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)

It has been suggested that the intensity of hypocalcaemic response to the administration of calcitonin may reflect the degree of osteoclastic activity and thus the state of the parathyroid function. We have performed the calcitonin test in 14 healthy volunteers and in 17 patients with chronic renal failure undergoing haemodialysis. The test involved the intramuscular injection of 100 MRC units of synthetic salmon calcitonin, serum calcium being determined before and after 5 h of the injections of the hormone. In 7 of the patients, the test was repeated using intranasal administration by means of a spray of calcitonin. In renal patients, serum calcium fell from 9.73 +/- 0.76 to 7.88 +/- 1.01 mg/dl (1.85 +/- 0.67 mg/dl). In the control group, serum calcium fell from 9.51 +/- 0.56 to 8.89 +/- 0.34 mg/dl (0.62 +/- 0.35 mg/dl). The calcium fall in renal patients was significantly greater than in the control group (p less than 0.001). In patients there was a statistically significant correlation between the fall in serum calcium and the level of alkaline phosphatase, but no with the serum concentration of immunoreactive parathormone (C-Terminal). After intranasal calcitonin, serum calcium fell from 9.81 +/- 0.55 to 8.83 +/- 0.72 mg/dl (1.42 +/- 0.42 mg/dl), a reduction comparable to that obtained after the intramuscular injection of the hormone in the same patients (1.84 +/- 0.69 mg/dl). These results provide evidence of an increase in osteoclastic activity in chronic renal failure, perhaps reflecting parathyroid hyperfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcitonin-induced hypocalcaemia as a possible index of osteoclastic activity in patients with chronic renal failure. 369 25

We wished to investigate the pathophysiology of hypertriglyceridemia in chronic renal failure. Our subjects were 30 patients under hemodialysis for at least five years who had never taken vitamin D analogues or calcitonin preparations. During those five years, triglycerides were high, with no significant changes, although the cholesterol level decreased significantly 10 to 12 months after the first hemodialysis treatment. There was a significant correlation between alkaline phosphatase and triglycerides (p less than 0.025) in these patients in the same assay. In the two patients with hypertriglyceridemia, serum triglycerides decreased to within the normal range by six months after parathyroidectomy, and remained there 30 months after surgery. These results suggested that secondary hyperparathyroidism may be involved in the pathophysiological mechanism of hypertriglyceridemia seen in chronic renal failure.
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PMID:Deranged metabolism of lipids in patients with chronic renal failure: possible role of secondary hyperparathyroidism. 371 61

Partial parathyroidectomy (PTX) was carried out 20 times in 15 dialitic patients with chronic renal failure. The operation was suggested by marked radiological abnormalities due to severe secondary hyperparathyroidism, that developed despite aggressive medical and dietetic management. The skeletal x-ray examination showed significant improvement following PTX, that was clearly visible already one month postoperatively at the level of the second and third phalanges of the hands. The improvement of the skeletal osteodystrophic patterns was always associated to a fall of parathyroid hormone and plasma alkaline phosphatase levels. The radiological examination of the hands may represent a usefull and simple method in the follow-up of patients after surgery to assess the efficacy of PTX.
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PMID:[Radiologic surveillance of uremic osteodystrophy after parathyroidectomy]. 373 84

The possible relationship between platelet dysfunction and secondary hyperparathyroidism (HPT) in chronic renal failure was examined in 23 uremic patients on conservative therapy (group I) and in 27 patients on maintenance hemodialysis (group II). Platelet function was assessed by measuring the degree of aggregation in response to various concentrations of adenosine diphosphate. Secondary HPT was evaluated by means of serum biochemistry (parathyroid hormone, calcium, phosphorus, and alkaline phosphatase) and radiographic examinations (x-ray films of the hand skeleton). This study showed impaired platelet aggregation in group I patients, compared to either group II patients or controls. There were no significant differences when group II patients were compared to controls. No significant correlations between platelet aggregation and the hematochemical changes associated with secondary HPT were found. No differences in platelet aggregation were found with regard to the activity (alkaline phosphatase) and the severity (x-ray findings) of secondary HPT. Effective treatment of secondary HPT with 1,25-dihydroxycholecalciferol in both group I and group II patients was not associated with consequent changes in platelet aggregation. It is concluded that secondary HPT is probably not a major factor in the pathogenesis of platelet dysfunction in chronic renal failure.
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PMID:Lack of evidence for the role of secondary hyperparathyroidism in the pathogenesis of uremic thrombocytopathy. 375 22

In view of the known toxicity of aluminum, we studied the effects of CaCO3 as an alternative phosphate binder in 12 chronic renal failure (CRF) children during 152 patient-months. Mean (+/- SD) serum creatinine concentration rose during that period from 3.7 +/- 1.8 to 5.1 +/- 3.0 mg/dl. 8 patients received CaCO3 from the start, and 4 were switched from A1(OH)3 after 2 months of interruption. In addition to CaCO3 (0.1-0.3 mg/kg BW) all patients received NaHCO3, and all but two received 1 alpha-hydroxyvitamin D3 [1 alpha(OH)D3] or dihydrotachysterol (DHT). Urine and blood variables were checked every 4-6 weeks and medication dosages were adjusted accordingly, aiming to keep serum Ca at 10.4-10.8 mg/dl, serum Pi at 3.5-5.5 mg/dl, and serum HCO-3 above 18 mEq/l. Bone X-rays were obtained every 6-9 months. With treatment, mean serum Ca increased from 8.9 +/- 0.7 to 10.3 +/- 0.4 mg/dl (p less than 0.01), serum Pi decreased from 6.3 +/- 0.9 to 4.2 +/- 0.5 mg/dl (p less than 0.01), and the mean Ca X P product decreased slightly and insignificantly. Mean serum alkaline phosphatase levels decreased significantly from 486 +/- 251 to 168 +/- 28 IU (p less than 0.01). Bone X-rays at the end of the study showed either healing of renal osteodystrophy or its prevention. Only one episode of mild hypercalcemia (serum Ca 11.7 mg/dl) was observed in 1 patient, but his Ca X P product remained low.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oral calcium carbonate as phosphate-binder in infants and children with chronic renal failure. 380 30

We evaluated the effectiveness of calcium carbonate as a phosphate binder in 19 children with chronic renal failure; ten children were undergoing dialysis therapy (eight maintained by CAPD and two by hemodialysis). Twelve children had previously received aluminum hydroxide, while calcium carbonate was the primary phosphate binder used in seven children. Among all the children, the serum phosphorus level on no phosphate binder was 7.4 +/- 0.9 mg/dL, which decreased significantly (P less than .001) to 5.9 +/- 0.8 mg/dL during calcium carbonate therapy, while the serum calcium, bicarbonate, and creatinine were unchanged. The reduction in the serum phosphorus level occurred while dietary intake of calcium and phosphorus were unchanged, as demonstrated by three-day dietary records. The dose of calcium carbonate required to maintain the serum phosphorus in the normal range varied from 600 mg to 15 g/d (mean 7.4 g/d). Among the 12 children and four others who had received aluminum hydroxide, serum aluminum levels fell from 108.8 +/- 121.8 ng/mL to 36.1 +/- 29.1 ng/mL after aluminum hydroxide was stopped (P less than .05). Serum alkaline phosphatase and parathyroid hormone (PTH) levels during aluminum hydroxide therapy were similar to levels obtained during calcium carbonate therapy, while PTH levels fell in children treated initially with calcium carbonate. All the children have been observed for a mean of 12.0 months (range 4 months to 3 1/2 years). Hypercalcemia occurred in seven children, usually when vitamin D therapy was initiated or the dose changed. Hypercalcemia resolved with adjustment of the vitamin D or calcium carbonate dose in all but one patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium carbonate is an effective phosphorus binder in children with chronic renal failure. 382 69

Dynamic skeletal histomorphometry was performed in 94 unselected patients receiving maintenance dialysis for chronic renal failure. An attempt was made to correlate the results with the clinical, biochemical and radiological findings. Skeletal histology was abnormal in each case. Hyperparathyroidism was present as the only abnormality in 18 patients and osteomalacia in 26; 50 patients showed both abnormalities. Osteomalacia, in contrast to hyperparathyroidism, increased in prevalence and severity with the duration of dialysis and with bone aluminum content. The majority of patients had histological osteosclerosis. It was impossible to predict either the nature or the severity of the histological lesions on the basis of symptoms and physical signs or on the basis of most biochemical parameters (including serum concentrations of three vitamin D metabolites). Serum alkaline phosphatase values and serum immunoreactive parathyroid hormone (iPTH) concentrations were positively correlated with the severity of histological hyperparathyroidism. Subperiosteal erosions of the phalanges were associated with severe histological hyperparathyroidism in each case but this radiological sign was absent in 66% of patients with histological hyperparathyroidism. Radiological osteosclerosis was associated with severe histological osteomalacia in each case, but this radiological sign was absent in 87% of patients with histological osteomalacia. No other radiological sign proved a reliable guide to the underlying skeletal histology. In the majority of dialysis patients, a skeletal biopsy is required for an accurate diagnosis of the nature and severity of azotemic osteodystrophy.
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PMID:Dialysis osteodystrophy. A study involving 94 patients. 383 91

The possible relationship between red blood cell (RBC) osmotic fragility and secondary hyperparathyroidism (HPT) in chronic renal failure was examined in 23 uremic patients on conservative therapy and in 42 patients on maintenance hemodialysis. Secondary HPT was evaluated by means of serum biochemistry (parathyroid hormone, calcium, phosphorus, and alkaline phosphatase) and radiographic examinations (X-ray films of the hand skeleton). This study showed increased RBC osmotic fragility in uremic patients when compared with controls, with no difference between those on conservative therapy and those on maintenance hemodialysis. No correlation between RBC osmotic fragility and the hematochemical changes associated with secondary HPT was found. No difference in RBC osmotic fragility was observed with regard to the activity (alkaline phosphatase) and the severity (X-ray findings) of secondary HPT. Effective treatment of secondary HPT by either pharmacological means (1,25-dihydroxycholecalciferol) or surgical removal was not associated with consequent improvement in RBC osmotic fragility. It is concluded that secondary HPT is probably not a major factor influencing RBC osmotic fragility in chronic renal failure.
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PMID:Lack of relation between secondary hyperparathyroidism and red blood cell osmotic fragility in chronic renal failure. 384 May 75

Quantitative bone histology, biochemistry and height velocities were studied in 18 children suffering from chronic renal failure. Eight received calcitriol, 7 ergocalciferol and 3, though alloted to a treatment group, failed to comply with therapy. A histochemical stain for aluminum showed heavy deposition at the calcification front in 3 patients; 2, in the calcitriol group had severe osteomalacia which worsened during treatment, and 1 in the ergocalciferol group had osteomalacia which did not improve. One had never undergone hemodialysis. Bone histology improved markedly in the remaining 12 patients, whichever vitamin D preparation was used; it was unchanged in 3 non-compliant children. Plasma calcium levels rose while parathyroid hormone and alkaline phosphatase levels fell following both treatments, and were unchanged in non-compliant children. Hypercalcemia occurred more frequently following calcitriol therapy (11 episodes) than following ergocalciferol therapy (3 episodes). Height velocities, studied in 11 children, increased in 5 (3 on ergocalciferol and 2 on calcitriol) and were unchanged in 6 (1 on ergocalciferol, 5 on calcitriol). Improved bone histology did not correlate with increase in height velocity. As ergocalciferol and calcitriol had similar therapeutic effects and as side-effects were more common with calcitriol, it is concluded that calcitriol provides no advantage over ergocalciferol in the treatment of renal bone disease in children.
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PMID:Treatment of childhood renal osteodystrophy with calcitriol or ergocalciferol. 387 85

We assessed the effects of ranitidine and cimetidine (histamine H2-receptor antagonists) on the serum concentrations of parathyroid hormone (PTH) in 22 patients with end-stage chronic renal failure. Treatment for 3 months induced a significant decrease in serum concentrations of PTH determined by radioimmunoassay directed at the mid portion of the PTH molecule. In contrast, significant increases were noted using an assay directed at the amino-terminal portion, whereas no change was noted with a carboxy-terminal assay. No significant changes in serum calcium, phosphate and alkaline phosphatase were noted after treatment with either agent, but serum concentrations of osteocalcin increased significantly. We conclude the H2-receptor antagonists do not favourably influence the natural history of hyperparathyroid bone disease in patients with end-stage chronic renal failure.
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PMID:Long-term effects of histamine H2-receptor antagonists on serum parathyroid hormone in chronic renal failure. 387 37


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