therapy, restoration of bowel continuity is strongly recommended.
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PMID:Oxalate nephropathy due to gastrointestinal disorders. 747 Oct 17

Bile acid malabsorption is often due to a disease or partial resection of the terminal ileum and more rarely a genetic defect in the distal ileum. It is often associated with diarrhoea with or without steatorrhoea, and it may be complicated by gallstone disease and hyperoxaluria. Bile acid malabsorption is rather easily diagnosed using the selenohomocholic acid taurine test. Patients with bile acid induced diarrhoea should be recommended a low-fat diet. Cholestyramine may be recommended in moderate bile acid diarrhoea. In patients with more severe bile acid malabsorption, cholylsarcosine may be used as a replacement therapy.
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PMID:Bile acid malabsorption: mechanisms and treatment. 854 66

Urolithiasis is one of the most frequent causes of morbidity in developed countries and its incidence is close to 5%. In our experience, 67.4% of urinary stones contain calcium oxalate as the main component, and hyperoxaluria plays an important role in the pathophysiology of this type of stone. The mechanisms responsible for the increment in urinary excretion of oxalate could involve oxalic acid synthesis. This increase could be due either to an increment of its endogenous formation or to an exogenous load of its precursors. Furthermore, an increased intestinal oxalate absorption is a frequent cause of hyperoxaluria and urolithiasis. Ingestion of oxalate rich foods, imbalance in the supply of other nutrients that influence oxalic acid absorption and GI disorders with malabsorption and/or decreased degradation of intraluminal oxalate can increase intestinal oxalate transport and cause hyperoxaluria. In this article we review the physiological mechanisms that control the oxalate pool: endogenous synthesis, exogenous supply, intestinal absorption and renal excretion of oxalic acid. We analyze the causes and the pathophysiological mechanisms that increase urinary oxalate excretion. We describe a protocol for the biochemical study of patients with hyperoxaluria and the therapeutic measures to reduce urinary oxalate are reviewed. Finally, possible research that may provide further insight into oxalate metabolism in patients with hyperoxaluria are discussed.
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PMID:[Hyperoxaluria and renal calculi]. 902 8

Urolithiasis is uncommon in adolescence and rare in early childhood. In pediatric populations, congenital urinary tract anomalies associated with stasis and infection, idiopathic urolithiasis (adolescents), and nephrocalcinosis (premature infants) account for the majority of urolithiasis patients. Inborn errors of metabolism, such as the primary hyperoxalurias, are rare causes of urolithiasis in childhood. We report six children (mean age at symptom onset 1.3 years; range 0.32-4.1 years) with moderate hyperoxaluria (mean 1.10 +/- 0.58 mmoL/1.73m2 per day; range 0.69-2.19 mmoL/1.73m2 per day). Urolithiasis was present in four. Stones from two children were comprised of calcium oxalate dihydrate. Calcium oxalate crystalluria was seen in two of the patients. Findings included a mean urine calcium concentration of 6.61 +/- 2.28 mg/kg per day, urine citrate of 925.5 +/- 291.29 mg/g of creatinine per day, and mean renal clearance of 99.83 +/- 23.27 mL/min. All children were born full term, none was receiving diuretics, and none had recurrent urinary tract infections. Secondary causes of hyperoxaluria, including dietary oxalate excess, pyridoxine deficiency, and malabsorption, were excluded. Urine glycolate and glycerate were normal in all patients. In one hyperoxaluric member of each sibship, hepatic alanine-glyoxylate aminotransferase and D-glycerate dehydrogenase/glyoxylate reductase activity were normal. The clinical and biochemical features of these children are unlike those in previously recognized hyperoxaluric states. Thus, our description of a separate hyperoxaluric entity, referred to as unclassified hyperoxaluria.
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PMID:Hyperoxaluria and urolithiasis in young children: an atypical presentation. 1060 14


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