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)

We report on the results of the clinical trial, where the effects of sucralfate on the serum phosphorus, calcium and alkaline phosphatase in 30 patients with chronic renal failure on intermittent hemodialysis were examined. After 14 days of treatment with sucralfate (1 gram four times daily), we found a significant reduction in serum phosphorus and alkaline phosphatase and an increase in serum calcium. On the basis of its proven hypophosphatemic and ulcer-healing effects, sucralfate can be recommended in treatment of hyperphosphatemia and secondary hyperparathyroidism in chronic renal failure. Serum phosphorus should be checked routinely in patients treated with sucralfate for the peptic ulcer disease.
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PMID:Changes in serum phosphorus, calcium and alkaline phosphatase due to sucralfate. 351 90

Peliosis hepatis is described in a renal transplant recipient and in a patient who was receiving long-term haemodialysis. This uncommon liver lesion has been reported in a number of patients, including 18 renal transplant recipients and two patients with chronic renal failure. However, its cause, clinical features, natural history and clinical significance remain to be determined. We emphasize that, although it is rare, peliosis hepatis should be considered in long-term haemodialysis and renal transplant patients who exhibit hepatomegaly and/or splenomegaly and/or disordered liver function (in particular, elevation of hepatic alkaline phosphatase levels).
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PMID:Peliosis hepatis in a renal transplant recipient and in a haemodialysis patient. 354 May 50

A prospective mammographic study was performed on 151 women to determine the prevalence of breast calcifications in patients with chronic renal failure. Frequency, size, structure, and location of calcific lesions were assessed in 15 patients with compensated renal insufficiency, 22 on hemodialysis, 14 who had renal transplants, and 100 who had normal kidney function. Serum levels of calcium, phosphorus, alkaline phosphatase, and parathyroid hormone were determined for all 151 women. The calcific lesions occurred preponderantly in dialysis patients (arteries, 55%; parenchyma, 68%; and ducts, 36%). Next in order were those with renal transplants (43%, 64%, and 29%, respectively) and those with renal insufficiency (33%, 53%, and 20%, respectively). Patients with renal disease had significantly more calcifications (p less than .001) than the patients with normal kidney function: arteries, 45% vs 8%; parenchyma, 61% vs 27%; and ducts, 29% vs 9%. Frequencies of calcifications correlated with serum levels of parathyroid hormone. None of the calcifications induced by renal disease simulated those seen in carcinoma of the breast.
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PMID:Breast calcifications in renal hyperparathyroidism. 355 17

Renal osteodystrophy is a common and incapacitating complication of chronic renal failure in children. Standard therapy with oral calcium supplements, phosphate binders, and vitamin D preparations is often inadequate to control progressive bone disease. We report the use of parenteral calcitriol therapy in two children, aged 2 and 15 years, respectively, with chronic renal failure. This treatment effectively suppressed secondary hyperparathyroidism in both patients, causing a nearly 50% reduction in circulating parathyroid hormone level and a parallel decline in serum alkaline phosphatase activity. In the younger patient, therapy was associated with healing of subperiosteal bone resorption and accelerated growth velocity. These findings indicate that parenteral administration of calcitriol may be an effective treatment option in some patients with refractory renal osteodystrophy and secondary hyperparathyroidism.
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PMID:Parenteral calcitriol for treatment of severe renal osteodystrophy in children with chronic renal insufficiency. 358 13

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

Ten children with end stage renal disease on chronic hemofiltration (HF) were studied for a 1-yr period to evaluate the efficacy of 1,25-dihydroxyvitamin-D3 (1,25(OH)2D3) therapy on biohumoral parameters of renal osteodystrophy and bone mineral content. In six of these children an acute study was done of the direct effect of the HF procedure on calcium and phosphate balance during 12 HF sessions. During the first 6 months of the study all children were treated with 1,25(OH)2D3 (0.25-0.50 microgram/day) to maintain plasma calcium at 9.5-11.0 mg/dl. There was a significant increase in plasma calcium (p less than 0.05) and a significant decrease in plasma phosphate (p less than 0.01) and alkaline phosphatase concentrations (p less than 0.05). The circulating levels of NH2 immunoreactive parathyroid hormone did not change, remaining at the upper limits of reference values. Immunoreactive parathyroid hormone-COOH terminal fragment levels decreased significantly (p less than 0.05). Bone mineral content rose significantly (p less than 0.01). During the last 6 months of the study, to evaluate the possibility that HF alone might control secondary hyperparathyroidism, 1,25(OH)2D3 treatment was discontinued in five children; plasma calcium and phosphate were well controlled whereas hyperparathyroidism worsened in all five, and one also developed intense pruritus and hypertension. The other five children remained on 1,25(OH)2D3 treatment; two of these were transplanted, and the other three continued to show an improvement of mineral balance. The results of the acute study showed that calcium balance was positive with a mean Ca++ gain of 140 mg/HF session. The mean total phosphate removed per HF run was 574 mg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of 1,25-dihydroxyvitamin-D3 treatment on mineral balance in children with end stage renal disease undergoing chronic hemofiltration. 375 54

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


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