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

100 g of spinach a day was added to the hospital diet of fifty-four patients with suspected malabsorption. Hyperoxaluria was found in thirty-eight patients; all of them had steatorrhoea. No patient with steatorrhoea had a urinary oxalate excretion of less than 40 mg a day. Ten other patients had hyperoxaluria, but the faecal fat determinations were regarded as unreliable in almost all and malabsorption could not be confirmed. It is suggested that in clinical practice determination of urinary oxalate after an oral load of oxalate could replace faecal fat determination in most patients with suspected malabsorption.
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PMID:Urinary oxalate on a high-oxalate diet as a clinical test of malabsorption. 7 94

Fourteen patients with ileal dysfunction due to resection or bypass were encountered over an 18-month period. Symptoms had been present for a mean period of 1.8 years. Diarrhoea was a universal symptom, and varied from mild to incapacitating. Weight loss, due in part to malabsorption and in part to the patients' fear of eating, occurred in 10 of 14 patients. The chief metabolic abnormalities were steatorrhoea and hypokalaemia. Vitamin B12 deficiency, folate deficiency, anaemia, hypoalbuminaemia, hypocalcaemia, hypomagnesaemia, hyperoxaluria, and an abnormal prothrombin ratio were less frequently seen. Treatment with cholestyramine and/or long-chain fat restriction effectively reduced diarrhoea in every case, and this was supplemented by replacement of specific deficiencies. There was little added benefit from non-specific antidiarrhoeal agents. It was found that the major symptoms of ileal dysfunction are readily treated, but that attention should also be given to a number of nutritional deficiencies.
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PMID:Consequences of ileal dysfunction: an approach to management. 10 34

To investigate the possibility of measuring urinary oxalate output instead of faecal fat excretion as an outpatient screening test for steatorrhoea, we determined 24 hour urinary oxalate and five day faecal fat excretion before and during an oral load of sodium oxalate 600 mg daily (oxalate 4.44 mmol), in 32 patients with suspected malabsorption on a diet containing oxalate 30 mg (0.33 mmol), fat 50 g (180 mmol), and calcium 1 g (25 mmol). Nineteen patients proved to have steatorrhoea (mean faecal fat 62 mmol/24 h, range 19--186 mmol) of varying aetiologies. On the diet alone, urinary oxalate was raised in only nine of these patients (mean 0.25 mmol/24 h, range 0.08--0.59 mmol) (normal less than 0.20). By contrast, when the diet was supplemented with oral sodium oxalate, all 19 patients with steatorrhoea had hyperoxaluria (mean 0.91 mmol/24 h, range 0.46--1.44 mmol) (normal less than 0.44). There was a significant positive linear relationship between urinary oxalate and faecal fat when the 32 patients were on the high oxalate intake (r = 0.73, P less than 0.001), but not when they were on the low oxalate intake. Mean percentage absorption of orally administered oxalate was 5.8 +/- 0.99% (+/- 1 SD) in normal subjects and 14.7 +/- 6.0% (P less than 0.002) in patients with steatorrhoea. Measurement of urinary oxalate output during oral sodium oxalate loading appears to be a reliable and convenient screening test for steatorrhoea.
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PMID:Oxalate loading test: a screening test for steatorrhoea. 52 84

This work was designed to investigate the site of oxalate hyperabsorption in malabsorption syndromes. 1) Urinary oxalate excretion was measured in 27 patients with ileal resection (IR) and steatorrhea. Mean urinary oxalate excretion was high in 13 patients with IR and intact colon and in 9 subjects with IR and right hemicolectomy (90.2 +/- 11.9 and 108 +/- 18.6 mg per 24 hours; mean +/- S.E.M.), whereas it was normal in 5 patients with IR and ileostomy (21.9 +/- 4.4 mg per 24 hours). Steatorrhea was similar in the three groups. 2) On one patient of the last group in whom the colon had not been removed initially but excluded closure of the ileostomy resulted in the development of frank hyperoxaluria. 3) Intracolonic perfusion of calcium (1.93 g per day) abolished or greatly reduced the hyperoxaluria in 3 patients. These results indicate that the colon is the major site of oxalate hyperabsorption, and the right colon is not necessary for the development of hyperoxaluria in malabsorption syndromes.
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PMID:Evidence for excessive absorption of oxalate by the colon in enteric hyperoxaluria. 63 58

143 patients (70 patients with Crohn's disease, 11 with ulcerative colitis, 40 with an intestinal by-pass operation, 9 with non-tropical sprue, 10 with short bowel syndrome, and 3 with other gastrointestinal disease) were studied during a metabolic regime including a fixed oral supply of 70 g fat, 800 mg calcium, and 200 mg oxalate. Faecal fat, 47Ca-absorption, 14C-oxalate absorption, and renal oxalate excretion were measured, and in the majority of patients a 14C-glyco-cholic acid breath test was also performed. 14Ca-absorption was practically identical (r = 0.92), whether determined by whole-body counting or from the accumulation of absorbed 47Ca in the skeleton of the underarm. 14C-oxalate absorption and renal oxalate excretion agreed well (r = 0.85). Steatorrhoea correlated weakly with renal oxalate excretion (r = 0.63, p less than 0.001), whereas no correlation was present between faecal fat and calcium absorption or between oxalate and calcium absorption under the constant conditions prevailing during the study. It is recommended that a "trifixed" regime with absorption studies of fat, calcium, and oxalate be undertaken previous to therapy that aims at a reduction of steatorrhoea or hyperoxaluria or an improvement of calcium absorption in chronic malabsorption syndromes, not least because therapy of these categories of patients most often continues for years.
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PMID:Standardized ("trifixed") diet in the study of chronic malabsorption syndromes. 67 51

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

The importance of intestinal resection, exclusion of the colon, and steatorrhoea for secondary hyperoxaluria was studied in 81 patients with Crohn's disease and 12 patients with ileostomy after colectomy for ulcerative colitis during a metabolic regime including a fixed oral supply of fat, calcium, and oxalate. Hyperoxaluria (greater than 48 mg (greater than 0.5 mmol) per 24 h) was present in 21 patients with Crohn's disease. All but one half or more of the colon preserved. Renal oxalate excretion was related to the amount of ileum resected. 14C-oxalate absorption was significantly higher in patients with ileal resection and the whole colon preserved than in patients with ileal resection plus hemicolectomy, despite the fact that the latter group had the most extensive ileal resections. Faecal fat and oxalate excretion agreed well in patients without ileostomy (r = 0.76, p less than 0.001), and renal oxalate excretion was significantly higher in patients with steatorrhea and the colon preserved than in patients without steatorrhoea. In all 93 patients 14C-oxalate absorption and renal oxalate excretion was positively correlated with a coefficient of correlation of 0.76 (p less than 0.001). No correlation was present between 47Ca- and 14C-oxalate absorption. The study confirm that a preserved colon is necessary for secondary hyperoxaluria and stresses the importance of ileal resection and steatorrhoea.
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PMID:Enteric hyperoxaluria: dependence on small intestinal resection, colectomy, and steatorrhoea in chronic inflammatory bowel disease. 70 53

To investigate the role of the colon in increased oxalate absorption, we measured urinary oxalate and fecal fat excretion in 26 patients with gastrointestinal disease. Eight patients with steatorrhea of various causes (Crohn's disease [two], chronic pancreatitis [four], jejunoileal bypass [one] and extrahepatic biliary obstruction [one]) had hyperoxaluria (greater than 45 mg per 24 hours). All these patients had intact colons. In contrast, none of five patients with ileostomies and steatorrhea secondary to ileal resection had hyperoxaluria. Absorption of 14C-oxalate was increased in three patients with steatorrhea and intact colons but not in three patients with steatorrhea and an ileostomy. Thus, the colon is both the site of and required for increased oxalate absorption in enteric hyperoxaluria. The lack of a direct relation between fecal fat excretion and urinary oxalate excretion in the patients with hyperoxaluria and steatorrhea suggests that steatorrhea, although important, is not the only determinant in the pathogenesis of hyperoxaluria.
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PMID:Importance of the colon in enteric hyperoxaluria. 83 Nov 27

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

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


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