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)

Aluminium-containing phosphate binders were replaced by a calcium and magnesium carbonate-containing antacid in 20 patients on long-term haemodialysis, over a three-month period in all of them, for 12 months in ten. After two months the serum aluminium level fell (mean +/- SD) from 3.0 +/- 1.6 to 1.4 +/- 0.5 mumol/l (P less than 0.001). After three months the serum phosphate level had fallen from 1.8 +/- 0.4 to 1.5 +/- 0.4 mumol/l (P less than 0.05), while during the same period parathormone (PTH-NH2) fell from 1.4 +/- 1.4 to 0.8 +/- 0.7 ng/ml (P less than 0.05). Serum total calcium concentration rose after two months from 2.2 +/- 0.2 to 2.4 +/- 0.2 mmol/l (P less than 0.001). In a third of patients the uraemic acidosis was corrected, standard bicarbonate rising from 18 +/- 2 to 21 +/- 3 mmol/l (P less than 0.05). Serum pH, potassium, sodium, magnesium and alkaline phosphatase did not change significantly. Hypercalcaemia was an expected disadvantage: repeated symptom-free episodes of hypercalcaemia occurred in six of 20 patients during the first three months and in a further two up to 12 months. These episodes were successfully controlled by a reduction of CaCO3/MgCO3 dosage and readministration of Al(OH)3. Extraosseous calcifications were not observed.
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PMID:[Replacement of aluminum-containing phosphate binders by calcium and magnesium carbonates in long-term hemodialysis]. 270 34

Six patients with progressive chronic renal failure not yet requiring dialysis and not consuming supplemental calcium or vitamin D developed hypercalcemia. Three had proven and 1 suspected tertiary hyperparathyroidism, 1 parathyroid carcinoma and 1 aplastic bone. None of the 3 patients who underwent bone biopsy had heavy bone aluminum staining. The patients with proven parathyroid-mediated hypercalcemia had marked elevation of C-terminal parathyroid hormone and alkaline phosphatase values and, when performed, radiographs consistent with osteitis fibrosa. When these findings are absent or the diagnosis is otherwise uncertain, a bone biopsy may provide a definitive diagnosis and guide management.
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PMID:Hypercalcemia in patients with advanced chronic renal failure not yet requiring dialysis. 275 79

Rats were subjected to a two-stage 5/6 nephrectomy and treated with aluminum for 2 and 4 weeks with a cumulative dose of 4.2 and 8.4 mg of aluminum, respectively. Other animals were parathyroidectomized and loaded with 8.4 mg of aluminum for 4 weeks. Histomorphometry and electron microscopy (tibiae), aluminum tissue (bone, kidney, liver) determination, serum (Ca, Mg, Zn, P, urea, creatinine, alkaline phosphatase, 1,25(OH)2D3, PTH) and urine (creatinine, A1) revealed that: (a) a dose of 8.4 mg aluminum was sufficient to induce rickets within 4 weeks of treatment and was associated with decreased serum calcitriol values and high aluminum accumulation within organs (electron-dense material was found in osteoblasts only); (b) previous parathyroidectomy prevented the occurrence of any aluminum-induced alteration of bone. It was associated with higher calcitriol and phosphorus values than in corresponding non-parathyroidectomized rats and significantly reduced aluminum accumulation within organs. The results was influenced neither by a drop in serum calcium values nor by different degrees of renal failure. We suggest that aluminum-induced rickets in growing uremic rats is prevented or delayed when previous parathyroidectomy has been performed.
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PMID:The influence of early parathyroidectomy on aluminum-induced rickets in growing uremic rats. 276 4

Since dialysis solutions in CAPD are now nearly aluminum free, the only source for elevated aluminum levels are aluminum-containing phosphate binders. Elimination with CAPD is insufficient to prevent aluminum accumulation. Therefore, we investigated a phosphate binder consisting of calcium alginate, a natural polyuronic acid, containing 100 mg calcium/g substance in 14 patients on CAPD over a period of one year. The patients had previously been treated with aluminum-containing phosphate binders for a period of 24.3 +/- 21.3 months. During a period of 3 weeks before changing to the new phosphate binder the mean (+/- SD) serum phosphorus concentration was 1.8 +/- 0.4 mmol/l, while at the end of one year of treatment with calcium alginate the concentration was 1.6 +/- 0.4 mmol/l. In order to lower serum phosphorus to this level, it was necessary to increase the mean (+/- SD) amount of calcium alginate from 6.9 +/- 1.3 g per day at the beginning of the study to 8.3 +/- 2.1 g per day at the end. The mean (+/- SD) serum calcium concentration did not change throughout the study period. Serum levels of alkaline phosphatase, 1.25 (OH)2 vitamin D3, and intact parathyroid hormone did not change as well. The mean (+/- SD) serum aluminum level declined from 36.0 +/- 20 to 14.0 +/- 11.3 micrograms/l after 6 months (p less than 0.001). In conclusion, calcium alginate is a good alternative to aluminum-containing phosphate binders and to phosphate binders on a calcium base as it does not lead to hypercalcemia. It prevents aluminum intoxication and has no serious side effects.
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PMID:Calcium alginate, an aluminum-free phosphate binder, in patients on CAPD. 276 87

Ten patients are reported following parathyroidectomy (PTX). In 9 all identifiable parathyroid tissue in the neck was deliberately removed, and in the tenth (operated 14 years ago) the remnant which had been left probably did not function. Their post-operative course resembled that of patients treated conventionally, and their subsequent course was likewise uneventful with disappearance of all symptoms associated with their osteodystrophy. All patients required oral calcium supplementation but none were given vitamin D compounds after the initial period of repletion following surgery. Mean serum values were (before PTX and current) for calcium 2.63 +/- 0.14 and 2.33 +/- 0.08 mmol/liter, P = NS, for phosphorus 1.96 +/- 0.13 and 1.38 +/- 0.09 mmol/liter, P less than 0.01, and for alkaline phosphatase 713 +/- 191 and 101 +/- 14 IU, P less than 0.05. Evidence for residual parathyroid tissue was present in each case; one patient remained mildly hyperparathyroid and several were mildly hypoparathyroid by the IRMA PTH assay. Bone histomorphometry in five subjects post-PTX showed either normal or low turnover. Radiologically, striking remineralization was seen with disappearance of all erosive changes. We suggest that residual areas of parathyroid tissue are stimulated and continue to secrete hormone even when all the discrete glands have been removed. It is recommended that when indicated, and in the absence of aluminum excess, total PTX without autotransplant should be the preferred form of therapy for long-term dialysis patients.
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PMID:Elective total parathyroidectomy without autotransplant in end-stage renal disease. 277 Jan 17

A total of 1,026 patients undergoing haemodialysis as the only chronic treatment were studied in all the dialysis units of the Veneto region, Italy. Aluminium was determined in water, dialysis fluids, and patients' serum. Aluminium mean concentration was 9.1 micrograms/l in tap water and 13.3 and 15.7 micrograms/l in bicarbonate and acetate haemodialysis fluids, respectively. Patients' serum aluminium mean level was 52.0 micrograms/l with the following frequency distribution: 59.2% below 60 micrograms/l, 25.5% between 60 and 100 micrograms, and 15.3% above 100 micrograms/l. The mean serum aluminium level was higher in patients undergoing haemodialysis with aluminium concentration in fluids over 10 micrograms/l. This was true also in patients not receiving aluminium hydroxide. Furthermore, we found higher average serum aluminium in those treated with aluminium hydroxide more than 3 g/day. No relationship was found between serum aluminium and sex, age, dialytic age, parathyroid hormone, and vitamin D treatment. Moreover, the patients with serum aluminium above 100 micrograms/l had higher serum alkaline phosphatase and lower mean cell volume values. Thus, in our haemodialysis population aluminium overloading occurred in spite of low concentration in water and fluid, and it was a result more of fluid pollution (over 10 micrograms/l) than aluminium hydroxide ingestion (over 3 g/day).
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PMID:Serum aluminium level in the veneto chronic haemodialysis population: cross-sectional study on 1,026 patients. 278

32 patients with slowly evolving predialysis chronic renal failure, who were not exposed to aluminum-containing antacids, were studied. A low aluminum intake was considered a useful condition to examine the bone deposition of the element as dependent variable, not interfering with PTH secretion and bone metabolism. Iliac bone biopsies for bone aluminum content and histomorphometric and histodynamic evaluations were taken. Serum aluminum, creatinine, calcium, phosphate, iPTH, osteocalcin (BGP), alkaline phosphatase (AP), 25-OHD3 and 1,25(OH)2D3 were also measured. 16 of the patients were on long-term treatment with 1,25(OH)2D3 (0.25 micrograms daily) for prevention and treatment of secondary hyperparathyroidism. Bone aluminum content of all patients showed a strong positive correlation with BGP and iPTH (p less than 0.001) while the correlation with serum creatinine was not significant. Multiregression analysis has singled out BGP as the most predictive variable of bone aluminum content (r2 = 0.419). The patients receiving 1,25(OH)2D3 had lower iPTH (p less than 0.01), lower bone aluminum content (p less than 0.05) and increased mineral apposition rate (p less than 0.05) compared to the untreated group. The results suggest that treatment with 1,25(OH)2D3 for long-term suppression of secondary hyperparathyroidism does not enhance aluminum accumulation in bone. The finding of lower bone aluminum together with increased mineral apposition rate, seems to indicate that 1,25(OH)2D3 is able to induce an osteoid mineralization process more selective against aluminum incorporation in bone than in case of more severe hyperparathyroidism and 1,25(OH)2D3 deficiency. At least in the present condition of low aluminum intake, 1,25(OH)2D3 may be considered to have protective effects on bone from aluminum deposition.
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PMID:Bone aluminum content in predialysis chronic renal failure and its relation with secondary hyperparathyroidism and 1,25(OH)2D3 treatment. 281 88

The clinical, biochemical, radiological and scintigraphical data related to renal osteodystrophy were followed in 18 patients on CAPD for 3 to 5 years. The majority maintained normal serum calcium, bicarbonate and alkaline phosphatase concentrations; serum phosphate concentration decreased after starting CAPD but remained somewhat elevated. Only half of the patients needed phosphate binders. Serum PTH concentrations fell in those with high values at the start and remained stable in most others. Serum aluminum concentrations never exceeded 50 micrograms/l while serum 25(OH)D3 levels remained low. Bone radiology and scintigraphy were characterized by their stability over time. We think that CAPD, with the addition of calcium carbonate, phosphate binders and vitamin D analogs can achieve good control of renal osteodystrophy. In addition, joint problems are not common in CAPD patients but we present evidence that they too are at risk of dialysis amyloidosis.
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PMID:[Bone and joint complications in patients treated with continuous ambulatory peritoneal dialysis (CAPD) for more than 3 years]. 281 91

Previous studies of surface modification of quartz particles have suggested that the biological activity of silica is at least in part related to its surface properties. In the present study, we exposed the tracheal lobe of 8 sheep to either 100 ml saline (saline group), 100 mg of quartz (Minusil-5) in 100 ml saline (SI group) or 100 mg of Al lactate treated quartz in 100 ml saline (SI-Al group). The 24 sheep were studied by bronchoalveolar lavage at days 0, 12, 24, 40, 60 and by autopsy at day 60. In the saline group, BAL analyses were as previously reported [1]. In the SI group, we found significant and sustained increases in total BAL cells (x 2, P less than 0.05), macrophages and lymphocytes (x 2, P less than 0.05), neutrophils (x 5-10, P less than 0.01), IgG (x 1.2-1.8, P less than 0.05), fibronectin (x 2-3, P less than 0.05), lactate dehydrogenase (x 3, P less than 0.01) and alkaline phosphatase (x 2, P less than 0.05). Histologically, a macrophagic and lymphocytic alveolitis was observed at day 60. In the SI-Al group, these changes were significantly attenuated and in the above parameters, SI-Al group did not differ from saline group after day 24. These data of BAL and histology of the sheep tracheal lobe model document clearly that aluminum lactate treatment alters the biological activity of quartz.
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PMID:Aluminum lactate treatment alters the lung biological activity of quartz. 301 7

Aluminum (Al) accumulation in bone is associated with low bone formation and mineralization rates; resorption may also be reduced. The mechanism of these Al-induced changes was investigated using cultured mouse osteoblast-like (OB) and osteoclast-like (OC) cells. The Al effect on bone resorption was measured by the in vitro release of 45Ca and beta-glucuronidase from mouse fetal limb-bones. Al had a biphasic effect. High concentrations (greater than 1.5 X 10(-6) M) of Al inhibited collagen and DNA synthesis, ornithine decarboxylase and alkaline phosphatase activity in OB, and depressed tartrate-resistant acid phosphatase activity in OC. Lower Al concentrations stimulated these cellular activities and 45Ca and beta-glucuronidase release from fetal bones. Al had no effect on basal cAMP levels in OB but inhibited the stimulating effect of bPTH on cAMP content. Al also altered the 1,25(OH)2D3 effects on the ornithine decarboxylase activity of OB cells. These data suggest that: (i) the low bone formation observed in vivo during Al intoxication may be due to the inhibition of collagen synthesis and to depressed cell proliferation; and (ii) Al may indirectly influence bone remodeling by interfering with the actions of bPTH and 1,25(OH)2D3 on bone cells.
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PMID:Aluminum action on mouse bone cell metabolism and response to PTH and 1,25(OH)2D3. 303 86


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