Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent data have shown that administration of prostaglandin inhibitors to patients with hypercalciuric nephrolithiasis decreased urinary calcium excretion, implying a possible role for prostaglandins in calcium excretion. To explore this hypothesis, we investigated the effect of single dose or 7 days' administrations of aspirin (100 mg/kg orally) or indomethacin (20 mg/kg, orally) on the urinary and serum concentrations of calcium, magnesium and inorganic phosphate. Experiments were performed in normocalcaemic and hypercalcaemic rats. Hypercalcaemia and hypercalciuria were induced in male Wistar albino rats by administration of vitamin D3 (20,000 IU/daily) for 7 days. Aspirin and indomethacin both significantly lowered the urinary calcium excretion in normocalciuric and hypercalciuric rats. The acute administration of indomethacin caused greater reduction of calcium excretion than that produced by the acute administration of aspirin, whereas aspirin showed greater activity than indomethacin after the long-term use of each. Aspirin induced hypocalcaemia in normocalcaemic rats and abolished the hypercalcaemia in hypercalcaemic rats. On the contrary, indomethacin, a specific prostaglandin biosynthesis inhibitor, increased serum levels of calcium. Hypophosphataemia was observed only after the administration of a single dose of aspirin in normocalcaemic rats, while the reduction of urinary phosphate excretion was investigated in hypercalciuric rats after the acute and chronic administration of indomethacin. Serum levels of phosphate were not altered significantly by acute or chronic administration of indomethacin. A single dose of indomethacin significantly reduced urinary excretion of magnesium in both groups of rats. However, the acute and chronic administration of aspirin resulted in non-significant changes in serum and urinary concentrations of magnesium. These data suggest that aspirin has hypocalcaemic and hypocalciuric actions while indomethacin has only a hypocalciuric effect. Aspirin may produce these actions by two mechanisms, one of them like that of indomethacin which is dependent on the inhibition of biosynthesis of prostaglandins, and another possible mechanism that is not related to the inhibition of prostaglandin biosynthesis. This suggestion may be supported by the discrepancy between the effects of aspirin and indomethacin on the renal handling and serum concentrations of magnesium and inorganic phosphate.
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PMID:Effect of aspirin and indomethacin on the serum and urinary calcium, magnesium and phosphate. 233 Mar 39

Caffeine ingestion increases urinary calcium excretion. The mechanism is not known, but prostaglandin synthesis has been implicated. We hypothesized that administration of a prostaglandin inhibitor such as acetylsalicylic acid (aspirin) along with caffeine would prevent caffeine-induced hypercalciuria. We measured 3-hour excretion in fasting subjects who each randomly ingested four treatments on nonconcurrent mornings: no drug, caffeine (5 mg/kg body weight), acetylsalicylic acid (650 mg), or caffeine plus acetylsalicylic acid. In experiment 1, nine healthy premenopausal female subjects were studied; each treatment was taken with 200 ml of orange juice. Water was provided hourly to encourage urine flow. Urinary calcium excretion rose with caffeine treatment; mean 3-hour calcium (mmol/mmol creatinine) was 0.49 +/- 0.07 compared with 0.23 +/- 0.04 during the no-drug treatment. Acetylsalicylic acid caused a significant reduction in urinary calcium to 0.13 +/- 0.08; when it was combined with caffeine, caffeine-induced calcium excretion fell significantly to 0.35 +/- 0.08. Sodium excretion tended to reflect calcium excretion. Urinary prostaglandin E(2) fell significantly with acetylsalicylic acid, with and without caffeine. There were no significant changes in creatinine, water, or potassium excretion. Experiment 2 was similar, except that water was substituted for orange juice to test the possibility that acetylsalicylic acid affected elevated but not basal calcium excretion. Similar and even more pronounced results were obtained, with caffeine causing a threefold increase in urinary calcium, acetylsalicylic acid causing a decrease by half, and the combined drug treatment being greater than no drug but less than caffeine alone. Urinary phosphorus rose significantly with caffeine alone. Prostaglandin synthesis may not be directly involved in caffeine-induced hypercalciuria, as the magnitude of the caffeine-induced increase was similar when treatments given the acetylsalicylic acid were compared with those without a prostaglandin synthesis inhibitor.
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PMID:Effect of prostaglandin inhibition on caffeine-induced hypercalciuria in healthy women. 1553 5