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)

Recent evidence suggests that the protein osteocalcin is like the bone alkaline phosphatase produced by osteoblasts and circulates in human blood. With the introduction of a radioimmunoassay for serum osteocalcin it was hoped that this test would provide a useful index of altered bone metabolism. Therefore serum osteocalcin was measured in 88 controls and 112 patients with disorders of calcium and phosphate metabolism, isolated elevation of alkaline serum phosphatase in the absence of disease (isolated hyperphosphatasaemia) and children prone to osteopenia. In the controls serum osteocalcin was higher in children less than 15 years (median and range: 11.9, 7.7-15.3 ng/ml) than in adults (3.7, 2.6-5.2 ng/ml) and was highly correlated to alkaline serum phosphatase activity (r = 0.87, n = 88, P less than 0.01). Osteocalcin was elevated in primary hypoparathyroidism, low in untreated hypoparathyroidism but normal in hypoparathyroidism (including pseudohypoparathyroidism) during vitamin D treatment. The bone protein was low-normal and increased to high-normal levels during vitamin D therapy in vitamin D deficiency rickets and familial hypophosphataemic rickets, but remained low in patients with end organ resistance to 1,25-dihydroxyvitamin D. Osteocalcin (and urinary hydroxyproline) were not elevated in isolated hyperphosphatasaemia, indicating that mechanisms other than increased bone turnover may account for the markedly elevated serum alkaline phosphatase activity in these subjects. Osteocalcin was decreased in children with diabetes mellitus type I and in patients on glucocorticoid treatment, indicating decreased bone formation. It is concluded that the measurement of serum osteocalcin seems to be a reliable index of bone formation provided that the vitamin D status and renal function are normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of serum osteocalcin as an index of altered bone metabolism. 301 28

During the last 4 years we observed four cases of neonatal rickets. The mothers of the infants suffered from osteomalacia for 1-3 years prior to its diagnosis shortly after the birth of their children. All four infants were born with craniotabes, and one infant had, in addition, a radial fracture. The diagnoses were confirmed by radiological and laboratory tests which revealed a rarefied bone structure, decreased serum 25-hydroxy-vitamin D and increased alkaline phosphatase levels in all patients. The disorder regressed under low-dose vitamin D3 therapy. As osteomalacia seems to be predominant in oriental women living in Berlin, it is necessary to consider vitamin D deficiency when clinical symptoms of this disease arise and to treat these women at least during pregnancy.
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PMID:Osteomalacia of the mother--rickets of the newborn. 303 31

Since Schmid (115) and Kruse (74) reported on osteopathies occurring after antiepileptic treatment in children, there have been numerous publications concerning the influence of antiepileptics on mineral metabolism in the bones. The investigators' results range from slight anomalies of the plasma levels of calcium, phosphate, alkaline phosphatase, parathormone and 25-hydroxycholecalciferol to severe bone alterations. In the majority of cases, the severe pictures occurred in retarded, neurologically abnormal, institutionalised children who were treated with a high-dose combination of several antiepileptics for epilepsy which was difficult to treat. The first case reports from adults were published by Dent et al. (26). These patients had also been treated since their early youth with an antiepileptic combination. They displayed fractures and suffered from bone pain and muscular weakness. The good response of the rachitic bone alterations to vitamin D treatment both in children and in adults indicated vitamin D deficiency. These reports prompted systematic investigations on the influence of antiepileptics on bone metabolism in numerous hospitals and outpatient departments. According to the available literature, it can be stated that antiepileptic therapy can lead to shifts in calcium and phosphate metabolism and to a raised activity of serum alkaline phosphatase. In studies comprising control groups, the patient treated with anticonvulsants more frequently displayed variations of clinical laboratory parameters. The frequent observation of vitamin D hypovitaminosis led to the assumption that alterations in vitamin D metabolism by enzyme induction are the cause of the disorders in calcium and vitamin D metabolism. This hypothesis was frequently contradicted in recent years after hypocalcaemia and alterations in the mineral content of the bone after antiepileptic therapy had been reported irrespective of the vitamin D level. Besides a restricted intestinal calcium absorption, an influence of antiepileptics on the hormones regulating calcium and phosphate metabolism was found. Thus, a multifactorial genesis of the disorders in bone mineral balance must be assumed. The fact that the vast majority of outpatients with long-term anticonvulsant therapy do not display any disorders of bone metabolism indicate that there are individually different compensation capabilities (possibly of genetic origin). According to the literature, the probability that adults will develop osteomalacia under antiepileptic therapy is associated with the joint presence of various risk factors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Osteopathia antiepileptica in adolescents and adults]. 306 13

We evaluated arginine-induced insulin and growth hormone (GH) secretion in ten children with vitamin D deficiency rickets and compared these values with those of eight age-matched control children. All rachitic children had biochemical (increased serum alkaline phosphatase activity and decreased calcium x phosphate product) and clinical evidence for rickets. After an intravenous infusion of arginine-HCl (10% solution, 0.5 g/kg), blood samples were obtained for the measurement of serum insulin and GH concentrations. The mean insulin level 30 min after the start of the infusion was 22.2 +/- 17.1 microU/ml for the rachitic children. This value is significantly below that for the normal children, 63.4 +/- 38.7 microU/ml (p = 0.004). Neither the fasting insulin level nor any others after the arginine infusion differed significantly from those for the control children. There were no significant differences in the fasting or the arginine-stimulated GH levels between the rachitic and control children. The concentrations of insulin-like growth factors did not differ between the two groups.
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PMID:Arginine-induced insulin and growth hormone secretion in children with nutritional rickets. 332 44

As part of a randomised controlled study to assess the effect of pasteurization of breast milk on the growth of very-low-birth-weight infants, the longitudinal changes in serum calcium, phosphorus, alkaline phosphatase, 25-hydroxyvitamin D, and bone-gla-protein concentrations were investigated. Infants fed untreated own mother's milk grew more rapidly than those fed pasteurized pooled preterm milk and had higher serum alkaline phosphatase and lower phosphorus values. Serum calcium and 25-hydroxyvitamin D (25-OHD) concentrations were similar in the two groups. Despite the provision of 750 IU vitamin D daily from the 2nd week of life, serum 25-OHD values remained low in a number of infants in both groups, suggesting that either malabsorption of vitamin D or hepatic immaturity might be responsible for the persistently low values. Bone-gla-protein rose significantly after birth and was correlated with alkaline phosphatase values, but not with 25-OHD or phosphorus values. The study supports previous work that indicates that the low phosphorus content of breast milk is probably responsible for biochemical evidence of inadequate bone mineralization and that despite vitamin D supplementation, 25-OHD values do not rise adequately. Thirty-six infants were reexamined between 4 and 11 months after birth. The 25-OHD values had risen significantly in all infants except one who had vitamin D deficiency rickets.
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PMID:Mineral homeostasis in very low birth weight infants fed either own mother's milk or pooled pasteurized preterm milk. 351 33

Serum levels of 25 OH-D, Calcium, Phosphorus and Alkaline phosphatase were measured in 53 children. These children, immigrants for 3/4, 3 to 6 years old, were in good health, and usually followed in a medical advice of PMI in the center of the city. During the month of february, march, april, the half of immigrant children have a serum 25 OH-D deficiency and high alkaline phosphatase, when european children have a normal 25 OH-D level and low alkaline phosphatase. After a stay in their origin country, in september, october, the children come back with a normal 25 OH-D level. Difference between winter and autumn is very significative. The risk factors of a vitamin D deficiency are studied.
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PMID:[25-Hydroxyvitamin D in children 3 to 6 years old followed at the Service de Protection Maternelle et Infantile]. 377 33

Forty patients with Crohn's disease were divided into undernourished (18) and well nourished (22) groups depending on whether their midarm circumference was below or above 90% of the ideal standard. Plasma 25-(OH)D3 and the dihydroxylated metabolites, 24,25-(OH)2D3 and 1,25-(OH)2D3 were measured in the summer. Results were related to clinical and biochemical parameters and also compared with results from patients with ulcerative colitis and healthy subjects who served as controls. Plasma 25-(OH)D3 was reduced in the undernourished Crohn's group compared with the well nourished Crohn's group, who did not differ from the controls. Over 50% of the undernourished Crohn's group had evidence of secondary hyperparathyroidism and raised alkaline phosphatase concentrations, although concentrations of 1,25-(OH)2D3 were normal. The low 25-(OH)D3 concentrations related to disease activity. It is suggested that undernourished Crohn's patients who have high levels of disease activity are at risk of vitamin D deficiency, and attempts should be made to improve their vitamin D nutrition.
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PMID:Vitamin D status in Crohn's disease: association with nutrition and disease activity. 387 63

A prospective study of 47 patients with otosclerosis was undertaken to investigate the possible etiologic role of vitamin D undernutrition. The population comprised 27 women and 20 men, with a mean age of 46.4 years (range 21 to 79). The disease was bilateral in 43 patients, and cochlear involvement was present in 84.4%. The mean duration of symptoms was 17.1 years. Vitamin D status was evaluated by measuring the plasma 25-hydroxy vitamin D3 (25-OHD), which is the main storage metabolite. Abnormally low 25-OHD levels were found in 10 patients (21.7%) and borderline low levels in another two. Raised serum alkaline phosphatase levels were present in 32.6%, calcium in 6.5%, and inorganic phosphate in 4.3%. Calcium and vitamin D replacement therapy resulted in significant hearing improvement in 3 of 16 patients; these data support a causal correlation. Vitamin D deficiency is probably a factor in the etiology of some cases of otosclerosis and is important, since the deafness resulting from cochlear involvement may be reversible.
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PMID:Vitamin D deficiency and otosclerosis. 392 24

The apparent decline over the last decade of vitamin D deficiency rickets among black infants in South Africa has suggested a significant improvement in their vitamin D status. Levels of serum 25-hydroxy-vitamin D, calcium, phosphorus and alkaline phosphatase, together with a radiograph of the left wrist, were obtained in 114 hospitalized black infants under the age of 2 years in order to establish the frequency of infants with or at risk of vitamin D deficiency. Mean 25-hydroxyvitamin D levels were found to be in the low normal range and showed no correlation with either age or season. Vitamin D stores were depleted in 7% and relatively deficient in 20,7% with suggestive radiological features of rickets in only 2 patients. The high prevalence of malnutrition and infection made a biochemical assessment of rickets impossible. The significance of these suboptimal vitamin D levels is uncertain, but the available literature would suggest that these infants are at increased risk of developing vitamin D deficiency rickets.
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PMID:Vitamin D status in hospitalized black children under 2 years of age. 401 77

Calciferol therapy for 12 months in white, Asian, and West Indian schoolchildren resulted in a highly significant increase in height and weight when compared with schoolchildren not so treated. The rate of fall of serum alkaline phosphatase was similar in both the treated and untreated schoolchildren and in other children treated in hospital for rickets. Dietary studies on 9% of the total survey by weighed inventory methods showed a low average intake of vitamin D, while random estimates of 25-hydroxycalciferol levels on 6% of the children were less than 3.8 ng/ml in 40% of those studied (principally Asian). It was concluded that there was a significant problem of vitamin D deficiency among Asian and West Indian teenagers and that white children were also affected to a less degree.
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PMID:Rickets, growth, and alkaline phosphatase in urban adolescents. 454 74


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