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

Oxalate-urolithiasis and hyperoxalaria have been reported to be a frequent complication in patients with small bowel disease, especially in patients with ileal resection due to Crohn's disease. Hyperabsorption of oxalate seems to be the main patholgenetic factor for "enteric" hyperoxalaria. Intestinal absorption and urinary excretion of oxalate was measured in patients with various gastrointestinal diseases after oral or rectal administration of 14C-oxalate. Kinetic data suggest that 14C-oxalate is absorbed in the small, the large bowel and the rectum as well. Oxalate absorption was decreased in patients with a colectomy and in active ulcerative colitis, but increased in patients with ileal resection, chronic liver disease, and steatorrhea due to chronic pancratitis or sprue. There existed a positive correlation between 14C-oxalate absorption and the amount of fecal fat excretion. The data suggest that hyperoxaluria and hyperabsorption of oxalate are not a specific finding in patients with bile acid malabsorption, but may occur too, in steatorrhea without alteration of bile acid metabolism.
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PMID:[Enteric hyperoxaluria. I. Intestinal oxalate absorption in gastrointestinal diseases (author's transl)]. 68 26

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

Urinary oxalate excretion was measured in healthy persons and patients with Crohn's disease, colitis ulcerosa, sprue and other diseases accompanied with malabsorption, and patients with insufficiency of the exocrine pancreas gland. Further measurements were made in patients after resection of parts of the small intestine or the colon. We found a clear increase of urinary oxalate excretion in patients with resected parts of the small intestine, sprue or other malabsorption syndromes. In 4 patients with resected parts of small intestine or pancreas we even found urolithiasis. Urinary oxalate excretion correlated significantly with steatorrhoea and increased if larger parts of small intestine were resected. Increased resorption of oxalate from food causes increased urinary excretion. Details about the patho-mechanism of this increased excretion are not known yet; an important factor seems to be the reduced absorption of fat in the small intestine.
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PMID:[Hyperoxaluriaas a complication of intestinal diseases (author's transl)]. 99 43

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

We have evaluated the urinary excretion of promoting (calcium, phosphorus, uric acid, oxalate) and inhibiting (citrate, magnesium, glycosaminoglycans) factors of crystallization in subjects with idiopathic hypercalciuria and calcium urolithiasis and in a control group. The examined children had a free diet and were drug free for the last 2 weeks. They were not affected by malabsorption, D-RTA, urinary tract infection, or urinary tract malformation (factors interfering with urinary excretion of citrate and oxalate). In the patients with calcium urolithiasis, the daily urinary excretion of oxalate was significantly higher (p less than 0.01), and the urinary excretion of citrate was significantly lower (p less than 0.001) than in the subjects with idiopathic hypercalciuria and in the control group. Among the subjects with idiopathic hypercalciuria, those aged 4-9 years had a significantly reduced, though in the normal range, urinary excretion of citrate as compared with those aged 10-15 years (362 +/- 189 and 503 +/- 198 mg/g creatinine/24 h, respectively; p less than 0.01). Our data show that hypocitruria may play an important role in the pathogenesis of urolithiasis in children with idiopathic hypercalciuria. In these cases, the urinary citrate excretion was not inversely related to age, as has been suggested by other authors.
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PMID:Promoters and inhibitors of calcium urolithiasis in children. 225 56

One hundred and sixty three children who received total parenteral nutrition (TPN), including 7 cases of short bowel syndrome, were studied to evaluate the role of TPN in the management of infants with extremely short bowel. Three of the seven were died of sepsis related with central venous catheter (CV catheter) during the period of malabsorption when TPN was necessary. Two children of other diseases were died of catheter sepsis, 5 out of 163 in total, making the mortality late of TPN 3%. Incidence of CV catheter related complications was significantly less frequent in Broviac catheter when compared with conventional Silastic catheter (p less than 0.01). Another significant complication of TPN in cases of short bowel syndrome was hepatic dysfunction. Cholestatic liver dysfunction seemed to be cleared when enteral feeding was started even with TPN going on. Oral feeding should be started in the early postoperative period with concomitant TPN covering the fluid loss. A case of copper deficiency with high output jejunostomy and a case of urolithiasis with hyperoxaluria complicated with short bowel were reported.
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PMID:[Long-term TPN for short bowel syndrome]. 314 68

Mg deficiency is a frequent complication of inflammatory bowel disease (IBD) demonstrated in 13-88% of patients. Decreased oral intake, malabsorption and increased intestinal losses are the major causes of Mg deficiency. The complications of Mg deficiency include: cramps, bone pain, delirium, acute crises of tetany, fatigue, depression, cardiac abnormalities, urolithiasis, impaired healing and colonic motility disorders. Serum Mg is an insensitive index of Mg status in IBD. Twenty-four-hour urinary excretion of Mg is a sensitive index and should be monitored periodically. Parenteral Mg requirements in patients with IBD are at least 120 mg/day or more depending upon fecal or stomal losses. Oral requirements may be as great as 700 mg/day depending on the severity of malabsorption.
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PMID:Magnesium and inflammatory bowel disease. 329 19

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

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

Although patients with Hirschsprung's disease (HD) carry some factors that increase the risk of urolithiasis this fact seems to be underestimated. Among 302 patients with HD, four patients (1.32%) with urolithiasis were encountered. Since factors increasing the risk of urolithiasis such as urinary tract infection, constipation, vesicoureteral reflux, enteric resections and malabsorption may be encountered during the course of HD, an increased risk of urolithiasis in these patients should be expected.
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PMID:Urolithiasis in patients with Hirschsprung's disease. 924


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