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)

Plasma levels of 25-hydroxycalciferol (25-OH-D) and the biological parameters of phosphocalcium metabolism were determined in 55 patients institutionalized in a geriatric hospital in Geneva. They were compared with two control groups, one of the same age and the other younger. The mean plasma 25-OH-D level of the hospitalized patients was 22.7 +/- SD 13.6 microgram/l, which is significantly lower (p less than 0.001) than the mean level obtained from both the control group of the same age (46.2 +/- SD 20.1 microgram/1 25-OH-D) and the control group of young subjects (48.6 +/- SD 16.8 microgram 25-OH-D/1). Among the 55 hospitalized patients, 27 (49%) had a deficient 25-OH-D plasma level lower than 20 microgram/1. Compared to the control group of the same age, the group of hospitalized subjects had lower mean plasma level of inorganic phosphate (27.1 +/- SD 4.34 mg/1; p less than 0.01) and an elevated mean plasma level of alkaline phosphatase (46.9 +/- SD 16.5 UI/1; p less than 0.005). For those 27 patients deficient in 25-OH-D, a positive correlation exists between the plasma values of 25-OH-D and the total calcium (r = 0.584). The high incidence of biological indicators of osteomalacia found in the group of hospitalized patients suggests that vitamin D deficiency is a current problem of the elderly in Switzerland necessitating a review of the prophylactic measures now in use.
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PMID:[Study of vitamin D deficiencies in the aged]. 87 25

In 100 infants with nutritional rickets, i.e., responsive to vitamin D therapy, we found a close inverse relationship between serum phosphorus, on the one hand, and serum alkaline phosphatase and the presence of radiological signs of rickets, on the other. There was no correlation between serum calcium and the severity of bone lesions. It is concluded that hypophosphatemia but not hypocalcemia is typical of rickets. Since hypophosphatemia and rickets can be produced experimentally by phosphate deficiency alone, we suggest our infants can be divided into two groups, one with true vitamin D deficiency that leads to hypocalcemia and no or mild bone lesions, and one with primary phosphate deficiency, resulting perhaps from a defect in phosphate transport, which leads to rickets and hypophosphatemia.
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PMID:Two types of nutritional rickets in infants. 99 37

Ten years of experience with daily prophylaxis of rickets brought about isolated knowledge which corrected old mistakes and demands a revision of older attitudes towards the usual prophylaxis. Prophylaxis of vitamin D according to the most modern and reliable knowledge in the best way promotes the growth and mineralisation of the skeleton with dosages of 400 to 800 I.U. smaller or higher dosages are disadvantageous. By observing the above given dosage, rickets and hypercalcaemia are rare and only conceivable under special pathological conditions. The diagnosis of beginning rickets must be well known, otherwise unspecific symptoms of rickets may induce the administration of unnecessarily high amounts of vitamin D. The symptoms of rickets show a gradual increase: the increase of serum alkaline phosphatase precedes the clinical and radiological symptoms. The reliable radiographic deformities of the hand can first be seen at the Ulna, then at the Radius and later at the secondary centers of Metacarpals. Among the relatively reliable clinical symptoms there its first the rosary later the Marfan-sign and eventually the deformation of the long bones. For infants protected by vitamin D, craniotabes as a sign of rickets is completely unreliable as well as the Harrison grooves and rachitic kyphosis. If one observes all these rules and rachitic kyphosis. If one observes all these rules and criterions vitamin D is as reliable in the prophylaxis as in the therapy of vitamin D deficiency rickets.
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PMID:[Ten years' daily prophylaxis against rickets--review and outlook (author's transl)]. 119 21

Unilateral nephrectomy causes a decrease in provision of vitamin D dihydro derivatives in pregnant rats, which correlated with the development of hypocalcemia and hypophosphatemia as well as with an increased content of parathyroid hormone. Fetuses of these females contained less amount of mineral components and active metabolites of vitamin D. Neonates, being born by these females with the nephrectomy, had vitamin D deficiency, which was manifested as a decrease in content of active vitamin D metabolites and minerals as well as an increase in activity of alkaline phosphatase and in the content of parathyroid hormone.
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PMID:[The effect of unilateral nephrectomy on vitamin D metabolism in pregnant rats]. 149 97

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

It has been suggested that hypertrophic cardiomyopathy (HCM) may be associated with hyperparathyroidism. We evaluated parathyroid function in 15 patients with HCM and 14 patients with primary dilated cardiomyopathy (DCM), measuring different parameters of calcium metabolism (total serum calcium, ionized calcium, PTH, vitamin D metabolites, alkaline phosphatase, osteocalcin). As a group PTH levels were normal in HCM (intact PTH 3.9 +/- 1.6 pmol/l, midmolecular PTH 59 +/- 13 pmol/l and carboxyterminal PTH 0.6 +/- 0.4 ng/ml), but in 3 patients carboxyterminal PTH levels were persistently higher than normal, while all other parameters of calcium metabolism were normal. We conclude that parathyroid function is normal in patients with HCM, although some of them may have an abnormal secretion and/or metabolism of carboxyterminal PTH fragments, or a circulating substance the interferes with this PTH assay. Parathyroid function in DCM patients was normal, except in a patient who had hyperparathyroidism secondary to vitamin D deficiency.
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PMID:[Parathyroid function in hypertrophic myocardiopathy]. 175 23

The influence of vitamin B6 deficiency on some vitamin D-dependent processes was studied in animals. The following parameters changing in relation to the level of vitamin D providing were investigated: activity of alkaline phosphatase in the serum and small intestine mucosa, the levels of Ca, P and parathormone, concentration of vitamin D metabolites and enzyme activity; and only 25-hydroxyvitamin D (25-OVD) concentration in the blood serum, under conditions of combined vitamin B6 and D deficiency was significantly lower as compared to cases with vitamin D deficiency alone. In the presence of vitamin B6 deficiency recovery of 25-OVD level in the blood serum, after vitamin D administration to the animals, had a tendency to delay as compared to that in the animals provided with vitamin B6. Vitamin B6 deficiency produced similar effect on 25-OVD 1-hydroxylase activity. The data obtained have evidenced a possibility of vitamin B6 influence on vitamin D metabolism.
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PMID:[Vitamin D and calcium metabolism in relation to different levels of vitamins B6 and D]. 179 51

The hypocalcemia that accompanies vitamin D deficiency is a major obstacle to proper interpretation of the role(s) of vitamin D metabolites in Ca-sensitive tissues. This paper describes the development and complete characterization of a dietary regimen with which normocalcemia was maintained in rats throughout the development of vitamin D deficiency. Normal weanling rats were fed diets containing 0.8% Ca, 0.5% P, and vitamin D3 (group A), or vitamin D-deficient diets containing 0.8% Ca and 0.5% P (group B); 2.0% Ca and 1.25% P (group C); or 2.0% Ca, 1.25% P, and 20% lactose (group D) for 19 wk. Group D rats were normocalcemic and normophosphatemic with normal parathyroid hormone (PTH) levels throughout the study. In contrast, from 4-19 diet wk, groups B and C were hypocalcemic with elevated PTH. Initially, plasma 25-hydroxyvitamin D3 [25(OH)D3] levels decreased most rapidly, and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] levels decreased least rapidly in group B rats, such that plasma 25(OH)D3 levels were reduced to 200-300 pg/ml before a decrease in 1,25(OH)2D3 levels was observed. However, vitamin D metabolite levels were similar in groups B, C, and D from 4-19 wk. Duodenal active Ca transport mirrored changes in plasma 1,25(OH)2D3 levels and was abolished after 10 wk. The results also suggested that vitamin D may not be necessary for normal bone mineralization since tibia mineral content and plasma alkaline phosphatase levels were similar in normocalcemic groups A and D throughout the study.
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PMID:Plasma Ca influences vitamin D metabolite levels as rats develop vitamin D deficiency. 184 6

Changes in bone structure like chondronecrosis and osteonecrosis occurred in a group of adolescent athletes especially gymnasts. To determine the etiology calcium, inorganic phosphorus, alkaline phosphatase activity and levels of 25-OH-Vit D were investigated. Single low calcium values were present in nearly the half of the athletes. In 37% the vitamin-D-levels were depressed. Such results were found in athletes with and without changes in bone structure. A vitamin D supplementation is recommended if low vitamin D levels are found. Vitamin D deficiency is not the only reason for the disturbances of the bone. Other factors are to take in consideration like nutrition, delayed bone maturation and its consequences, and the mechanical load.
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PMID:[Parameters of mineral metabolism in children and adolescents in athletic training]. 192 Nov 65

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


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