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 double-blind randomized study of 29 patients with symptomatic Paget's disease was conducted comparing the clinical, biochemical, and histomorphometric responses to 3-month treatment with placebo (10 patients), low-dose disodium etidronate (EHDP) (5-7 mg/kg/day) (10 patients), and low-dose EHDP plus 1 alpha-hydroxyvitamin D3 (1 alpha D3) 0.5 mcg daily (9 patients). In placebo-treated patients no significant changes were observed in symptoms, biochemistry, or bone histomorphometry. Histologically apparent mineralization defects developed after 3 months of therapy in 90% of patients in the EHDP group, compared with 45% of patients in the EHDP/1 alpha D3 group. In 19% of the patients treated with active medication, the mineralization defects in pagetic bone were accompanied by histological evidence of continued osteoclastic resorption. The development of mineralization defects was not related to serum levels of vitamin D metabolites, alkaline phosphatase, or intestinal calcium absorption but did correlate with the occurrence of hyperphosphatemia during treatment, which was most marked in patients treated with EHDP alone. Although mineralization defects were less frequent in the EHDP/1 alpha D3 group, these patients also responded less well symptomatically, thus limiting the potential usefulness of this drug combination in Paget's disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of 1 alpha-hydroxyvitamin D3 on the mineralization defect in disodium etidronate-treated Paget's disease--a double-blind randomized clinical study. 313 73

The efficacy and safety of calcium carbonate as a phosphate binder was evaluated in 20 patients on chronic hemodialysis who had previously received aluminum hydroxide. During the control period the patients were on aluminum hydroxide and calcitriol therapy and had plasma phosphorus levels less than 6 mg/dL (4.95 +/- 0.8 mg/dL). Aluminum hydroxide was then discontinued and no phosphate binder was prescribed for 1 month. Every patient developed hyperphosphatemia so that calcium carbonate treatment was begun and calcitriol dose was adjusted in relation to plasma calcium changes. After 24 months of calcium carbonate therapy, plasma phosphorus was 4.85 +/- 0.7 mg/dL, using a daily dose of calcium carbonate of 2.57 +/- 1.3 g (range, 1 to 6 g). The daily dose per patient of calcitriol was not different from that prescribed during the control period, but in five patients calcitriol was permanently withdrawn for hypercalcemia. At the end of the study plasma calcium, magnesium, bicarbonate, alkaline phosphatase, and parathyroid hormone values were unchanged in comparison with the control period, whereas a significant reduction in plasma aluminum and plasma aluminum increase induced by deferoxamine infusion was observed. The frequency of hypercalcemic and hyperphosphatemic episodes during the last 12 months of calcium carbonate therapy (6.2% and 16.6%, respectively) was not different from that observed during the 12 months on aluminum hydroxide therapy preceding the control period (4.5% and 14.7%, respectively). It was concluded that calcium carbonate is effective in the control of hyperphosphatemia and secondary hyperparathyroidism in patients on chronic hemodialysis and that the incidence of hypercalcemia is low when the daily dosage is less than 6 g.
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PMID:Efficacy and safety of long-term treatment with calcium carbonate as a phosphate binder. 314 60

The medical records of 14 hyperthyroid cats with thyroid carcinoma were analyzed retrospectively regarding historical, physical, laboratory, and thyroid scintiscan findings, treatment, and treatment outcome. Breed predilection was not detected, and older castrated male cats were most commonly affected. The most common clinical signs detected by owners were weight loss, polydipsia, polyuria, polyphagia, hyperactivity, and anorexia. Physical examination findings included tachycardia, palpable cervical mass, hyperactivity, cardiac murmur, and abnormal coat. Common abnormal laboratory findings were high serum thyroxine and triiodo-thyronine concentrations and high serum alanine transaminase, alkaline phosphatase, and aspartate transaminase activities. Azotemia, hyperphosphatemia, and hyperglycemia were noticed less frequently. The most common thyroid scintiscan findings were multiple nodular areas of high radionuclide uptake in the cervical region, thoracic inlet, and cranial mediastinum. The most common morphologic diagnosis was mixed compact and follicular carcinoma, with follicular and papillary carcinomas being less common. Most cats responded well to treatment of the thyroid tumor, with rapid resolution of the historical and physical examination findings. The most common necropsy findings were local tumor invasion, regional lymph node metastases, cardiomyopathy, and interstitial nephritis.
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PMID:Thyroid carcinoma causing hyperthyroidism in cats: 14 cases (1981-1986). 318 90

The authors describe a boy with precocious puberty due to adrenal hyperplasia associated with rickets, hypocalcemia, hyperphosphatemia, elevated PTH and alkaline phosphatase levels, and concentrations of 25-OH-D and 1,25-(OH)2D at the upper limit or above normal range. Treatment with hydrocortisone for 9 months did not normalize hypocalcemia and hyperphosphatemia. The addition of 1,25-(OH)2D3 (0.5-2 micrograms/day) to the corticoid treatment for 1 year was followed by a progressive normalization of plasma calcium, phosphorus, PTH and alkaline phosphatase concentrations with improvement of the osteomalacia on bone biopsy.
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PMID:Congenital adrenal hyperplasia associated with hyperphosphatemic rickets. 337 Sep 5

In order to investigate the dietary effect of calcium on aluminum-induced hypophosphatemia, five types of diet, sucrose, lactose, milk, casein and soy protein, were prepared. These diets differed with regard to Ca concentration, and carbohydrate or protein sources which were expected to modify intestinal Ca absorption. Weanling Wistar rats were fed these diets for 67 days with the addition of Al at a concentration of 2000 ppm. Nutritional constituents had little effect on Al accumulation in the duodenum and bone. Al treatments had no effects on increases of body weight. The Al treatments significantly increased duodenum alkaline phosphatase (ALPase) activity and serum phosphorus concentration in all of the dietary groups. Slight but significant decreases of bone weight were observed. There were no significant increases in serum Al concentration but bone and kidney ALPase activities were also observed. These results suggest that Al ingestion can cause hyperphosphatemia in the intact animal. Effects of Al on nutrition should be considered even if serum Al concentration does not increase.
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PMID:Increases of serum phosphorus concentration and duodenal, renal and femur alkaline phosphatase (EC 3.1.3.1) activities of normal rats fed 2000 ppm aluminum diets. 338 46

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

In 93 children, end-stage renal disease was treated with the new dialytic methods of continuous ambulatory peritoneal dialysis (CAPD) or continuous cycling peritoneal dialysis (CCPD) over 5 years. Modality survival rates at 36 months with CAPD, CCPD, or both were 20%, 93%, and 87%, respectively. Use of CCPD as the primary dilaytic method increased during the study period. The peritonitis rate was one episode per 11.8 patient treatment months and was similar with both CAPD and CCPD. Gram-positive organisms were cultured in 34% of these episodes of peritonitis. Staphylococcus aureus peritonitis was associated with a recurrence rate of 40% and led to catheter replacement in 45% of the episodes. Peritoneal membrane failure necessitating switching to hemodialysis was related to peritonitis in three patients. Of the 74 peritoneal catheters that required replacement, 70% were infected. Serial serum levels of urea nitrogen, potassium, calcium, phosphorus, albumin, and alkaline phosphatase remained stable, whereas serum creatinine level rose slightly over time. Episodes of hyperkalemia, hypercalcemia, and hyperphosphatemia were observed at a frequency of one episode per 12.2, 4.6, and 2.5 treatment months, respectively. Blood transfusions were required in once per 1.5 and 3.3 treatment months in seven anephric patients and in 35 patients with their own kidneys, respectively (P = 0.05). In prepubertal patients who received CAPD or CCPD for greater than 1 year, little or no improvement in growth occurred in relationship to either chronologic or bone age.
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PMID:Five years' experience with continuous ambulatory or continuous cycling peritoneal dialysis in children. 365 81

The pathophysiology, clinical presentation, prevention, and treatment of aluminum-related osteomalacia in renal-failure patients are reviewed. Aluminum-related osteomalacia can develop in patients exposed to high concentrations of aluminum either in dialysis solutions or through gastrointestinal aluminum absorption from aluminum-containing antacids used to treat hyperphosphatemia. Although the exact etiology of aluminum-related osteomalacia is unknown, aluminum is believed to inhibit bone mineralization by forming an inhibitory complex with citric acid at physiologic concentrations. The complex is deposited along bone mineralization fronts and in bone marrow. The major symptoms of aluminum-related osteomalacia include skeletal pain, fractures, and vertebral collapse. The disease is difficult to diagnose because patients may have normal or slightly elevated serum concentrations of calcium, phosphate, alkaline phosphatase, and parathyroid hormone. Direct measurement of bone aluminum content (using biopsy) is often needed to confirm diagnosis. The aluminum-chelating agent deferoxamine mesylate can be used to measure bone aluminum content indirectly. Aluminum intoxication can be managed either by preventing exposure to aluminum or by removing deposited aluminum from bone. New standards restrict aluminum content in dialysis solutions, and prevention now focuses on the use of aluminum-free phosphate binders for treatment of hyperphosphatemia. Calcium carbonate may be as effective as aluminum-containing antacids in controlling serum phosphate concentrations, but it should be used cautiously in patients who are hypercalcemic or at risk of developing metastatic calcification. Chelation therapy with deferoxamine has improved the symptoms and bone histology in a small number of patients. Clinical improvements have been seen in patients receiving intravenous deferoxamine 2-6 g per week for 20 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aluminum-related osteomalacia in renal-failure patients. 389 71

Hyperphosphatemia leads to the development of osteitis fibrosa in patients with chronic renal failure. In contrast, crippling osteomalacia may appear in uremic patients who are hypophosphatemic or aluminum intoxicated or who undergo total or subtotal parathyroidectomy. Thus, strict phosphorus control by use of aluminum-containing gels may ameliorate renal osteitis fibrosa, but may potentiate the development of osteomalacia. To evaluate this possibility, we compared the bone histologies of 10 chronic renal hemodialysis patients who consistently maintained predialysis phosphorus levels between 4-5 mg/dl (Strict-P) to those of 46 randomly selected dialysis patients (Random-P). We found that the Strict-P group had lower circulating immunoreactive PTH (P less than 0.02) and alkaline phosphatase (P less than 0.05) levels and, as expected, less evidence of hyperparathyroid bone disease. On the other hand, the Strict-P patients had osteomalacia, as evidenced by moderate osteoid accumulation and reduced capacity of bone to assume a fluorescent tetracycline label. Furthermore, all Strict-P patients had histological evidence of bone aluminum accumulation. We conclude that maintenance of normal serum P levels with aluminum-containing gels in hemodialysis patients prevents severe hyperparathyroid bone disease. Such treatment, however, is also attended by a moderate degree of aluminum-associated osteomalacia.
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PMID:Does strict phosphorus control precipitate renal osteomalacia? 394 54

Three cases of pseudohypoparathyroidism with roentgenographic evidence of hyperparathyroid bone disease are described. Renal resistance to exogenous parathyroid hormone (PTH), the hallmark of pseudohypoparathyroidism, was documented by markedly blunted or absent urinary phosphate and cyclic AMP responses to parathyroid extract. At the time of diagnosis all patients were hypocalcemic and hyperphosphatemic with elevated serum alkaline phosphatase levels and subperiosteal resorption noted on skeletal films. Bone biopsy in one patient revealed a histologic appearance consistent with hyperparathyroidism. Serum PTH levels, measured in two patients while they were hypocalcemic, were elevated. None of the patients had short stature, brachydactyly, subcutaneous calcification or mental deficiency. These cases are compared to the 15 well-documented cases previously reported. The presently available information on pseudohypoparathyroidism indicates a variable skeletal response to PTH mediated by several factors extrinsic to bone and suggests that pseudohypoparathyroidism with hyperparathyroid bone disease is one extreme of a clinical spectrum of skeletal responsiveness to PTH. This disorder is part of an expanding clinical picture which makes pseudohypoparathyroidism a diagnostic consideration in any patient with unexplained hypocalcemia, hyperphosphatemia, elevated alkaline phosphatase levels or metabolic bone disease.
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PMID:Skeletal responsiveness in pseudohypoparathyroidism. A spectrum of clinical disease. 624


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