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)

Clinical signs of rickets developed in a previously healthy 13-year-old girl with normal features. She had hypocalcemia, hyperphosphatemia, elevated alkaline phosphatase and parathyroid hormone levels, and normal vitamin D metabolite levels, with osteitis fibrosa cystica on bone biopsy specimen. Her renal function was normal. Treatment with 1 microgram of calcitriol each day resulted in symptomatic and clinical relief and improvement of the serum chemical values. This patient probably has pseudohypoparathyroidism type 1, with renal nonresponsiveness and bone responsiveness. This disorder has the clinical features of rickets, but represents hyperparathyroid bone disease.
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PMID:Renal-nonresponsive, bone-responsive pseudohypoparathyroidism. A case with normal vitamin D metabolite levels and clinical features of rickets. 654 1

Fifteen children undergoing continuous ambulatory peritoneal dialysis for 0.3 to 2.4 years were evaluated longitudinally for renal osteodystrophy. Immunoreactive parathyroid hormone, 25-OHD, total and ionized calcium, inorganic phosphate, and alkaline phosphatase levels were measured regularly. Skeletal radiographic studies were performed at the onset and conclusion of CAPD and at six-month intervals during therapy. All children received 1,25(OH)2D3 and aluminum hydroxide, and nine received supplemental calcium. Plasma 25-OHD concentrations were normal to elevated, and calcium increased steadily to high normal levels despite a trend to persistent hyperphosphatemia. The increased calcium levels suppressed parathyroid hormone overactivity in only one patient. At the onset of CAPD, nine patients had hyperparathyroid bone disease seen radiographically, three of whom also had rachitic lesions. At the end of CAPD, the hyperparathyroid lesions had improved in four patients, completely resolved in three, and deteriorated in two. Rachitic lesions had completely healed in two patients and improved in the third. However, among the six children without radiographically evident lesions at onset of CAPD, hyperparathyroid bone lesions developed in two and rachitic lesions in two others during CAPD. Although CAPD and appropriate therapy benefited most patients with renal osteodystrophy, the benefits were not uniform, and bone lesions deteriorated in some.
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PMID:Renal osteodystrophy in children undergoing continuous ambulatory peritoneal dialysis. 663 99

Hyperphosphataemia with levels of 65 mg/l was found in a black African aged 20 with a 10-year history of tumour calcinosis. Levels of blood calcium, plasma ionised calcium, serum alkaline phosphatase, 24-hour urinary calcium and phosphate were all normal, as was renal function. Tubular phosphate reabsorption (TmP) was greater than 90 mg per litre of glomerular filtrate (N = 22-42). Levels of circulating parathyroid hormone, nephrogenic cAMP and serum vitamin D metabolites [25 OH D3, 24,25 (OH)2 D3 and 1,25 (OH)2 D3] were normal. The TmP fell by 36% on exogenous PTH stimulation (N = 30.25 +/- 6.7), and by 7.9% 120 min. after injection of acetazolamide. Our results confirm the conclusions of recent studies: patients with tumour calcinosis have disordered renal phosphate excretion with normal PTH secretion, normal PTH action on the renal tubule and normal vitamin D metabolism. In fact in these hyperphosphataemic patients, circulating 1,25 (OH)2 D3 levels would be expected to be low, whereas they were normal in our patient. An attempt at treatment with acetazolamide and phosphate chelating agents gave no significant results.
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PMID:[Phosphorus metabolism in a case of tumoral calcinosis]. 671 63

True reference values (TRV) should ultimately be determined in blood from inactive, unstimulated rats but in practice, acceptable reference values (ARV) may be established using blood from decapitated or anesthetized animals if one is cognizant of variations associated with blood sampling procedures. Data reported here illustrate some variations in serum biochemical values following decapitation or anesthesia. Decapitation does not provide serum in which ARV for sodium, potassium or lactate dehydrogenase can be found but ARV can be determined for glucose, insulin and several other parameters. It is suggested that both TRV and ARV for serum electrolytes be determined using serum from cannulated rats. All three anesthetics raised glucose levels and ether and halothane increased alkaline phosphatase activity. Both halothane and Innovar-VetR decreased insulin:glucose ratios suggesting inhibition of insulin release from the pancreas. Innovar-VetR also produced hypoxia due to severe respiratory depression and bradycardia as well as hyperuricemia, hyperglycemia and hyperphosphatemia. Techniques most likely to provide ARV should be of the shortest possible duration, afford least respiratory and cardiovascular suppression and minimize stimulation of the sympathetic nervous system.
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PMID:Variation of rat serum biochemical values following decapitation or anesthesia with ether, halothane or Innovar-VetR: rapid Innovar-VetR-induced hyperuricemia and hyperglycemia. 704 81

Clinically asymptomatic patients undergoing hemodialysis and with histologically proven renal osteodystrophy were treated with 1,25-dihydroxycholecalciferol (1,25[OH]2D3) or with placebo for 9-37 weeks. Serum concentrations of total calcium were frequently increased when the ionized calcium was raised into the normal range. Serum magnesium was in the upper normal range due to the presence of magnesium in the aluminum hydroxide used to lower the hyperphosphatemia, which was difficult to control. Basal serum parathyroid hormone (PTH) levels were increased and seven times higher when measured with a radioimmunoassay recognizing mainly COOH-terminal fragments of human PTH-(1-84) (C-terminal assay) as compared to another assay measuring predominantly intact PTH-(1-84) (N-terminal assay). During treatment with 1,25 (OH)2D3, serum PTH returned towards the normal range with increasing calcium levels. Mean PTH concentrations decreased significantly by 34% (p less than 0.05) when measured with the N-terminal assay and by only 14% (p greater than 0.1) in the C-terminal assay. Serum alkaline phosphatase activity and the mineral content of the forearm estimated by photon absorptiometry remained unchanged.
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PMID:1,25-Dihydroxycholecalciferol in dialysed patients with clinically asymptomatic renal osteodystrophy. A controlled study. 735 81

Persistent hypercalcemia is most often due to tumor. Other causes are best eliminated by clinical methods combined with simple tests. Hypocalcemia is most often a result of hypoalbuminemia. Hyperphosphatemia induced by phosphate infusion or enema may cause profound hypocalcemia. Biochemical profiling may uncover severe hypophosphatemia necessitating phosphate administration. Markedly elevated serum alkaline phosphatase in the absence of hepatic disease is most likely to reflect either Paget's disease of bone or metastatic prostate cancer.
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PMID:Calcium and phosphorus studies: interpretation of results and strategies for further testing. 739 85

Pseudohypoparathyroidism (PHP) is a condition characterized by hypocalcemia, hyperphosphatemia, and an impaired phosphaturic response to exogenous parathormone (PTH). A minority of patients with PHP have associated bone disease, and in some the radiological appearances have been suggestive of rickets. We report a patient with PHP who had epiphyseal enlargement and bowing of the long bones similar to that seen in rickets. Radiology showed generalized osteomalacia with failure of epiphyseal calcification and several pseudofractures. Bone biopsy showed increased osteoid seams. The phalanges of both hands showed subperiosteal erosions consistent with hyperparathyroidism. Biochemically, he had persistent hypocalcemia, hyperphosphatemia, and an elevated alkaline phosphatase. Plasma calcitonin, magnesium, and 25-hydroxycholecalciferol levels were normal. The 1,25-dihydroxycholecalciferol level was within the normal adult range but was probably inappropriately low for an adolescent. Plasma parathormone was elevated (1.3--1.7 microgram/liter; normal, < 0.73). His diet was not deficient in vitamin D. Gastrointestinal function was normal. Renal function was normal, apart from an increase in the maximum tubular reabsorption of phosphate (46--52.6 mg/liter glomerular filtration rate; normal, 38 +/- 5). Intravenous PTH infusion tests were performed on the patient and a control subject before and 6 months after serum calcium levels had returned to normal. The maximum increases in cAMP excretion in the patient were 0.03 and 0.05 mmol/g creatinine before and after treatment, respectively (control, 0.53 and 0.24); the maximum increases in phosphate excretion in the patient were 0.14 and 0.04 mmol/g creatinine before and after treatment, respectively (control, 0.32 and 0.07). He responded to initial treatment with a high dose of calciferol and later to 1,25-dihydroxycholecalciferol in a dose of 1 microgram/day. It is considered that renal resistance to PTH is his primary abnormality, with the bone disease representing a secondary phenomenon.
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PMID:Pseudohypoparathyroidism presenting with rickets. 741 91

We prospectively studied the long-term effects of intravenous calcitriol in 17 hemodialysis patients with severe secondary hyperparathyroidism (HPT) for 25.7 +/- 3.4 (+/- SE) months. Calcitriol was given thrice weekly after dialysis. Subsequently, changes were made every 3-4 weeks based upon serum chemistries. Total calcium and inorganic phosphorus were measured weekly; alkaline phosphatase (AP) and IRMA-PTH were measured monthly. Inorganic phosphate was controlled with calcium supplements. With calcitriol therapy both IRMA-PTH and AP decreased from 876 +/- 113 to 65 +/- 13 pg/ml (p < or = 0.001) and 432 +/- 106 to 103 +/- 15 U/ml (p < or = 0.001), respectively. Each patient had a reduction in IRMA-PTH and AP. Nadir IRMA-PTH occurred at 55.4 +/- 7.3 weeks. The maximum and mean maximum doses of calcitriol were 8.0 and 4.1 +/- 0.4 micrograms thrice weekly, respectively. Hypercalcemia tended to occur in those patients who were hypercalcemic prior to the initiation of intravenous calcitriol therapy. All hypercalcemic episodes were asymptomatic and reversed either by temporary withdrawal or lowering of the calcitriol dose. Hyperphosphatemia developed in those patients with a history of elevated serum phosphates and was mostly related to dietary and medication noncompliance. We conclude that intravenous calcitriol was uniformly effective and safe for the long-term therapy of severe HPT in ESRD. Careful attention to serum phosphate control is required.
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PMID:Long-term high dose intravenous calcitriol therapy in end-stage renal disease patients with severe secondary hyperparathyroidism. 763 48

We report three neonates with transient hypoparathyroidism with elevated parathyroid hormone (PTH) levels to clarify further the pathogenesis of late neonatal hypocalcemia and calcium homeostasis. Clinical signs were seizures starting at age of 10 and 11 days. The biochemical features were characterized by transient hypocalcemia and hyperphosphatemia due to a high transport maximum of the phosphate/glomerular filtration rate, despite high PTH levels. All had normal magnesium and calcidiol levels (at least 5 micrograms/l) for their age, and this precludes hypoparathyroidism due to low magnesium levels and hyperparathyroidism due to overt vitamin D deficiency. To diagnose pseudohypoparathyroidism type I, intravenous human PTH (1-34) infusions were performed; however, they showed brisk responses of plasma and/or urine cyclic AMP in response to the PTH infusion, but the phosphaturic response to the PTH was sluggish compared to the controls. All three showed an increase in serum alkaline phosphatase activity, suggesting PTH stimulation of osteoblasts. They were treated initially with calcium lactate or (1 alpha)-hydroxycalciol/calcitriol. Their hypoparathyroid condition, however, was transient; they maintained normal serum calcium and PTH levels without medication before the age of 6 months. The etiology, possibly intracellular signal transduction distal to cyclic AMP and/or distinct from adenylate cyclase in the kidney, is developmental and the condition was resolved completely within 6 months of age. We have termed this condition "transient pseudohypoparathyroidism of the neonate".
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PMID:Transient pseudohypoparathyroidism of the neonate. 765 38

This study was undertaken to evaluate the long-term effect of single weekly oral pulse calcitriol therapy (0.05 mcg/kg) in 16 uremic patients. Eight (5 female, 3 male; aged 51.6 +/- 8.5 years) were on continuous ambulatory peritoneal dialysis (CAPD) for 28.8 +/- 12.7 months with basal intact parathyroid hormone (iPTH) 247 +/- 60 pg/mL. Eight (6 female, 2 male; aged 53 +/- 17.9 years) were on hemodialysis (HD) for 76.3 +/- 55 months with basal iPTH 270.9 +/- 92. Calcium dialysate was 1.75 mmol/L in all patients and serum phosphorus was controlled with CaCO3 2-4 g/day. Ca and P were measured weekly; iPTH and alkaline phosphatase were measured monthly. After two months, iPTH decreased to 132.4 +/- 89 (p < 0.05 vs basal values) in the HD patients and to 158.2 +/- 61 (p < 0.05) in the CAPD group. After six months, iPTH decreased to 108.6 +/- 73.2 (p < 0.01) in the HD patients and to 126.5 +/- 48 (p < 0.01) in the CAPD patients. Two patients (1 HD and 1 CAPD) who were not compliant with phosphate binder therapy were dropped. To control hyperphosphatemia in 1 HD patient we reduced bolus to 0.03 mcg/kg. Two CAPD patients presented hypercalcemia and required calcium dialysate of 1.25 mmol/L. In conclusion, single weekly oral pulse of calcitriol appears to be effective in suppressing mild hyperparathyroidism both in CAPD and in HD patients, even though some variations in the protocols may be required.
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PMID:Long-term effect of oral calcitriol single weekly pulse in CAPD and in HD. 799 42


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