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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

We prospectively studied 15 infants who, before 3 months of age, underwent resection of the small intestine-proximal in 3 infants, mid in 6, and distal in 6. Two died before one year of age. Many required prolonged parenteral nutrition, but by one year, 12 of the 13 survivors were on oral feedings only, and seven were above the third percentile for height and weight. Developmental delay occurred in the early postoperative period but diminished with time. There was compensatory adaptation of the remaining gut, shown by improving fat and B12 absorption and duodenal bile-salt concentrations. Bacterial contamination complicating end-to-side anastomoses occurred in two cases (P), gastric hyperacidity in four of 12 (1P, 3M), and hyperoxaluria in eight of 14 (1P, 5M, 2D). Studies of immune competence revealed normal cellular immune function (11/11), transient hypogammaglobulinemia (3/14), hypocomplementemia (1/12), and serum autoantibodies (3/10). Thus, massive resection of the small intestine did not preclude spontaneous improvement in absorptive function, growth, and development.
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PMID:A clinical study of young infants after small intestinal resection. 10 3

The effects of some putative inhibitors of oxalate production or urinary oxalate excretion have been investigated in the Cynamolgus monkey and in patients with Type I primary hyperoxaluria (hyperoxaluria with glycollic aciduria). Sodium-1-hydroxybutan-sulphonate, D,L-phenyllactate, succinimide and isocarboxazide did not reduce the urinary oxalate excretion in the monkeys. Pyridoxine reduced the excretion of oxalate and glycollate in some patients, and its therapeutic use has been documented over a five-year period. Succinimide, which has been used by other workers for the treatment of non-hyperoxaluric stone formers, did not decrease the excretion of either oxalate or glycollate in three patients in whom it was tried. It did not change the inhibitory activity of the urine with respect to the growth and aggregation of calcium oxalate crystals in any of the three patients, and it did not have any consistent effect on the excretion of calcium oxalate crystals in the one patient who had detectable crystaluria before treatment. We have identified several metabolites of succinimide in the urine of patients taking the drug. These include 2,3-dehydrosuccinamic, 2-hydroxysuccinamic and 3-hydroxysuccinamic acids. Isocarboxazide, cholestyramine and thiamine did not affect the urinary oxalate excretion in the patients. The significance of these observations from the viewpoint of the treatment of primary hyperoxaluria is discussed.
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PMID:Studies on some possible biochemical treatments of primary hyperoxaluria. 11 1

A 61 year old man had chronic renal failure because of oxaluria and renal calculi. Two years before death, while on hemodialysis, he developed severe progressive peripheral neuropathy. At autopsy calcium oxalate crystals were found in the peripheral nerves and other tissues. Nerve lesions included segmental demyelination, axonal degeneration and crystalline deposits within the myelin sheath. Ultrastructurally there were foci of osmiophilic granular material within myelin lamellae and endoneurium, and pleomorphic lamellar bodies in the perinuclear Schwann cell cytoplasm. It is probable that chronic hemodialysis favors the deposition of oxalate in the Schwann cells and the development of neuropathy in patients with primary hyperoxaluria and renal failure.
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PMID:Peripheral neuropathy in oxalosis. A case report with electron microscopic observations. 17 8

A patient with chronic renal disease due to primary hyperoxaluria developed a rapidly progressing motor neuropathy with marked impairment of nerve conduction. Pathological studies demonstrated the presence of both axonal degeneration and segmental demyelination, together with the presence of oxalate crystals within axons. It is suggested that the development of peripheral neuropathy complicating hyperoxaluria is a consequence of the increased life-span mad possible by haemodialysis.
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PMID:Peripheral neuropathy complicating primary hyperoxaluria. 18 38

A child with hyperoxaluria, probable Type I, was noted to have a "flecked retina" on funduscopic examination at age 2 1/2 months; it persisted throughout his seven years of life. The relationship of the ocular findings to his metabolic disease is discussed.
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PMID:"Flecked retina" --an association with primary hyperoxaluria. 19 75

Eighty patients with proved calcium urolithiasis participated in an outpatient study designed to define the most likely metabolic problem related to the cause of the stone disease. Diagnostic categories included absorptive hypercalciuria (33 patients), renal leak hypercalciuria (20 patients), hypomagnesiumuria (27 patients), hyperuricemia and hyperuricuria (16 patients), hyperoxaluria (15 patients), normal stone-former (4 patients), renal tubular acidosis (2 patients) and suspicion of hyperparathyroidism (7 patients). Of the 80 patients 40 had more than 1 defect. Patients with a high suspicion of hyperparathyroidism were excluded from the study. Based on these criteria treatment plans incorporating medications, diet or both were instituted. Of 21 patients observed for greater than 2 years 90 per cent have shown no new stone disease.
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PMID:Outpatient evaluation of patients with calcium urolithiasis. 43 49

The causes of, and physiopathological factors underlying the most common metabolic disorders implicated in the formation of renal stones are reviewed. These include hypercalciuria, hyperoxaluria, renal tubular acidosis, cystinuria and disturbances of purine metabolism. Apart from metabolic disorders the risk of stone formation is also influenced by a low inhibitor activity in urine. Though some aspects in the pathogenesis of urolithiasis remain uncertain, the exact knowlege of important aetiological factors of stone formation is the basis of correct treatment and the prevention of recurrence of urinary calculi.
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PMID:[The evaluation of patients with urinary calculi discloses disturbances of metabolism in 75% of all cases (author's transl)]. 47 69

The incidence of urolithiasis was registered in 87 patients with chronic inflammatory bowel disease and compared with that of renal oxalate excretion. All patients were studied while on a standardized diet with fixed amounts of fat, calcium, and oxalate. Pyelography had been performed in all. Nine, or 35%, of 26 hyperoxaluric patients had urolithiasis, compared with 14, or 23%, of 61 patients were normal renal oxalate excretion, the difference being statistically insignificant. No significant difference in urinary oxalate or urinary calcium in stone-formers as compared with non-stone-formers could be demonstrated. Oxalate was a more frequent component of calculi in patients with normal renal oxalate excretion than in patients with hyperoxalura. Thus, we were unable to demonstrate an increased incidence of urolithiasis in patients with hyperoxaluria compared with a control group with normal renal oxalate excretion. Our results cast doubt on the concept that enteric hyperoxaluria per se is the cause of stone diathesis in chronic inflammatory bowel disease.
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PMID:Urolithiasis and hyperoxaluria in chronic inflammatory bowel disease. 48 60


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