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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence is presented that many of the enteric and systemic manifestations after jejunoileal bypass can be related to an inflammatory process within the bypassed small bowel rather than to the surgically induced sequelae of a short bowel syndrome with malabsorption. Invasion of the excluded segment by fecal flora was associated with a histologically demonstrable inflammatory response of the mucosa. The disorder was of variable severity and duration and occurred in the majority of 28 bypass patients. Progression to a clinical syndrome resembling an acute abdomen occurred in about 15% of the patients. Small bowel ileus and, in some patients, obstruction of the colon were suggested by physical signs and x-ray findings. Surgical exploration in such instances demonstrated an inflammaotry process of the excluded small bowel loops with severe distention of this segment and of the colon, but not organic obstruction. Pneumatosis cystoides intestinalis was a sequal in two patients. Exudative protein loss was documented in the severe cases. Most of the systemic sequelae are comparable to those seen with inflammatory diseases of the bowel such as Crohn's disease. Fever, excessive weight and lean tissue loss, and the involvement of skin, blood vessels, joints and possibly, the liver suggest an immune response as a common factor in the pathogenesis. The clinical improvement with antibiotics such as metronidazole or with restitution of normal bowel continuity indicates that the bacterial flora in the excluded small bowel segment or its byproducts are causally related to the systemic complications. Hyperoxaluria may be primarily the sequela of steatorrhea and not of the inflammatory process.
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PMID:Bypass enteropathy: an inflammatory process in the excluded segment with systemic complications. 83 42

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

A 45-year-old man underwent a jejunoileal shunt procedure for obesity. Twenty months later he developed severe oxalosis and chronic renal failure, which required maintenance hemodialysis. The sequential observation of two biopsy specimens and the necropsy (over a span of 39 months) suggests that oxalate deposition caused tubular obstruction and destruction with subsequent atrophy of nephrons. This indicates that patients undergoing intestinal bypass are at risk for developing irreversible renal failure due to enteric hyperoxaluria.
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PMID:Oxalosis and chronic renal failure after intestinal bypass. 83 9

A perfusion technique has been used to study the effect of sodium chenodeoxycholate (5 mmol 1-1) on absorption of oxalate (2 mmol 1-1) from the surgically excluded colon in two patients with chronic liver disease. Colonic absorption of oxalate increased at least fivefold when sodium chenodeoxycholate was incorporated in the perfusion solutions. This observation may explain enteric hyperoxaluria after ileal resection and in some other gastrointestinal disorders.
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PMID:Effect of sodium chenodeoxycholate on oxalate absorption from the excluded human colon--a mechanism for 'enteric' hyperoxaluria. 85 53

The effect of fat malabsorption on the absorption and renal excretion of dietary oxalate was studied in four patients with sprue and in two patients with dermatitis herpetiformis and sprue-like jejunal histology. Hyperoxaluria was present in all patients with sprue when fat malabsorption was severe. Urinary oxalate excretion decreased in two of the three patients with coeliac sprue when their fat malabsorption had improved after three months of dietary gluten restriction. Neither patient with dermatitis herpetiformis and sprue had steatorrhoea. In these patients, urinary oxalate excretion was always within normal limits. A significant positive linear relationship (y=28.25 +4-84x; r=0-82; P less than 0-01) was demonstrated between faecal fat and urinary oxalate excretion. The results of this study support the concept that severe malabsorption of dietary fat plays a primary causative role in enteric hyperoxaluria.
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PMID:Hyperoxaluria correlates with fat malabsorption in patients with sprue. 87 37

The effect of oral administration of cholestyramine, neomycine, calcium, and bile acids on intestinal 14C-oxalate absorption and urinary oxalate excretion was assessed in patients with normal or increased ('enteric' hyperoxaluria) urinary oxalate excretion. Cholestyramine, neomycine and acute administration of chenodeoxycholic acid (2.75 g/24 h) did not affect significantly 14C-oxalate absorption or urinary oxalate excretion. Oral administration of calcium markedly reduced 14C-oxalate absorption (88.2%) and urinary oxalate excretion (46%). Calcium-induced reduction of intestinal oxalate absorption was more pronounced in patients with hyperabsorption of oxalate than in subjects with normal oxalate absorption or excretion. Patients on treatment with high doses of chenodeoxycholic acid (1.5-2.0 g/day) for dissolution of cholesterol gallstones had increased oxalate absorption and excretion, patients on long-term treatment with lower doses of chenodeoxycholic acid (0.75-1.0 g/day) exhibited normal absorption or urinary excretion of oxalate. The results do suggest that calcium and bile acids do play an important role in the pathogenesis of 'enteric' hyperoxaluria. It is suggested that the beneficial therapeutic effect of cholestyramine in hyperoxaluria due to ileal resection is rather caused by its bile acid binding property than by direct binding of oxalate within the intestinal lumen.
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PMID:'Enteral' hyperoxaluria. Effect of cholestyramine, calcium, neomycin, and bile acids on intestinal oxalate absorption in man. 88 68

Fourteen patients underwent small bowel bypass (SBB) takedown for complications such as chronic nausea and vomiting, excessive flatus, intractable diarrhea, liver dysfunction, electrolyte imbalance, hyperoxaluria with renal stones, and arthritis. The average weight loss in these 14 patients after SBB was 93 pounds (34% of initial weight), with a mean follow-up of 23 months. Four of the 14 patients had SBB takedown only and gained an average of 36 pounds over the ensuing 14 months. Similarly, three patients had SBB takedown with delayed (asynchronous) gastric bypass (GB) and gained an average of 55 pounds during the 14 months prior to GB. Following GB these three patients lost only an additional 8 pounds over a 12 month period, leaving them 47 pounds heavier than at the time of SBB takedown. In contrast, seven patients treated with SBB takedown and synchronous GB not only maintained the weight reduction obtained with SBB, but, in addition, had further modest weight reductions (average, 18 pounds), for a mean follow-up of 8 months. There were no serious operative or late complications with any of the above operations. In addition, the complications leading to SBB takedown resolved in each case. It is concluded that synchronous GB is an effective means of maintaining the weight reduction in the morbidly obese patient after SBB takedown.
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PMID:Management of the morbidly obese patient after small bowel bypass failure. 88 3

In the female rat intoxicated with ethylene glycol the oxaluria increases with the degree of intoxication. The increase is less in the animals treated with succinimide. The comparative study of the results of the dosages made with gas-liquid-chromatography and by various colorimetric methods show that this later gives varying results and underestimates high concentrations of oxalic acid. The result is that any study based on results of dosages of urinary oxalic acid made by colorimetry must be taken with some reserve, and this on whether the oxalic lithiasis is experimentally induced or human, or whether its evolution is spontaneous or influenced by a therapeutic.
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PMID:Effect of succinimide on hyperoxaluria in the rat estimated value of the different dosing methods of oxaluria. 88 49

The current concepts of normal fat absorption and the entero-hepatic circulation of bile acids are being reviewed with emphasis on the steps which are clinically important. Based on an understanding of normal physiology, diseases associated with steatorrhea can be classified according to pathogenetic mechanisms. In some diseases the pathogenesis of the steatorrhea is not understood. Malabsorption of fat and bile salts can have characteristic consequences such as nutritional deficiencies, diarrhea, hyperoxaluria with nephrolithiasis, and cholelithiasis. For quantitative assessment of steatorrhea chemical analysis of fecal fat is necessary.
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PMID:[Absorption and malabsorption of fat and bile acids (author's transl)]. 89 17

alpha-Ketoglutarate: glyoxylate carboligase activity has been reported by other laboratories to be present in mitochondria and in the cytosol of mammalian tissues; the mitochondrial activity is associated with the alpha-ketoglutarate decarboxylase moiety of the alpha-ketoglutarate dehydrogenase complex. The cellular distribution of the carboligase has been re-examined here using marker enzymes of known localization in order to monitor the composition of subcellular fractions prepared by differential centrifugation. Carboligase activity paralleled the activity of the mitochondrial matrix enzyme citrate synthase in subcellular fractions prepared from rat liver, heart and brain as well as from rabbit liver. Whole rat liver mitochondria upon lysis released both carboligase and citrate synthase. The activity patterns of several other extramitochondrial marker enzymes differed significantly from that of carboligase in rat liver. In addition, the distribution pattern of carboligase was similar to that of alpha-ketoglutarate decarboxylase and of alpha-ketoglutarate dehydrogenase complex. The data indicate that alpha-ketoglutarate: glyoxylate carboligase activity is located exclusively within the mitochondria of the rat and rabbit tissues investigated. There is no evidence for a cytosolic form of the enzyme. Thus the report from other laboratory that the molecular etiology of the human genetic disorder hyperoxaluria type I is a deficiency of cytosolic carboligase must be questioned.
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PMID:Cellular localization of alpha-ketoglutarate: glyoxylate carboligase in rat tissues. 91 88


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