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)

Fifty-nine chronic hemodialysis patients who had been on dialysis for an average of 77 months underwent bone biopsies and the pathologic findings were correlated with biochemical and demographic data. All but two had evidence of renal osteodystrophy, 23 with osteitis fibrosa (OF), 19 with osteomalacia and/or adynamic disease (OM/AD), and 15 with mixed osteodystrophy (MOD). Patients in each group were similar with regard to age, sex distribution, duration of dialysis, unstimulated serum aluminum, calcium and phosphorus. Patients with osteitis fibrosa (OF) had statistically higher DFO stimulated aluminum, alkaline phosphatase and PTHC levels than the other two groups although there was marked individual variation. The bone biopsies were also evaluated for the amount of aluminum deposited in the osteoid seam. All 23 of the patients with OF and 11 of the 15 patients with MOD had no, mild, or minimal aluminum deposition but 12 of the 19 patients with OM/AD had moderate to marked aluminum deposition. Patients with minimal to mild aluminum deposition were similar in age, duration of dialysis, sex distribution, unstimulated and DFO stimulated aluminum levels, calcium, phosphorus, alkaline phosphatase to those with moderate to marked deposition but had significantly higher parathormone levels. All patients had been treated in a similar fashion regarding diet, oral phosphate binders and vitamin D; therefore, the observed differences in bone pathology were not readily explicable. However, patients who were found to have osteitis fibrosa and those with minimal to mild aluminum deposition had significantly higher parathormone levels when compared with patients in the other groups at the inception of dialysis.
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PMID:The clinical spectrum of renal osteodystrophy in 57 chronic hemodialysis patients: a correlation between biochemical parameters and bone pathology findings. 201 18

The preventive effect of beta-alanyl-L-histidinato zinc (AHZ) on the toxic action of aluminium on bone metabolism was investigated in the femoral diaphysis of weanling rats. Aluminium chloride (5.0, 10.0 and 20.0 mumol A1/100 g body weight) was orally administered for 3 days. The dose of 10.0 and 20.0 mumol A1/100 g caused a significant increase in serum calcium concentration and bone acid phosphatase activity, while bone alkaline phosphatase activity and calcium content were not altered significantly. Moreover, the bone DNA content was significantly decreased by the doses of 10.0 and 20.0 mumol A1/100 g. Meanwhile, the increase in serum calcium concentration caused by the administration of aluminium (20 mumol/100 g) was completely prevented by the simultaneous administration of AHZ (1.0 and 2.5 mg/100 g) for 3 days, although AHZ alone did not have any effect. Also, the effects of aluminium (20.0 mumol/100 g) to increase bone acid phosphatase activity and to decrease the bone DNA content were completely blocked by the simultaneous administration of AHZ (1.0 and 2.5 mg/100 g). AHZ (1.0 and 2.5 mg/100 g) alone had the effect to increase bone DNA content but not bone acid phosphatase activity. The present study indicates that AHZ can prevent the revelation of the toxic effect of aluminium on bone metabolism in rats.
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PMID:Beta-alanyl-L-histidinato zinc prevents the toxic effect of aluminium on bone metabolism in weanling rats. 209 94

We measured serum aluminum concentrations in 104 haemodialysis patients from 3 centres in Hong Kong. We found that the 52 patients dialyzed in unit A had much higher mean aluminium levels (100 micrograms/L) than those from the other two units (61 and 39 micrograms/L respectively). In unit A, where water treatment by reverse osmosis had been introduced only recently, 30.8% of patients had fractures/looser zones, 46.2% had rugger-jersey spine and 28.8% had skeletal erosions. When these patients were divided into two groups according to whether their serum aluminium concentration was below or above 100 micrograms/l, the latter patients had significantly lower alkaline phosphatase, serum phosphate, and higher total prescribed dose of aluminium hydroxide. It was concluded that both dialysate aluminium and oral aluminium intake seemed to have contributed to the high incidence of osteomalacic fractures among Unit A patients. In eight of these patients serum aluminium increased by more than 150 micrograms/L after four weeks of receiving 1.5 g desferrioxamine twice weekly. Serial X-rays showed that the mean time after dialysis for the appearance of fractures/Looser zones was 72 months. Three patients developed fractures/Looser zones after successful renal transplantation; and it was postulated that the prompt excretion of aluminium permitted increased osteoclastic activity, resulting in fractures in these patients.
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PMID:Newcastle bone disease in Hong Kong: a study of aluminum associated osteomalacia. 218 35

Fluoride, in the presence of aluminum ions, reversibly inhibits the temperature-mediated inactivation of unoccupied glucocorticoid receptors in cytosol preparations from mouse L cells. The effect is concentration-dependent, with virtually complete stabilization of specific glucocorticoid-binding capacity at 2 mM fluoride and 100 microM aluminum. These concentrations of aluminum and fluoride are ineffective when used separately. Aluminum fluoride also stabilizes receptors toward inactivation by gel filtration and ammonium sulfate precipitation. Aluminum fluoride prevents temperature-dependent transformation of steroid-receptor complexes to the DNA-binding state. Aluminum fluoride does not inhibit calf intestine alkaline phosphatase, and unoccupied receptors inactivated by this enzyme in the presence of aluminum fluoride can be completely reactivated by dithiothreitol. The effects of aluminum fluoride are due to stabilization of the complex between the glucocorticoid receptor and the 90-kDa mammalian heat-shock protein hsp90, which suggests that aluminum fluoride interacts directly with the receptor. Endogenous thermal inactivation of receptors in cytosol is not accompanied by receptor dephosphorylation. However, inactivation is correlated with dissociation of hsp90 from the unoccupied receptor. These results support the proposal that hsp90 is required for the receptor to bind steroid and dissociation of hsp90 is sufficient to inactivate the unoccupied receptor.
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PMID:Aluminum fluoride inhibition of glucocorticoid receptor inactivation and transformation. 219 18

Renal osteodystrophy is multifactorial. Decreased calcium absorption from the GI tract, secondary to low calcitriol levels; hyperphosphatemia; skeletal resistance to the action of parathormone; and aluminum deposition on the surface of the bones are its main pathogenetic mechanisms. Its biochemical features include abnormalities in serum calcium, phosphate, alkaline phosphatase, parathormone, calcitriol, and aluminum concentration. Radiographic methods are of little use in the characterization of the type of osteodystrophy present, but they may be of help in assessing mineral loss from the skeleton. Clinical manifestations are from bones (pain, deformities, fractures) or from metastatic calcifications. Bone biopsy is the definitive means of diagnosis. The main histologic types of osteodystrophy include osteitis fibrosa, osteomalacia, mixed form (with features of both osteitis fibrosa and osteomalacia), and aluminum osteodystrophy (presenting as either osteomalacia or aplastic lesion). The management of renal osteodystrophy should address all the pathogenetic mechanisms. Correction of the abnormalities in calcium and phosphate metabolism and prevention of aluminum osteodystrophy are the cardinal rules of management. Specific measures (parathyroidectomy, chelation of aluminum) have clear-cut indications and usually require a bone biopsy.
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PMID:Diagnosis and management of bone disorders in chronic renal failure and dialyzed patients. 219 65

A 42-year-old woman presented to our institution with a 2-week history of bone pain in the lower extremities. Her history was remarkable for duodenal ulcer and long-term treatment with a magnesium-aluminum hydroxide antacid (Maalox) and sucralfate. Initial laboratory studies showed severe hypophosphatemia and elevated alkaline phosphatase and serum 1,25-dihydroxyvitamin D levels. Bone scan showed multiple areas of increased uptake consistent with osteomalacia and microfractures. The patient recovered completely following withdrawal of antacids and sucralfate and short-term treatment with phosphate. Although hypophosphatemia induced by aluminum-containing antacids is rare, treatment of peptic ulcer disease with a combination of two aluminum-containing agents may increase the risk of clinically significant hypophosphatemia. Awareness of this condition is important, because early recognition can prevent morbidity and lead to safe and effective treatment.
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PMID:Antacid and sucralfate-induced hypophosphatemic osteomalacia: a case report and review of the literature. 225 22

We analyzed transiliac bone biopsy specimens obtained after tetracycline double labeling from 24 patients with aluminum-related bone disease who had undergone long-term hemodialysis. The specimens were selected by the following criteria: Al deposits at the mineralization fronts, a dramatic reduction in double-labeled surfaces, reflecting a low mineralization rate, and a significant increase in osteoid volume and osteoid surfaces. The bone formation rate at the tissue level and at the basic multicellular unit level was decreased in all patients. Seventeen biopsy specimens (group 1) showed morphologic and dynamic evidence of osteomalacia, as defined by an increase in the osteoid seam thickness and a decreased mineralization rate. In one specimen from group 1, thickened osteoid seams were present only in a small part of the specimen. In seven specimens (group 2), the osteoid seam thickness index was normal, indicating "aplastic bone." Two specimens from group 2, however, showed morphologic and dynamic evidence of focal osteomalacia either in trabecular or in cortical bone. Specimens from group 2 patients differed from those in group 1 in their significantly lower values of osteoid volume and lower levels of serum alkaline phosphatase and parathyroid hormone. These data show that the absence of significant increase in osteoid seam thickness and the focal distribution of thickened osteoid seams in patients with Al overload and low rate of bone formation reflect the marked reduction of bone matrix formation at the cellular level. It is suggested that low parathyroid activity might play a role in the reduction of bone matrix formation.
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PMID:Low rate of bone formation with or without histologic appearance of osteomalacia in patients with aluminum intoxication. 241 May 22

This study evaluates the use of calcium carbonate in chronic renal failure. Forty-eight patients (25 male, 23 female, mean age 54.3 years, six pre-dialysis. 12 CAPD, 30 haemodialysis) on phosphate restriction and requiring aluminum hydroxide (mean 2.4 +/- 0.8 g/day) to control serum phosphate, were converted to an equivalent dose of calcium carbonate (2.5 +/- 0.6 g/day). None received vitamin D analogues. Three months post-conversion there was a significant decrease in mean (+/- SEM) serum phosphate (1.86 +/- 0.08 versus 1.66 +/- 0.05 mmol/l P less than 0.01) and serum aluminum (28.3 +/- 5.4 versus 13.2 +/- 3.0 micrograms/l, P less than 0.0001): calcium/phosphate product was unchanged. Post-conversion there was an increase in serum bicarbonate, (20.6 +/- 0.5 versus 22.1 +/- 0.6 mmol/l, P less than 0.01) and serum calcium (2.32 +/- 0.02 versus 2.45 +/- 0.03 mmol/l, P less than 0.0001). No change in serum creatinine, alkaline phosphatase or parathormone occurred. No adverse effects were reported but nine (18%) patients became hypercalcaemic (2.7 to 2.93 mmol/l), eight of whom responded to dose reduction. Hypercalcaemia did not correlate with pre-conversion serum calcium, parathyroid hormone, alkaline phosphatase or aluminium. Calcium carbonate is an effective alternative to aluminium-based phosphate binders. It produces a beneficial increase in serum calcium and bicarbonate and a significant decrease in serum aluminium. Hypercalcaemia is unpredictable but is easily reversible in the majority of patients.
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PMID:The use of calcium carbonate to treat the hyperphosphataemia of chronic renal failure. 251 82

Parathyroidectomy (PTx) is indicated in hemodialysis (HD) patients who have severe osteitis fibrosa unresponsive to vitamin D therapy or in whom the latter treatment is contraindicated. Immediately after PTx, plasma immunoreactive parathyroid hormone, calcium and phosphorus concentrations decline abruptly. However, little is known in such patients about the short-term effects of PTx on plasma alkaline phosphatase (AP) activity and plasma aluminum (Al) levels. The present, preliminary study was performed to determine such parameters in 37 HD patients, and to correlate them with data of bone histology. Mean plasma AP activity started to increase after PTx from day 4 onwards. Thus, AP values significantly higher than pre-PTx values were observed at day 7 and 14 (415 +/- 54 vs. 619 +/- 77 and 749 +/- 83 IU/liter, means +/- SEM; N = 37; P less than 0.05 and 0.001, respectively). This increase, in the absence of changes in liver function, was mainly due to the bone-specific iso-AP. Moreover, the degree of increase in plasma AP activity was higher in the subgroup with negative (group I, 21 patients) than in that with positive bone Al staining (group II, 16 patients). However, plasma osteocalcin (BGP) did not change after PTx (N = 8). Basal plasma Al levels were significantly higher in group II both before and two weeks after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Short-term effects of parathyroidectomy on plasma biochemistry in chronic uremia. 257 18

The effects of CaCO3 were investigated in 7 patients undergoing maintenance hemodialysis who had been treated with 1 microgram/day 1 alpha (OH)D3 and 2 g/day Al(OH)3. CaCO3 (3 g/day) was administered instead of Al(OH)3. The levels of serum total calcium and ionized calcium were significantly increased, the level of C-terminal parathyroid hormone was appreciably decreased and the levels of serum aluminum in all patients were reduced. There were no significant changes in the levels of serum phosphate, calcium x phosphate product, alkaline phosphatase, calcitonin, magnesium and bicarbonate. It is concluded that 3 g/day CaCO3 is equivalent to 2 g/day Al(OH)3 in terms of its phosphate-binding effect, and the prescription of CaCO3 together with 1 alpha (OH)D3 ameliorates secondary hyperparathyroidism.
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PMID:Treatment of secondary hyperparathyroidism in patients on maintenance hemodialysis. 261 19


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