Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A previous short-term study of 10 weeks in 8 patients had shown us that with half the dose of elemental calcium, calcium acetate (CaAc) could control predialysis plasma phosphate (PPO4) as well as calcium carbonate (CaCO3) but that the incidence of hypercalcemia was not decreased. To better appreciate the value of CaAc in comparison to CaCO3, CaAc was given to 28 patients on chronic hemodialysis (6 men, 22 women, age 61 +/- 14 years; dialyzate Ca:1.5 mmol/l) for 6 months to replace CaCO3 at half the dose of elemental calcium (1,235 +/- 521 versus 2,375 +/- 1,470 mg/day). Because of gastrointestinal intolerance, CaAc had to be discontinued in 5 patients after 1-5 months. Magnesium hydroxide [Mg(OH)2] given in 18 of them in association with CaCO3 was discontinued and reintroduced in 6 patients in order to keep PPO4 < 2 mmol/l. Mean dosage of Mg(OH)2 was 2.09 +/- 1.4 g/day with CaCO3 and 0.9 +/- 0.5 with CaAc. Predialysis plasma concentrations of calcium and phosphate were monitored weekly during the 3 months of the control period under CaCO3 and during the 6-month administration of CaAc. Plasma calcium (PCa) was comparable with the 2 treatments (2.47 +/- 0.11 vs. 2.5 +/- 0.10 mmol/l), but PPO4 was significantly lower with CaAc (1.82 +/- 0.26 vs. 1.73 +/- 0.23 mmol/l). Plasma alkaline phosphatase remained constant (122 +/- 66 vs. 122 +/- 70; normal < 170 UI/l) as well as plasma intact PTH (121 +/- 153 vs. 121 +/- 146; normal < 54 pg/ml) and plasma aluminum (0.34 +/- 0.23 vs. 0.32 +/- 0.20 mumol/l).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term (6 months) cross-over comparison of calcium acetate with calcium carbonate as phosphate binder. 844 61

Persistent hypercalcemia attributable to parathyroid gland hyperplasia was identified in 6 dogs with primary hyperparathyroidism. Clinical signs included polydipsia (n = 4), polyuria (n = 4), and signs caused by cystic calculi (n = 3). Abnormal clinical pathologic findings included hypercalcemia (mean, 13.6 mg/dl; range, 12.6 to 14.7 mg/dl; n = 6), hypophosphatemia (mean, 2.2 mg/dl; range, 1.4 to 2.9 mg/dl; n = 6), high serum alkaline phosphatase activity (mean, 222 IU/L; range, 161 to 286 IU/L; n = 3), and isosthenuria (mean, 1.012; range, 1.006 to 1.017; n = 6). Serum parathyroid hormone concentration was within the reference range or high (mean, 23 pmol/L; range, 7 to 119 pmol/L; reference range, 1.5 to 13 pmol/L) in all dogs. At surgery, the number of large parathyroid glands was variable, being limited to 1 gland in 3 dogs, 2 glands in 2 dogs, and 4 glands in 1 dog. All visibly large parathyroid glands were surgically removed from each dog. Serum calcium concentration decreased into or below the reference range within 72 hours of surgery in all dogs, confirming the diagnosis of primary parathyroid disease. Multiple nodules of adenomatous hyperplasia were identified in each dog. All 6 dogs were treated with vitamin D and calcium carbonate following surgery. The dog from which all 4 parathyroid glands were removed has remained eucalcemic for more than 1 year with vitamin D supplementation. Vitamin D and calcium administration was discontinued within 4 to 12 weeks of surgery in the remaining 5 dogs. These dogs remained eucalcemic without vitamin D supplementation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Primary parathyroid gland hyperplasia in dogs: six cases (1982-1991). 847 30

Standard therapy with orally administered active metabolites of vitamin D3 often does not satisfactorily control the biochemical manifestations of secondary hyperparathyroidism in uremic patients. This may be due to inadequate serum concentrations of 1,25 (OH)2D3 achieved during the treatment. Eighteen patients on chronic hemodialysis (HD) with severe hyperparathyroidism were given high doses of calcitriol (1,25 (OH)2D3) or alphacalcidol (1 alpha-OH-D3) orally, in ten evenings preceding each HD session. The effect of the treatment on circulating parathyroid hormone (PTH), serum hydroxyproline, serum alkaline phosphatase and bone isoenzyme was examined in a pilot study during 5 weeks. Irrespective the preparation given the treatment caused 71.7 +/- 22.2% reduction of intact serum PTH concentration with only moderate rise of serum calcium. A decrease of serum hydroxyproline and activity of alkaline phosphatase with its bone fraction, the direct indexes of bone turnover reduction, was also observed. With ongoing calcium carbonate therapy (3-6 g/day) 5 episodes of mild, asymptomatic hypercalcemia was observed for the 108 times of the total number of examinations; in those cases the dose of alphacalcidol was reduced. Our observations indicate that intermittent administration of 1,25 (OH)2D3 as well as 1 alpha-OH-D3 in high oral doses effectively suppress PTH synthesis in uremic hyperparathyroidism already in a couple of weeks. The effect is similar to that obtained with intravenous administration of the vitamin D3 active metabolites.
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PMID:[Oral pulsatile therapy with active vitamin D3 metabolites--an efficient method of parathyroid hormone synthesis suppression in uremic patients with severe hyperparathyroidism. A pilot study]. 850 2

A randomized, prospective, double-blind test was carried out to compare the effects of heated oyster shell-seaweed calcium (AAA Ca), calcium carbonate, and placebo in 58 elderly, hospitalized women with the mean age of 80 divided into three groups. Group A received 900 mg/day Ca as AAA Ca, Group B 900 mg/day Ca as CaCO3, and Group C placebo besides regular hospital diet containing approximately 600 mg Ca/day for 24 months. From the 25th to the 30th month, all groups were given AAA Ca. Lumbar spine and radial bone mineral density (BMD) were measured at 3-month intervals. Urinary Ca/Cr and serum alkaline phosphatase, intact and midportion serum parathyroid hormone (PTH), and calcitonin were also measured at intervals. From the 6th to the 24th month of the study, the ratio of lumbar spine BMD (L2-L4 by DPX, Lunar) to the basal pretest value was consistently and significantly higher in Group A than Group C but not higher in Group B than in Group C. PTH, measured 12 months after the beginning of the study, was lower in Group A than in Group C, but no significant difference was found between Groups B and C. At 3 months after the placebo was switched to AAA Ca in Group C, serum PTH was significantly decreased from the level during placebo supplement. Morning urine Ca/Cr decreased in Groups A after 18 months and in B after 12 months, but not in C. Serum alkaline phosphatase decreased in Group A significantly compared with Group C, but not in Group B. AAA Ca appears to be effective for increasing BMD in elderly subjects.
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PMID:Heated oyster shell-seaweed calcium (AAA Ca) on osteoporosis. 866 52

Forty-five subjects (41 women and 4 men) in long-stay and medium-stay facilities, aged 74 to 95 years (mean 86.4 years), with 25-hydroxy-vitamin D levels less than 12 ng/ml, were treated for six consecutive months with two tablets per day of a preparation containing vitamin D3 (800 IU/day) and calcium carbonate (1 g elemental calcium/day). Serum levels of 25-hydroxy-vitamin D were very low at baseline (5.6 +/- 0.4 ng/ml) and rose significantly under treatment, to normal values, 33.2 +/- 1.2 and 40.9 +/- 2.1 ng/ml after three and six months, respectively (p < 0.001 for both comparisons). Serum calcium increased significantly, by 4.5% (p < 0.001) during the first three months, and remained at a plateau thereafter. Corrected serum calcium rose by 8.9% (p < 0.001) during the trial. No patient developed hypercalcemia. Serum parathyroid hormone levels, which were elevated at baseline (71.6 +/- 5.8 pg/ml; normal, 12 to 54 pg/ml), decreased gradually and significantly throughout the treatment period, by 43.0% and 67.1% after three and six months, respectively (p < 0.001 for both comparisons). Serum alkaline phosphatase activity fell concomitantly, by 9.9% after three months (p < 0.01) and 36.5% after six months (p < 0.001). In conclusion, the preparation used in our study is effective in correcting both the vitamin D deficiency that is prevalent in elderly institutionalized patients and the resultant increase in bone turnover.
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PMID:Biochemical effects of calcium and vitamin D supplementation in elderly, institutionalized, vitamin D-deficient patients. 868 85

It is still unclear whether dialysis modality, i.e., continuous ambulatory peritoneal dialysis (CAPD) versus hemodialysis (HD) specifically affects bone mineral density (BMD). To answer this question, 34 patients on HD and 25 on CAPD were matched for age, sex, height, and body weight with 125 normal subjects. BMD was measured using dual-energy X-ray absorptiometry (DXA; Hologic QDR 1000/W) at the lumbar spine (trabecular bone), the femoral neck (mixed cortical and trabecular bone), the distal tibial diaphysis (cortical bone), and the epiphysis (trabecular bone) in all subjects. No significant difference for blood hemoglobin, albumin, total and ionized calcium, intact parathyroid hormone (PTH) or phosphorus concentrations, as well as for alkaline phosphatase activity, failed renal allograft, prior steroid therapy, prior parathyroidectomy, duration of uremia, or of dialysis was found between patients on HD and those on CAPD. However, the residual daily urine volume and renal function at the time of the absorptiometry were higher in CAPD than in HD patients (p < 0.05) as well as the mean dialysate calcium concentration during dialysis, the blood bicarbonate concentration, and the residual renal function at the initiation of dialysis (p < 0.01, p < 0.05, and p < 0.005, respectively). In contrast, the total dose of calcium carbonate was lower in CAPD than in HD patients (p < 0.01). Results of BMD were expressed as Z scores (the number of standard deviations from the appropriate mean of BMD of 623 healthy subjects adjusted for age and sex). At the lumbar spine, no significant difference with respect to BMD was observed between the three groups. At the femoral neck and tibial epiphysis, HD patients had lower BMD (p < 0.001) than normal controls, whereas no difference was observed between HD and CAPD patients. At tibial diaphysis, patients on HD had lower BMD (p < 0.001) than patients on CAPD and than normal controls, with the values being similar in patients on CAPD and in normal controls. The results remained identical after exact matching of HD (n = 25) and CAPD (n = 25) patients for dialysis duration (1.9 +/- 0.3 and 1.7 +/- 0.3 years, respectively). Multiple regression analysis revealed significant negative correlations between Z scores at the lumbar spine (p < 0.05), femoral neck (p < 0.02), tibial diaphysis (p < 0.005), and tibial epiphysis (p < 0.05) on the one hand and plasma alkaline phosphatase activity on the other. The Z score at tibial diaphysis was also correlated with residual renal function at the initiation of dialysis (p < 0.05). In conclusion, this study provides evidence for the preservation of cortical bone with CAPD as opposed to HD. The higher residual renal function observed in the former treatment modality might account, at least in part, for this finding.
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PMID:Evidence for preservation of cortical bone mineral density in patients on continuous ambulatory peritoneal dialysis. 877 Jul 2

We studied 26 non-dialysed patients with chronic renal failure [creatinine clearance (CCr) 32.6 +/- 12.7 ml/min]. They were divided into three groups according to their CCr and serum intact parathyroid hormone (PTH) and were given 0.5 micrograms/day oral calcitriol (calcitriol group, n = 8), 3 g/day calcium carbonate (CaCO3 group, n = 10), or neither (control uraemic group, n = 8). Serum intact PTH decreased from 154 +/- 75 to 90 +/- 43 pg/ml in the calcitriol group (P < 0.01) and from 162 +/- 97 to 77 +/- 62 pg/ml in the CaCO3 group (P < 0.001). Calcium carbonate was also effective in suppressing serum tartrate-resistant acid phosphatase, alkaline phosphatase and intact osteocalcin levels, while calcitriol did not suppress serum osteocalcin. Secretion of interleukin-1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha) by phytohaemagglutinin A (PHA)-activated peripheral blood mononuclear cells (PBMC) was greater in uraemic patients than in age-matched healthy controls (n = 8). Calcitriol was effective in suppressing secretion of both cytokines, while calcium carbonate was capable of suppressing only TNF-alpha secretion. CCr decreased from 37.4 +/- 15.4 to 33.0 +/- 11.8 ml/min (P < 0.05) in the CaCO3 group, while it did not decrease in either the calcitriol group or the control uraemic group during a 6 month period. These results suggest that supplementation with calcitriol is necessary to maintain bone formation and normalize IL-1 beta and TNF-alpha secretion by activated PBMC in uraemic patients.
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PMID:Comparison of effects of calcitriol and calcium carbonate on secretion of interleukin-1 beta and tumour necrosis factor-alpha by uraemic peripheral blood mononuclear cells. 884 Mar 6

Recently, several reports have suggested that there is a higher incidence of low turnover bone in the absence of aluminium exposure in peritoneal dialysis patients than in hemodialysis patients. Relative hypoparathyroidism with mild hypercalcemia, induced by a positive calcium balance, is considered to be one of the major causes of this disorder. Thus, we recruited 9 continuous ambulatory peritoneal dialysis (CAPD) patients with relative hypoparathyroidism and low bone turnover [intact parathyroid hormone (iPTH) < 50 pg/mL, intact osteocalcin < 10.0 ng/mL] who had been prescribed 1.75 mmol/L calcium (Ca) dialysate for 5.0 +/- 0.3 years. They were then treated by low Ca (1.25 mmol/L) dialysate for nine months without vitamin D and aluminum administration. Intact PTH and bone metabolic markers [intact osteocalcin, alkaline phosphatase (ALP)] were measured every three months. Intact PTH levels increased from 21.1 +/- 3.8 to 159.2 +/- 32.8 pg/mL after the first three months; thereafter, those levels were maintained at around 150 pg/mL. On the other hand, intact osteocalcin levels rose consecutively from 6.7 +/- 1.2 to reach 22.0 +/- 3.8 ng/mL after nine months. Interestingly, the pattern of time course changes between PTH and intact osteocalcin was different. ALP activity did not change during the nine-month period. Corrected serum calcium was significantly decreased (p < 0.001) to approximately 0.25 mmol/L within one month, and the level remained almost the same thereafter. The serum phosphate level did not change without adjusting the original dose of calcium carbonate as a phosphate binder. We concluded that low Ca dialysate (1.25 mmol/L) is effective for the treatment of CAPD-related hypoparathyroidism with low bone turnover.
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PMID:Low calcium (1.25 mmol/L) dialysate can normalize relative hypoparathyroidism in CAPD patients with low bone turnover. 886 14

In this study, we prospectively evaluated the efficacy of calcium acetate in patients with chronic renal insufficiency on hemodialysis programme with secondary hyperparathyroidism and hyperphosphatemia, which are difficult to control by means of the usual finders (calcium carbonate and aluminium hydroxide) and who were treated with pulses of calcitriol. We studied 10 patients. The inclusion criteria were: a serum phosphorus higher than 6.5 mg/dl, a serum PTHi higher than 250 pg/ml and a serum calcium higher than 9.5. The former therapy was stopped at the time of the patient was included in the study. Calcium acetate was initially introduced with doses between 2.5-4 g/day according to previous calcium and phosphate values. Also, all patients were initially treated with intermittent subcutaneous bolus of Calcitriol were modified and adjusted according to serum concentrations of calcium, phosphorus and PTHi. The concentration of calcium in the dialyzed was of 1.25 mmol/l. Fortnightly total calcium, phosphate and alkaline phosphatase serum determinations and monthly aluminium and PTHi serum determinations were carried out. During the 6 months treatment, a decrease was observed in serum concentrations of phosphate (p < 0.01), aluminum (p < 0.02) and PTHi (p < 0.001) with no changes in the values of calcium (p = ns) nor alkaline phosphatase (p = ns). The incidence of hypercalcemia was low during the follow-up period (11% of all biochemical serum determinations) and was easily controlled. We can conclude that calcium acetate is a sure and effective finder of phosphorus with a very good tolerance. Administered together with pulses of calcitriol, and the use of a low calcium concentration in the dialysate, it does not increase the risk of hypercalcemia.
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PMID:[Usefulness of calcium acetate as a chelating of phosphorus in patients in hemodialysis with secondary hyperthyroidism]. 892 27

Degradable hydroxyapatite (HA) implants complexed with the resorption inhibiting agent bisphosphonate (PCP) and the mineralizing agent alkaline phosphatase (ALP) can theoretically maintain alveolar bone mass directly after extraction of teeth. The present in vitro study investigated the surface properties of PCP-ALP-complexed HA implants in relation to the requirements of implant behavior and action. Adsorbed PCP (pH 3.49) resulted in a flattening and broadening of the phosphate peaks and the formation of carbonate peaks in the HA pattern of the implant indicating a chemical alteration of the HA surface. Adsorption of ALP onto PCP-altered HA surfaces was 26% lower than onto HA implant blank surfaces. PCP-ALP-complexed HA implants released the PCP and ALP steadily and continuously over observation periods of, respectively, 75 and 14 days. During these observation periods, the ceramic grains of the HA implant became smaller and intergrain boundaries became broader. These morphologic characteristics suggested preconditioning of the HA implant surface for future bonding and degradation in vivo. Individual grains were no longer bonded to other grains and detached from the implant which had become rounded in shape. From in vitro mice experiments we found that PCP concentrations between 10(-4) and 10(-3) M resulted in 45Ca-release from the bone HA. Our calculations showed, however, that only a total concentration of 1.4 x 10(-4) M PCP was gradually released over the whole observation period. In another experiment, it appeared that a PCP concentration in solution < 10(-3) M did not reduce ALP activity. It is concluded that release of PCP by the PCP-ALP-complexed implants is maintained at levels in the range to impair osteoclast bone resorption but not high enough to block osteoblast activity. The amount of ALP released can lead to induction of bone formation onto implant surfaces. pH-induced alterations in the microstructure and chemistry of the HA surface allow for controlled degradation of the HA implants in vitro. A PCP-ALP-complexed HA implant acting as temporary scaffolding for alveolar bone growth enhancement, mineralization, and maintenance seems to be a reasonable concept for preservation of the edentulous alveolus.
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PMID:Degradable bisphosphonate-alkaline phosphatase-complexed hydroxyapatite implants in vitro. 928 69


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