Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of vitamin D2 (VD2) on hypocalcemia were studied in 54 hypocalcemic patients (29 males and 25 females) on chronic hemodialysis. Calcium lactate (3 g/day) or VD2 (10,000 IU/day, 50,000 IU/day and 80,000 IU/day) were administered for 4 months in order to correct the hypocalcemia. Serum calcium, phosphate and alkaline phosphatase levels were measured and the effects of VD2 on these parameters of calcium metabolism were followed. 1) Calcium lactate or 10,000 IU/day of VD2 were not effective for the correction of hypocalcemia, while 50,000-80,000 IU/day of VD2 were effective. The effects of VD2 on serum calcium concentrations were dose-dependent, and the normalization of serum calcium concentrations was achieved more rapidly with higher doses of VD2. However, in the group treated with 80,000 IU/day of VD2, many patients developed hypercalcemia, but in the group treated with 50,000 IU/day of VD2, only a few patients did it. From these results, suitable dose (initial and maintenance doses) of VD2 in dialysed patients would be 50,000 IU/day. 2) When the responder group (normal serum calcium levels after 4 months of treatment with 50,000 IU/day of VD2) and the non-responder group serum calcium levels lower than 4.2 mEq/liter on the same condition) were compared, the durations of dialysis were significantly shorter in the former than those in the latter. This fact may suggest that the effects of VD2 administration on hypocalcemia in dialysed patients are partly dependent on the residual renal function concerning the conversion of 25-OH-D3 into 1,25 (OH)2D3.
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PMID:The effect of vitamin D2 on hypocalcemia in patients under chronic hemodialysis. 696 6

The potential value of xylitol in calcium therapy was evaluated by comparing the effect of dietary xylitol (50 g/kg diet) + calcium carbonate with the effects of calcium carbonate, calcium lactate and calcium citrate on bone repair of young male rats after the rats consumed for 3 wk a calcium-deficient diet (0.2 g Ca/kg diet). After this calcium-depletion period, the rats were fed for 2 wk one of four diets, each containing 5 g Ca/kg diet as one of the four dietary calcium sources. The diet of the control animals was supplemented with CaCO3 (5 g Ca/kg diet) throughout the study. The Ca-deficient rats showed low bone mass, low serum calcium and high serum 1,25-dihydroxycholecalciferol, parathyroid hormone (1-34 fraction) and osteocalcin concentrations. They also excreted magnesium, phosphate and hydroxyproline in the urine in high concentrations, and had high bone alkaline phosphatase and tartrate-resistant acid phosphatase activities. Most of these changes were reversed by the administered of the calcium salts. The highest recoveries of femoral dry weight, calcium, magnesium and phosphate were observed in the groups receiving xylitol+CaCO3 and calcium lactate. Calcium lactate and calcium citrate caused low serum phosphate concentration compared with rats receiving CaCO3 and with the age-matched Ca-replete controls. Xylitol-treated rats excreted more calcium and magnesium in urine than did the other rats, probably due to increased absorption of these minerals from the gut. These results suggest that dietary xylitol improves the bioavailability of calcium salts.
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PMID:Bone repair in calcium-deficient rats: comparison of xylitol+calcium carbonate with calcium carbonate, calcium lactate and calcium citrate on the repletion of calcium. 820 45

The effect of histamine H2-receptor antagonist (famotidine) on the phosphorus-binding abilities of calcium carbonate and calcium lactate were examined in 13 chronic hemodialysis patients. In seven patients receiving calcium carbonate, famotidine (20 mg/d) was given because of gastroduodenal disorders, and calcium carbonate was replaced with calcium lactate as a phosphorus binder after 4 wk of treatment with famotidine. With the 4-wk administration of famotidine accompanied by calcium carbonate, the serum phosphorus level increased from 6.3+/-0.9 to 7.1+/-0.5 mg/dl (P<0.05). However, with the substitution of calcium lactate, the serum phosphorus level decreased significantly when compared to that before substitution (6.3+/-0.2 and 6.0+/-0.9 mg/dl after 4 and 8 wk of substitution, respectively), despite continued administration of famotidine. Serum calcium, creatinine, alkaline phosphatase, high sensitive parathyroid hormone, blood urea nitrogen, arterial blood pH, and bicarbonate were not significantly altered during the trial period. In six control patients treated with calcium carbonate alone, there were no statistical changes in serum calcium and phosphorus levels after substitution of calcium lactate for calcium carbonate. These results suggest that famotidine significantly affects the phosphorus-binding ability of calcium carbonate, but not that of calcium lactate. A careful observation of changes in the serum phosphorus level should be required in hemodialysis patients receiving calcium carbonate and histamine H2-receptor antagonists. Calcium lactate may be useful as a phosphorus binder in such hemodialysis patients.
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PMID:Effect of histamine H2-receptor antagonist on the phosphorus-binding abilities of calcium carbonate and calcium lactate in hemodialysis patients. 1023 96