Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of gastrectomy, especially total gastrectomy, on the serum levels of 25-hydroxyvitamin D and vitamin D-binding protein and on mineral metabolism were examined. The serum 25-hydroxy-vitamin D levels were markedly decreased in patients with total gastrectomy and Billroth II gastrectomy. Decreased levels of serum vitamin D-binding protein and serum calcium, and increased levels of serum alkaline phosphatase were observed in both patients with partial gastrectomy and patients with total gastrectomy. The results show that vitamin D deficiency could develop in high frequency patients with total gastrectomy and Billroth II gastrectomy, and that deranged mineral metabolism could develop in patients with any type of gastrectomy with or without vitamin D deficiency. The decreased levels of serum vitamin D-binding protein in postgastrectomy patients may be a sensitive reflection of the failure of hepatic protein synthesis.
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PMID:Serum 25-hydroxyvitamin D and vitamin D-binding protein levels and mineral metabolism after partial and total gastrectomy. 689 89

Different methods for the prevention and treatment of vitamin D deficiency were studied in 42 institutionalized elderly people. One group received ultraviolet radiation (UVR) on a large area of the body surface once a week for three months. The results were compared with those in groups receiving either 450 IU vitamin D2 together with 420 mg calcium daily, 420 mg calcium alone, or no treatment. A significant increase in serum 25-hydroxyvitamin D was obtained with UVR. A similar increase was obtained with oral vitamin D2. A small but significant decrease in serum alkaline phosphatase was observed in subjects receiving vitamin D and calcium or calcium alone. No effects on serum phosphate, urinary cyclic adenosine monophosphate and urinary calcium were seen. Though brief UVR at one-week intervals is an efficient and safe method for prevention of vitamin D deficiency in the elderly, it is in our experience time-consuming for the ward staff and thus less convenient than oral vitamin D supplementation.
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PMID:Oral vitamin D and ultraviolet radiation for the prevention of vitamin D deficiency in the elderly. 698 7

The occurrence of anticonvulsant osteomalacia was studied in 23 epileptic outpatients, and in age and sex matched controls. Hypocalcaemia was observed in 10, hypophosphataemia in 1, and increased serum alkaline phosphatase in 8 of the patients. The serum 25-hydroxyvitamin D concentration was significantly lower In the patients than in the controls, but no difference was found in the serum 24,25-dihydroxyvitamin D concentration between the patients and the controls. There was no difference in bone mineral density between the patients and the healthy controls. In the histomorphometric study, no differences were found in the amount of trabecular bone or osteoid between the patients and the controls, but the patients had a slightly more extensive trabecular resorption surfaces. Histological osteomalacia was found in two of the 23 cases (9%). We conclude that epileptic outpatients on long-term anticonvulsant therapy have vitamin D deficiency and may develop osteomalacia.
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PMID:Anticonvulsant osteomalacia in epileptic outpatients. 713 82

The effects of long term, low dosage anticonvulsant drug therapy on the vitamin D and folacin status of young children was studied. Biochemical and dietary parameters including serum calcium, phosphorous and alkaline phosphatase; serum and red blood cell folacin; serum drug concentrations; hematocrits; and dietary intakes of vitamin D and folacin were measured in seven subjects. All subjects were taking low dosages of medication. Four subjects were considered at risk for developing a folacin deficiency based on red blood cell folacin concentrations. Two of these subjects had inadequate dietary intakes of folacin. Serum calcium and alkaline phosphatase levels were within normal ranges for all subjects; two subjects had subnormal levels of serum phosphorous. Dietary intake of vitamin D was below fifty percent of the Recommended Dietary Allowance for four subjects. The data of the present study suggest that young children undergoing chronic anticonvulsant drug therapy of minimal dosage are susceptible to developing folacin deficiency especially if dietary intake of folacin is inadequate. These children do not appear to be at risk for developing vitamin D deficiency probably due to the low dosage of medication coupled with adequate sunlight exposure.
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PMID:Folic acid and vitamin D status of young children receiving minimal anticonvulsant drug therapy. 732 58

One hundred and four children aged 0-15 years, with suspicion of malabsorption were studied. They had a proximal jejunal biopsy and, at the same time, the following measurements: 25-hydroxycholecalciferol (25-OH-CC), calcium, phosphorus and serum alkaline phosphatase, bone age on X-ray of the left hand and wrist, cortical thickness of the 2nd, 3rd, 4th metacarpal bones. For the analysis of the results, the patients were divided into two groups according to the season (winter vs. summer). None of the patients in either group had clinical or radiological signs of rickets. The following results were obtained: 1. The 25-OH-CC serum levels were significantly lower during the winter than during the summer months. This was observed more frequently in the cases with atrophy of the jejunal mucosa. 2. During the summer, the 25-OH-CC serum levels were not different in the cases with normal or pathological mucosa. This demonstrates the importance of the skin synthesis of vitamin D during the summer months. 3. The mean of the serum calcium levels was significantly lower in the group of children with atrophy of the jejunal mucosa than in children with normal intestinal biopsy. The serum calcium levels were not correlated with the serum 25-OH-CC levels. 4. The serum phosphorus levels were significantly lowered during the winter months in the children aged 0-3 years with pathological jejunal biopsy. 5. The serum alkaline phosphatase levels were lowered in cases of total atrophy of the jejunal epithelium cells. 6. Cortical thickness of the metacarpal bones becomes thinner with the progression of the alteration of the jejunal epithelium cells, independently of season or age. However, only the group of children aged 0-3 years studied during the winter months and with total atrophy of the jejunal mucosa have a significantly diminished cortical thickness of the metacarpal bones. The lowering of the calcium levels and the decrease of the cortical thickness are probably secondary to an impaired intestinal absorption of calcium. In the syndrome of malabsorption, the integrity of the jejunal epithelial cells seems to play a more important role than a vitamin D deficiency in the genesis of this calcium malabsorption.
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PMID:[Phosphorus-calcium metabolism and plasma 25-hydroxycholecalciferol in intestinal malabsorption]. 745 Dec 35

Vitamin D nutrition in pregnancy was investigated in 115 Asian women living in London, and in 50 of their newborn infants. Mean serum 25-hydroxy cholecalciferal (25-OHD) concentration at the beginning of the last trimester was 20.2 nmol/l, and fell to 16.0 nmol/1 post partum. Thirty-six per cent of the women post partum and 32 per cent of the infants had undetectable 25-OHD concentrations (less than 3 nmol/l). Such low values are commonly associated with osteomalacia and rickets. The bone isoenzyme of alkaline phosphatase was elevated in 20 per cent of the women post partum, and in 50 per cent of the infants, indicating the presence of sub-clinical bone disease. Five infants had symptomatic hypocalcaemia. Vitamin D deficiency was most likely to occur in Pakistanis, Hindu Indians and East African Asians, and in vegetarians. All British Asians should receive supplementary Vitamin D during pregnancy.
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PMID:Observations on the vitamin D state of pregnant Asian women in London. 745 87

Nutritional vitamin D deficiency rickets was established in 41 Sudanese children aged from 3 months to 7 years by clinical, radiological and therapeutic response supported by biochemical investigations. There were 25 boys and 16 girls, of whom 42% were infants of less than 1 year. Forty-seven per cent of rachitic children were underweight. Six infants had early rickets with no bony swellings but had other clinical features and radiological evidence of rickets. One of them, aged 3 months, presented with hypocalcaemic convulsions. Three children had icthyosis. Serum alkaline phosphatase was raised in 75%, hypophosphataemia occurred in 68% and hypocalcaemia in 54% of patients. Anaemia, mostly hypochromic, was detected in 79%. Possible causes were poor socio-economic background, inadequate dietary intake in both mothers and children, prolonged breastfeeding, prematurity, limited sun exposure and type of residence. Nutritional vitamin D deficiency rickets should be looked for in Sudanese children, especially in preterms and in those living in flats.
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PMID:Nutritional vitamin D deficiency rickets in Sudanese children. 759 40

Phenytoin therapy is a well recognized cause of gingival hyperplasia, a condition characterized by increased gingival collagen synthesis, and may also cause acromegalic-like facial features. Based on these clinical findings suggestive of anabolic actions, we sought to test the hypothesis that phenytoin acts on normal bone cells to induce osteogenic effects. To test the direct actions of phenytoin on human bone cells, we measured the dose responses to phenytoin for [3H]thymidine incorporation, cell number, alkaline phosphatase specific activity, and collagen synthesis in human hip bone-derived cells. Phenytoin significantly and reproducibly increased [3H]thymidine incorporation, cell number, alkaline phosphatase specific activity, and collagen synthesis in a biphasic manner with optimal stimulatory doses between 5-10 mumol/L. Thus, micromolar concentrations of phenytoin can act directly on human bone cells to stimulate osteoblast proliferation and differentiation. We next sought to test the hypothesis that phenytoin stimulates bone formation in humans in vivo. Accordingly, three serum biochemical markers of bone formation, i.e. osteocalcin, skeletal alkaline phosphatase, and procollagen C-terminal extension peptide, were measured in 39 male epileptic patients, 20-60 yr of age, with an average duration of phenytoin therapy of 10.5 +/- 1.62 yr (mean +/- SEM). In this group of patients, the mean serum phenytoin level was 9.56 +/- 0.90 mg/L (mean +/- SEM; equivalent to 34.9 +/- 3.3 mumol/L). Thirty apparently healthy male subjects of similar age and taking no medication were included as controls. Serum calcium, 25-hydroxyvitamin D3, and PTH levels in the phenytoin-treated patients were not significantly different from those in the age-matched controls and were within the clinical laboratory normal range of our hospitals, indicating that the patients did not develop hypocalcemia, vitamin D deficiency, or secondary hyperparathyroidism. Serum levels of osteocalcin, skeletal alkaline phosphatase, and procollagen peptide in the phenytoin-treated patients were significantly increased compared to those in the age-matched subjects; in each case these biochemical markers were significantly correlated with the serum phenytoin level, but not with the dose or duration of phenytoin treatment. These findings are consistent with the interpretation that phenytoin increases the bone formation rate in humans in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Phenytoin increases markers of osteogenesis for the human species in vitro and in vivo. 762 28

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

A population of 125 adult Ethiopian women immigrants to Israel was screened for serum levels of calcium, phosphorus, and alkaline phosphatase. After the first instance of hypocalcemia was observed at a clinic in Afula Ilit (northern Israel), case finding was initiated among the 131 adult Ethiopian subjects 20 years or older. Over the course of 4 years, 125 patients (95%) were investigated. In 5 patients for whom these values deviated from the norm, values of parathyroid hormone (PTH), 1,25 hydroxy (OH) D, and 25 OH D were determined. Their diet was assessed for vitamin D-fortified foods and calcium intake. 5 subjects (prevalence of 4%) had hypocalcemia with normophosphatemia, 2 of them also having elevated levels of alkaline phosphatase. In 1 of them osteomalacia was found. Before and after treatment, high serum PTH and 1,25 OH D and low 25 OH D were found in all patients. All 5 patients had low serum levels of 25 hydroxy (OH) vitamin D3 and high parathyroid hormone (PTH) levels. In 4 of the 5 patients, clinical and biochemical manifestations of vitamin D deficiency were detected during pregnancy or lactation. Treatment with vitamin D2 for 4-13 months resulted in clinical improvement and partially corrected the biochemical abnormalities, but low serum vitamin D levels and elevated FTH levels persisted. Vitamin D deficiency among female Ethiopian immigrants to Israel can be ascribed either to dark skin or to low calcium and vitamin D intake, or to both. As far as it is known this is the first report of vitamin D deficiency among such immigrants. The study suggests the need to be alert to the possibility of vitamin D deficiency in Ethiopian women who have immigrated to Israel, in particular those who are pregnant or are breast-feeding.
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PMID:High prevalence of vitamin D deficiency among Ethiopian women immigrants to Israel: exacerbation during pregnancy and lactation. 864 79


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