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

Metabolic disorders are the most frequent risk factor for the development of urolithiasis. They are manigenic substances or deficiency of inhibitors of crystalgenic substances or deficiency of inhibitors of crystallization and aggregation. The authors use for their diagnosis a modification of Pak's procedure. It involves examination of 24-hour urine with the patient on a low-calcium diet, supplemented by urine examination on fasting and after a 1000 mg calcium load. The procedure includes also examination of serum and bacteriological examination of urine. A total of 93% of patients with calcium lithiasis had a metabolic disorder, 42% suffered from idiopathic hypercalciuria, 32% from hyperuricosuria, 19% from hyperoxaluria, 15% from magnesium deficiency and 38% from hypocitraturia. On the other hand, patients with uric acid lithiasis had a detectable metabolic disorder only in 62%. Active detection of metabolic disorders is essential for the introduction of effective, specific metaphylaxis of urolithiasis.
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PMID:[Detection of metabolic disorders as a cause of urolithiasis in clinical practice]. 272 Jul 28

A shortened small intestine may end at a stoma or be anastomosed to the colon. Patients with a jejunostomy, but not those with a colon, lose large amounts of sodium. The intake and absorption of sodium can be increased by sipping a sodium-glucose solution; stomal loss can be reduced by restricting water or low-sodium drinks. If a stoma is situated less than 100 cm along the jejunum, a constant negative sodium balance may necessitate parenteral saline supplements. Gastric anti-secretory drugs or a somatostatin analogue reduce jejunostomy losses in such patients but do not restore a positive sodium balance. Loperamide or codeine phosphate benefit some patients. Magnesium deficiency can usually be corrected by oral magnesium oxide supplements. An elemental or hydrolysed diet is not beneficial. Patients with a jejunostomy can maintain a normal diet without fat reduction. When the colon is present, unabsorbed carbohydrate is fermented to absorbable short chain fatty acids. Unabsorbed long chain fatty acids and bile salts cause watery diarrhoea and increased colonic oxalate absorption with hyperoxaluria. Such patients benefit from a high carbohydrate, low-fat and low-oxalate diet. Parenteral nutrition is needed only by the few patients unable to maintain health or avoid socially disabling diarrhoea despite these measures.
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PMID:Review article: practical management of the short bowel. 769 44

Male weanling rats were maintained on magnesium-deficient diet for 30 d and compared with pair-fed control rats fed magnesium-supplemented diet. Magnesium deficiency led to slow growth and finally to a significant decrease in body weight (P < 0.001) accompanied by a significant hypomagnesaemia, hypomagnesuria and hyperoxaluria (P < 0.001 in each case) in experimental rats as compared to the control rats. Magnesium deficiency altered the glyoxylate metabolism in the liver and kidney mitochondria by significantly decreasing glyoxylate oxidation (by 26 per cent in liver and 17 per cent in kidney) and activity of alpha-ketoglutarate:glyoxylate carboligase enzyme (by 35 per cent in liver and 27 per cent in kidney) in the experimental animals. A significant increase in the specific activities of glycolic acid oxidase (P < 0.001) and glycolic acid dehydrogenase (P < 0.01) and a significant decrease in alanine transaminase (P < 0.01) was also observed in magnesium-deficient rats. No change in liver and kidney lactate dehydrogenase was observed. Thus magnesium deficiency in rats leads to accumulation of glyoxylate in the tissues, a part of which is converted into oxalate, thereby promoting hyperoxaluria.
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PMID:Oxalate metabolism in magnesium-deficient rats. 827 58