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

Excretion of oxalic acid in urine was measured in 28 healthy and 97 patients with gastrointestinal diseases. We found significantly higher values in the following groups: patients after resection of parts of the small intestine, patients with sprue and other diseases with malabsorption, patients with M. Crohn of the small intestine, colitis ulcerosa and granulomatosa, patients with chronical diseases of the pancreas gland and patients with cirrhosis of the liver. In 4 patients after resection of parts of the small intestine or pancreas urolithiasis could be verified. Reduction of fat and food without ballast reduced the excretion of oxalic acid in urine. Hyperoxaluria correlied significantly with the following parameters: excretion of fat in feces, exhalation of 14CO2 in the glykocholate breath test, resorption of vit. B12 and the length of resected small intestine. This form of hyperoxaluria is caused by hyperresorption of oxalic acid from food. The mechanism of this hyperresorption is not clarified yet, an important factor seems to be ill resorption of fat.
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PMID:[Hyperoxaluria in intestinal and liver diseases]. 83 13

The increased oxalic acid absorption is a well documented finding in gastroenterological diseases. The malabsorption of bile acids and fat is important in the pathogenesis of the hyperoxaluria. The enteric absorption of 14C-labelled oxalic acid was measured in 49 patients with different diseases. The dihydroxy-trihydroxy-ratio of bile acids is significantly decreased in patients with hyperoxaluria over 20% of the ingested dosage. We didn't find any correlation between the excretion of oxalic acid and the intraduodenal pancreatic lipase activity.
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PMID:[Pancreatico-biliary secretion in enteral hyperoxaluria]. 325 36

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