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)

Vitamin D deficiency reduces insulin secretion and still occurs in East London Asians in whom the prevalence of diabetes mellitus is at least four times that of Caucasians. Vitamin D status was assessed in 44 of 65 non-diabetic subjects 'at risk' of diabetes (spot blood glucose level >6.0 mmol/l <2 h post cibum, or>4.6 mmol/l >2 h post cibum on two separate occasions) and in 15 of 60 age and sex-matched 'low-risk' control subjects who attended for oral glucose tolerance test (OGTT) after screening of 877 omnivorous subjects not known to have diabetes. It was found that 95% of at-risk and 80% of low-risk subjects were vitamin D deficient (serum 25-hydroxy-vitamin D <11 ng/ml). Diabetes was present in 16, impaired glucose tolerance in 12 and normoglycaemia in 19 at-risk subjects, imparied glucose tolerance in 2, and normoglycaemia in 13 low-risk subjects. Correlation of 30-min OGTT blood glucose, specific insulin and C-peptide levels with 25-hydroxy-vitamin D concentrations in 44 at-risk subjects were -0.31 (p=0.04), 0.59 (p=0.0001) and 0.44 (p=0.006). In 15 'not-at-risk' subjects 30-min OGTT specific insulin and C-peptide levels correlated with 25-hydroxy-vitamin D, r=0.39 (p=0.04) and 0.16 (p=0.43), respectively. Serum alkaline phosphatase concentration was higher in at-risk than not-at-risk subjects (59.6 vs 46.5 IU/l, p=0.012); corrected calcium concentrations were comparable (2.38 vs 2.39 mmol/l, p=0.7). Following treatment with 100,000 IU vitamin D by i.m. injection, specific insulin, C-peptide [30 min on OGTT] and 25-hydroxy-vitamin D concentrations had risen 8-12 weeks later [mean +/- DS] from 57 +/- 62 to 96.2 +/- 82.4 mU/l [p=0.0017], 1.0 +/- 0.4 to 1.7 +/- 0.8 pmol/ml [p=0.001] and 3.6 +/- 1.8 to 13.5 +/- 7.4 ng/ml [p=0.0001], (but not to low-risk group values of 179 +/- mU/l, 2.7 +/- 1.14 pmol/ml and 8.16 +/- 6.4 ng/ml), respectively. Both total serum alkaline phosphatase and corrected calcium concentrations rose following vitamin D treatment in the at-risk subjects by 11.1 +/- 8.22 (from 44 to 55 IU/l) and 0.15 +/- 0.18, (2.43 to 2.57 mmol/l), respectively (p=0.004). Abnormal glucose tolerance was unchanged by vitamin D treatment. The value of early and sustained repletion with vitamin D in diabetes prophylaxis should be examined in communities where vitamin D depletion is common.
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PMID:Glucose intolerance and impairment of insulin secretion in relation to vitamin D deficiency in east London Asians. 869 Jan 78

The sera from 158 healthy Thai volunteers (77 males and 81 females), aged 20-80 years, were studied. The vitamin D status, parathyroid gland activity and the magnitude of bone turnover were assessed by measurement of serum 25-hydroxycholecalciferol (25-OH-D), intact parathyroid hormone (N-tact-PTH), osteocalcin and alkaline phosphatase. The mean serum 25-OH-D, N-tact-PTH, osteocalcin and alkaline phosphatase concentrations in men were 67.4 +/- 31.6 (S.D.) [Range (R): 20.6-147.1 ng/ml], 23.3 +/- 10.3 (R: 5.6-56.6 pg/ml) 3.4 +/- 1.5 (R: 1.2-10.5 ng/ml), and 19.9 +/- 6.6 (R: 7.5-35.7 IU/L), respectively, and the mean levels in women were 42.4 +/- 23.9 (R: 13.8-127.8 ng/ml), 26.1 +/- 11.3 (R: 10.5-68.7 pg/ml), 3.7 +/- 2.1 (R: 0.5-11.5 ng/ml), and 19.5 +/- 6.0 (R: 9.1-41.5 IU/L), respectively. There is no evidence of vitamin D deficiency in ambulatory elderly Thais. Serum N-tact PTH increased with advancing age in both men and women whereas increasing serum osteocalcin and alkaline phosphatase with age were observed only in women. In addition, serum alkaline phosphatase correlated to serum osteocalcin only in women suggesting an increase in bone turnover after menopause. These basic data would be useful for the study of metabolic bone diseases in Thai population.
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PMID:Serum vitamin D, parathyroid hormone and biochemical markers of bone turnover in normal Thai subjects. 885 32

: There is a decline in serum 25 hydroxyvitamin D (25OHD), 1,25 dihydroxyvitamin D (1,25(OH)2D), and calcium absorption with advancing age, which may lead to secondary hyperparathyroidism and bone loss. Studies show a relationship between serum 25OHD and bone density in older men and women, with an inverse correlation between bone density and parathyroid hormone (PTH). Vitamin D supplementation in this age group improves calcium absorption, suppresses PTH, and decreases bone loss. Vitamin D many also reduce the incidence of hip and other nonvertebral fractures, particularly in the frail elderly who are likely to have vitamin D deficiency. Patients with established vertebral osteoporosis have lower calcium absorption than age-matched control subjects, possibly due to reduced serum 1,25(OH)2D or to relative resistance to the action of vitamin D on the bowel. Malabsorption of calcium in women with vertebral crush fractures does not usually respond to treatment with physiological doses of vitamin D, but can be corrected by pharmacological doses of vitamin D or by low doses of calcitriol or alfacalcidol. In a recent randomized, controlled study in 46 elderly women with radiological evidence of vertebral osteoporosis, alfacalcidol 0.25 micro;g twice daily improved calcium absorption, decreased serum PTH, and reduced alkaline phosphatase, whereas vitamin D2 500-1000 IU daily had no effect over the 6-month study period. Studies of the effect of the vitamin D metabolites in the management of elderly women with established vertebral osteoporosis have yielded conflicting results, but suggest that alfacalcidol and calcitriol may decrease spinal bone loss and reduce the incidence of vertebral fractures. Although vitamin D supplementation decreases bone loss and fracture risk in the frail elderly, vitamin D metabolites may prove more useful in the treatment of elderly women with vertebral osteoporosis.
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PMID:Is there a differential response to alfacalcidol and vitamin D in the treatment of osteoporosis? 903 Apr 91

To determine the biological criteria for neonatal vitamin D deficiency, serum 25-hydroxyvitamin D (calcidiol), parathyroid hormone (PTH), calcium, phosphates, and alkaline phosphatase (ALP) activity were measured during the winter-spring period in 80 healthy neonates and their mothers 3-6 d after delivery. A longitudinal 3-mo survey of the serum biology of 52 of these neonates consuming formula was also performed to test the influence of their neonatal vitamin D status on the effects of two oral ergocalciferol supplements (500 and 1000 IU or 12.5 and 25 micrograms/d). At birth, 63.7% of the infants had calcidiol concentrations < or = 30 nmol/L. Most of them had no other biological sign evocative of vitamin D deficiency, but 14 neonates had low calcidiol concentrations and serum PTH concentrations > 60 ng/L, the upper limit of the adult normal range. They also had a significantly lower mean serum calcium concentration than did neonates with calcidiol concentrations > 30 nmol/L. On the basis of the association of low calcidiol concentrations (< or = 30 nmol/L) and high PTH concentrations (> 60 ng/L) as criteria for vitamin D deficiency, 24% of the neonates born to unsupplemented mothers were found to be vitamin D-deficient. Neonatal vitamin D status influenced the response of the infants to vitamin D supplements. Neonates with no sign of vitamin D deficiency showed similar changes in their serum calcidiol, calcium, phosphate, and PTH concentrations and ALP activity and no toxic effect (hypercalcemia or highly elevated calcidiol concentration) was observed whatever their vitamin D intake. In contrast, neonates with subclinical vitamin D deficiency had normalized serum PTH within 1 mo only when they were given 1000 IU ergocalciferol (25 micrograms)/d in addition to their formula.
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PMID:Subclinical vitamin D deficiency in neonates: definition and response to vitamin D supplements. 906 28

The present study was designed to investigate whether enhanced bone formation due to intermittent PTH administration is dependent on vitamin D metabolites. Forty-eight female Sprague-Dawley rats were randomized into four groups: 1) vitamin D-sufficient, saline-injected (+D Sal); 2) vitamin D-sufficient, human (h) PTH-(1-38)-treated (+D PTH); 3) vitamin D-deficient, saline-injected (-D Sal); and 4) vitamin D-deficient, hPTH-(1-38)-treated (-D PTH) animals. The -D diet contained 2% calcium (Ca), 1.25% phosphorus (P), and 20% lactose to maintain normocalcemia and normophosphatemia despite vitamin D deficiency. The +D diet contained 0.8% Ca, 0.5% P, 20% lactose, and 1000 IU/kg vitamin D. After 45 days of either diet, the rats were injected with 50 microg/kg BW PTH or saline, s.c., daily for 2 weeks. Serum Ca, Mg, P, albumin, and creatinine were similar in all groups. PTH administration decreased endogenous PTH concentrations in the -D PTH compared with those in the - D Sal group. Serum alkaline phosphatase activity, bone mass measurements, dual energy x-ray absortiometric analysis of mineral density, and mechanical testing values in vertebrae and femora of the -D Sal animals did not significantly differ from those in +D Sal animals. Moreover, in both diet groups, PTH improved bone biochemical activity (as assessed by serum alkaline phosphatase), bone mass, mineral density, and biomechanical properties. These results indicate that mineral supply, more than vitamin D itself, may be important for normal bone mineralization and to enable PTH to enhance bone formation. A balance study performed during the last 3 days of the experiment revealed that PTH increased apparent intestinal magnesium absorption in the +D group only. Ca and P retention, however, were augmented in both diet groups after PTH treatment. In conclusion, in normocalcemic and normophosphatemic -D rats, PTH treatment reduced the increased endogenous hormone concentration and improved Ca and P retention. Furthermore, PTH may have a vitamin D-dependent influence on intestinal magnesium absorption. Finally, short term PTH treatment is anabolic in bone of vitamin D-deficient rats when adequate mineral amounts are provided in the diet.
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PMID:Parathyroid hormone increases bone formation and improves mineral balance in vitamin D-deficient female rats. 916 35

Rickets of prematurity is not uncommon in neonatal intensive care units. Nutritional rickets in childhood is usually caused by vitamin D deficiency, but the rickets of prematurity is mainly attributable to calcium and phosphorus deficiencies. We present a premature infant with sequelae of necrotizing enterocolitis who needed prolonged administration of total parenteral nutrition (TPN), and who sustained ricketic fracture. After high calcium-fortified TPN supplementation the fracture healed well, and serum alkaline phosphatase dropped. This finding shows (1) serum calcium and phosphorus levels are of predictive value regarding rickets, (2) regular follow-ups of alkaline phosphatase levels combined with radiography in high-risk groups of premature infants are good tools for monitoring rickets, and (3) prolonged TPN administration needs to contain higher calcium and phosphorus concentrations in prematurity than in childhood.
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PMID:Rickets of premature infants induced by calcium deficiency. A case report. 926 Mar 76

We describe a 13 year-old Ethiopian girl with vitamin D deficiency rickets. Hypercalcemia, increased serum alkaline phosphatase and PTH levels, together with low serum levels of 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D suggested the co-existence of primary hyperparathyroidism. The surgical removal of a parathyroid adenoma led to bone healing and normalization of blood chemistry. We conclude that vitamin D deficiency masked the hyperparathyroidism and hypercalcemia, while excess PTH secretion delayed the cure of rickets until successful parathyroidectomy had been carried out.
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PMID:Recovery from metabolic bone disease in a girl with vitamin D deficiency rickets associated with primary hyperparathyroidism. 936 60

Biochemical markers of bone turnover have been shown to provide valuable information for the diagnosis and monitoring of metabolic bone disease. However, these dynamic indexes are influenced by a number of factors that need to be clearly identified to improve their clinical usefulness. To evaluate the contributions of anthropometric, life style, and environmental variables on bone turnover, biochemical markers of bone metabolism were determined in a population-based sample of 580 adults, aged 50-81 yr (297 men and 283 women). Subjects were recruited during 14 consecutive months within the framework of the European Vertebral Osteoporosis Study. Serum total and bone-specific alkaline phosphatase (S-BAP), serum C-terminal propeptide of type I collagen, and serum osteocalcin (S-OC) were measured as bone formation markers. Urinary total pyridinoline and deoxypyridinoline were included as bone resorption indexes. In females, serum levels of 25-hydroxyvitamin D3 were significantly higher (P < 0.01) in summer (May-September) than in winter (October-April), whereas no significant differences were found in males. In both sexes, no seasonal changes were seen in serum PTH. In males, serum total alkaline phosphatase (P < 0.01), S-BAP (P < 0.001), and S-OC (P < 0.05) were significantly higher in winter than in summer. During the same period, females had higher values of S-BAP (P < 0.05), S-OC (P < 0.01), and urinary pyridinoline and deoxypyridinoline (P < 0.001, respectively). Univariate analyses of the effects of life style habits on markers of bone metabolism revealed that in females, regular alcohol consumption and current smoking led to a suppression of markers of bone turnover, whereas in males, only alcohol intake was associated with such changes. In contrast, physical activity was associated with higher levels of bone formation markers and reduced levels of bone resorption indexes in both sexes. As shown by multivariate regression analyses, seasonal variations accounted for more of the variability in most biomarkers (up to 12%) than any of the other anthropometric or life style factors except age. This effect may be attributed to subclinical vitamin D deficiency during the winter period, which is common in countries of the northern hemisphere. We conclude that seasonal variation contributes significantly to the biological variability of bone turnover and needs consideration when interpreting the results of bone marker measurements.
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PMID:Seasonal variation of biochemical indexes of bone turnover: results of a population-based study. 943 18

Secondary hyperparathyroidism is a common feature of chronic renal failure and vitamin D deficiency plays an important role in the development of this abnormality. Several therapeutical calcitriol schedules have been used in treating uremic hyperparathyroidism but recently oral boluses have been proposed as more effective. In this study we compare the efficacy of three different oral calcitriol regimens in suppressing iPTH secretion in predialytic chronic renal failure. Sixteen (16) patients (mean age 51 +/- 16 years; creatinine clearance 22.9 +/- 9.8 ml; range 8-32 ml/min) were treated in a cross-over randomized design with oral daily calcitriol 0.5 micrograms/die (Treatment A), three oral boluses of 2 micrograms of calcitriol a week (Treatment B) and a single oral bolus of 2 micrograms of calcitriol a week (Treatment C). All treatment periods lasted three months and were followed by a wash-out period of one month. Serum iPTH (Allegro Nichols), 1-25 vitamin D (IRMA-MAB), total and ionized calcium (Nova 8 Pabish), serum phosphate, alkaline phosphatase and creatinine clearance were measured every two weeks. Serum iPTH was also determined in a control group of fifteen (15) patients (mean age 47 +/- 12 years, creatinine clearances of 21 +/-12 ml/min) observed for three months without calcitriol treatment. Daily oral intake of 0.5 micrograms of calcitriol prevents an increase of iPTH without causing hypercalcemia, but only oral boluses (B and C) decreased iPTH: from 270 +/- 169 pg/ml to 135 +/- 76 pg/ml (p < 0.01; B) and to 165 +/- 121 pg/ml (p < 0.05; C). Serum iPTH increased from 293 +/- 121 to 323 +/- 129 pg/ml (p = n.s.). No significant differences in renal function were observed during the different study periods. Our results confirm the good efficacy of multiple calcitriol oral boluses but also suggest for the first time a single weekly bolus as a reliable approach to the treatment of secondary hyperparathyroidism in pre-dialytic renal failure.
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PMID:Calcitriol oral therapy for the prevention of secondary hyperparathyroidism in patients with predialytic renal failure. 958 56

The assessment of bone quality by quantitative ultrasound (QUS), a transportable and relatively cheap method, shows some correlations with bone mineral density (BMD) as measured by dual-energy X-ray absorptiometry (DXA) and with fracture risk. To examine its correlation with bone metabolism in a population of institutionalized elderly people known to be at high risk for vitamin D deficiency and secondary hyperparathyroidism, QUS of the calcaneus and biochemical parameters were measured in 264 women aged 85 +/- 7 (SD) years and in 103 men aged 81 +/- 8 years living in 19 nursing homes. Vitamin D deficiency was frequent in this population: 41.9% of the women and 31.4% of the men had a serum 25-hydroxyvitamin (25OHD) level below the 2.5th percentile level of 3276 normal Swiss adults (6.2 micrograms/l or 15.5 mmol/l). Hyperparathyroidism was less frequent: serum parathyroid hormone (PTH) levels were above the 97.5th percentile level of normal adults (70 pg/l) in 18.9% of women and 9.8% of men. In women, QUS data correlated significantly with age (r = -0.297), body mass index (BMI) (r = 0.403), calcium (r = 0.220), PTH (r = -0.296), 25OHD (r = 0.298) and alkaline phosphatase (AP) (r = -0.170) for broadband ultrasound attenuation (BUA), and with age (r = -0.195), BMI (r = 0.208), PTH (r = -0.174), 25OHD (r = 0.140) and AP (r = -0.130) for speed of sound (SOS). In men, ultrasound data correlated with BMI (r = 0.326), calcium (r = 0.199), 25OHD (r = 0.258) and AP (r = -0.311) for BUA, and with AP (r = -0.196) for SOS. In women, but not in men because of their smaller number, a multivariate analysis was performed to examine relationships between age, BMI, biochemical markers and QUS. Age, BMI, PTH and phosphate explained 30% of the variance of BUA and 10% for SOS. In conclusion, QUS of bone evaluates characteristics of bone that are influenced, at least partially, by age, BMI and the secondary hyperparathyroidism due to vitamin D deficiency.
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PMID:Influence of anthropometric parameters and biochemical markers of bone metabolism on quantitative ultrasound of bone in the institutionalized elderly. 966 33


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