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)

Parameters of mineral metabolism were examined in 6 patients with moderately severe anticonvulsant drug-induced osteomalacia. Compared to 15 matched controls, the patients exhibited significantly reduced serum calcium, inorganic phosphate, and 25-hydroxyvitamin D concentration, elevated serum alkaline phosphatase and immunoreactive parathyroid hormone (iPTH) concentration, reduced intestinal 47Ca absorption, reduced urinary calcium and increased urinary hydroxyproline excretion, and reduced forearm bone mass. Intestinal absorption of vitamin D3 was normal. Following 4 months of treatment with vitamin D3 (4000 units/day), serum 25-OHD concentration was increased to 3 times mean normal values and all parameters except serum iPTH, urinary calcium excretion, and forearm bone mass were returned to levels not significantly different from normal. Serum iPTH concentration was reduced by 39% (P less than 0.05); 24-h urinary calcium excretion rose by 98% (P less than 0.001), and forearm bone mass increased by 5.6% (P less than 0.05). It is concluded that moderate-dose vitamin D3 supplementation is effective in normalizing parameters of mineral metabolism in this disorder, despite evidence of resistance to the biologic effects of vitamin D.
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PMID:Anticonvulsant drug-induced osteomalacia: alterations in mineral metabolism and response to vitamin D3 administration. 22 50

Thirty-four patients were studied 2--6 years after jejunoileal bypass for morbid obesity. The serum concentration of 25-hydroxyvitamin D (25-OHD) were reduced and related to the frequency fo stools and to the weight reduction. Fifteen patients were not able to normalize serum 25-OHD following a long-term regular vitamin D intake. The serum immunoreactive parathyroid hormone concentration (iPTH) and the alkaline phosphatase levels were elevated in this group, indicating a secondary hyperparathyroidism. The mean bone mineral content of the forearm was reduced 3--6 years after the operation, most severely in those with elevated serum iPTH. The desired weight reduction by jejunoileal shunt was obtained at the expense of a severely disturbed vitamin D metabolism. We suggest, that all patients with an intestinal bypass for obesity should receive regular vitamin D supplement, and serum 25-OHD should be measured in order to monitor the effect of therapy.
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PMID:Impairment of vitamin D and bone metabolism in patients with bypass operation for obesity. 28 17

A randomized controlled study was performed to investigate the effect of 2 years' monitored diphenylhydantoin (DPH) therapy on plasma 25-hydroxyvitamin D (25-OHD) in non-epileptic, non-institutionalized subjects. Mean +/- SEM plasma 25-OHD of 18 DPH-treated subjects at the end of 2 years' drug treatment was 59 +/- 8 nmol/l (23.6 +/- 3.2 ng/ml), which was not decreased compared to that of eighteen control subjects (54 +/- 8 nmol/l, 21.6 +/- 3.2 ng/ml). In addition, mean plasma 25-OHD had not changed 1 month after ceasing DPH. The treated group had a higher mean serum alkaline phosphatase (SAP) during DPH treatment, attributable to hepatic enzyme induction. It is concluded that therapeutic doses of DPH without other anticonvulsants do not have a clinically significant effect on plasma 25-OHD.
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PMID:Chronic diphenylhydantoin therapy does not reduce plasma 25-hydroxy-vitamin D. 38 83

Plasma 25-hydroxyvitamin D (25-OHD) values in 22 hyperthyroid patients did not differ significantly from those of controls matched for age, sex, and the time of year that plasma samples were taken. In the hyperthyroid group, plasma alkaline phosphatase was significantly higher than in controls, and an increase in bone type alkaline phosphatase occurred in 50%. In the 18 female hyperthyroid patients the plasma gamma-glutamyl transferase was significantly increased compared with controls. Mean values for plasma albumin, alanine transferase, and calcium showed no significant difference between hyperthyroid and control patients.
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PMID:Plasma 25-hydroxyvitamin D and alkaline phosphatase isoenzymes in hyperthyroidism. 73 91

The development of alkaline phosphatase influenced by 1 alpha-OH-D3 (a synthetic active form of vitamin D3) and cortisone was studied in chick duodenal organ cultures. The administration of cortisone to the embryo in ovo on the 14th day of incubation resulted in a precocious increase in alkaline phosphatase after six days (20-day embryo). When duodena from 14-, 18- and 20-day embryos were cultured in the presence of cortisone, there was no significant enhancement of alkaline phosphatase activity except for a marginal effect observed in the 18-day duodenum. On the other hand, the alkaline phosphatase activity in cultured duodena from 20-day chick embryos was significantly stimulated by the addition of 1 alpha-OH-D3. The effects of cortisone and 1 alpha-OHD-3 were not additive. The activity of maltase, another intestinal enzyme, was not influenced by 1 alpha-OH-D3. Studies on inactivation of alkaline phosphatase by EDTA suggest that the observed increase in alkaline phosphatase activity induced by the administration of 1 alpha-OH-D in vitro may be related to the qualitative changes in the enzyme that take place during development in vivo.
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PMID:The effect of 1alpha-hydroxyvitamin D3 and cortisone on the development of chick duodenal alkaline phosphatase in organ culture. 82 39

The synthesis of osteocalcin or bone gla protein by osteoblasts is markedly stimulated by 1,25-(OH)2D, a key hormone in the regulation of bone mineralization. The circulating levels of osteocalcin have been shown to reflect both the osteoid matrix production and the formation rate of mineralized bone in several metabolic bone diseases (osteoporosis, thyrotoxicosis, primary hyperparathyroidism) in which both mechanisms are tightly coupled because of the absence of mineralization defect. In this study, we measured in 12 patients (7 women, 5 men, 56 +/- 15 yr old) with untreated osteomalacia serum osteocalcin and vitamin D metabolites (25OHD and 1,25-(OH)2D). The results were correlated with biochemical and histomorphometric assessment of bone remodeling. Osteomalacia was due to vitamin D deficiency (5 cases), to vitamin D malabsorption (6 cases), and to hypophosphataemia in 1 case. When compared to control values, serum osteocalcin was increased in patients with osteomalacia (7.4 +/- 4 vs. 3.7 +/- 1.3 ng/mL; P less than 0.001) and was positively correlated with serum alkaline phosphatase (r = 0.65; P = 0.03) and negatively with 25 OHD (r = -0.61; P = 0.04). Serum osteocalcin was not correlated with 1,25-(OH)2D [r = -0.45; not significant (NS)] even after exclusion of the patient with hypophosphataemia. Serum osteocalcin was positively correlated with the osteoid volume and osteoid perimeter (r = 0.71 and 0.69 respectively; P less than 0.01) but not with any of the tetracycline-based parameter of bone mineralization at the tissue level (r ranging from -0.41 to +0.42, NS). Serum 25 OHD, but not 1,25-(OH)2D, was positively correlated with the mineralization rate (r = 0.59; P less than 0.05 and r = 0.54; NS). We conclude that in patients with osteomalacia, a condition which is characterized by an increased osteoid accumulation due to a decreased mineralization rate, the increased level of serum osteocalcin reflects the increased osteoid synthesis but not the mineralization defect. In this disease, serum osteocalcin is inversely correlated to the severity of vitamin D deficiency reflected by serum 25 OHD, but not to the serum levels of 1,25-(OH)2D.
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PMID:Serum osteocalcin is increased in patients with osteomalacia: correlations with biochemical and histomorphometric findings. 156 62

Eleven Nigerian children with clinically and radiologically proven rickets were assessed biochemically. The children had low or low normal concentrations of total and corrected calcium, and elevated plasma alkaline phosphatase (ALP) activity, but normal plasma phosphate concentrations. Their serum 25-hydroxyvitamin D (25-OHD) and 1,25-dihydroxyvitamin D (1,25-(OH)2D) concentrations were not significantly different from those in controls, but the ratio of 1,25-(OH)2D to 25-OHD was significantly greater than that in controls. Parathyroid hormone (PTH) concentrations were greater in rachitic children, and there was a significant correlation between 1,25-(OH)2D and PTH concentrations. Osteocalcin concentrations in rachitic children were not significantly different from those in controls, but they were markedly elevated in the three patients with the highest 1,25-(OH)2D and PTH concentrations. One child, from whom a sample of bone (from a corrective osteotomy) was available for histological examination, showed markedly thickened osteoid seams, characteristic of rickets. All the rachitic children had a calcium intake of less than 150 mg daily. Treatment of these rachitic children with calcium gluconate (1 g/d) led to clinical, radiological, and biochemical healing of rickets. We conclude that rickets in Nigerian children is not due to vitamin D deficiency, but to a lack of calcium. This observation has implications regarding the pathogenesis, treatment, and prevention of rickets/osteomalacia in Nigeria and possibly other African and tropical countries.
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PMID:Rickets in Nigerian children: a consequence of calcium malnutrition. 198 79

We report serum 25-hydroxyvitamin D (25-OHD), 24,25-dihydroxyvitamin D [24,25-(OH)2D], and 1,25-dihydroxyvitamin D [1,25-(OH)2D] levels in untreated Paget's disease and the effect of treatment with either calcitonin (CT) or etidronate (EHDP) on these levels. In untreated Paget's patients serum 25-OHD (73 +/- 29 nmol/liter, n = 36, mean +/- SD) and 24,25-(OH)2D (0.3-12.9 nmol/liter, median 2.2, n = 36) levels were significantly lower than in age-matched controls (94 +/- 30 nmol/liter, n = 32, p less than 0.005, and 1.3-16.4 nmol/liter, median 5.3; n = 32, p less than 0.001, respectively). Also, the 24,25-(OH)2D levels correlated with the 25-OHD levels in the untreated Paget's patients (r = 0.56, p less than 0.01) and in the controls (r = 0.39, p less than 0.05). The percentage molar ratio of 24,25-(OH)2D to 25-OHD in Paget's patients had a median value of 3.7% (range 0.4-14.3%), which was not significantly different from controls, who had a median value of 5.6% (range 2.2-18%). There was no difference between the 1,25-(OH)2D, and immunoreactive PTH (iPTH) levels of Paget's patients and control subjects. The percentage molar ratio of 1,25-(OH)2D to 25-OHD in untreated Paget's patients (0.157 +/- 0.09%) was not significantly different from controls (0.124 +/- 0.05%) despite lower 25-OHD levels in Paget's patients. There was a significant inverse correlation between the severity of Paget's disease as measured by plasma alkaline phosphatase (AP) levels and 25-OHD levels (r = 0.392, p less than 0.02); however, 24,25-(OH)2D and 1,25-(OH)2D levels were not correlated with AP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in vitamin D metabolites during treatment of Paget's disease of bone with calcitonin or etidronate. 212 1

Metabolism of calcium and vitamin D was studied in young rats administered with trichothecene-related mycotoxin deoxynivalenol (vomitoxin) at a daily dose of 10 mg/kg perorally within 7 days. The vomitoxin treatment caused a moderate hypocalcemia, a decreased absorption of calcium in small intestine as well as led to decrease of alkaline phosphatase activity in blood and small intestine mucosal membrane. Density and saturation of bone tissue with minerals were not altered. Concentration of 25-OHD in blood and activity of vitamin D3(25)-hydroxylase in liver tissue were decreased by 40% and 30%, respectively. Development of 1,25(OH)2D3 and 24,25(OH)2D3 as well as concentration of total and free 1,25(OH)2D3 receptors were not altered in kidney. At the same time, these impairments of calcium and vitamin D metabolism were prevented by providing high content of vitamin D in the ration--0.25 mg/kg of food. Impairments in calcium metabolism caused by vomitoxin may be partially related to development of a secondary deficiency in vitamin D.
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PMID:[The effect of the trichothecene mycotoxin deoxynivalenol (vomitoxin) on calcium homeostasis, vitamin D metabolism and receptors in rats]. 217 86

Twenty-five hydroxycalciferol (25-OHD), 1,25-dihydroxyvitamin D (1,25(OH)2D), calcium (Ca), phosphorus (P), alkaline phosphatase, and total protein were estimated in 86 Saudi pregnant women. They were divided into two groups, group I, parity 5 or more, and group II, parity 4 or less. The mean level of 25-OHD was 10.4 (S.D. 6.5) ng/ml in group I, and for group II 8.2 (6.1) ng/ml with no significant statistical difference between the groups. 1,25(OH)2D mean levels, in group I 45.5 (S.D. 30.2) ng/ml and in group II 36.9 (S.D. 27.1) pg/ml, also showed no significant difference. Levels of vitamin D metabolites were comparable with non-pregnant levels in Saudi Arabia but lower than others reported in Western populations. We found no effect of increasing parity on levels of vitamin D metabolites in our study.
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PMID:Parity and vitamin D metabolites. 244 72


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