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)

Vitamin D treatment was tried when renal osteodystrophy was first recognized in the early 20th century, using vitamin D2, D3, or dihydrotachysterol. Large doses of vitamin D2 or D3 (150,000-500,000 IU) were prescribed by monitoring serum calcium, phosphate, and alkaline phosphatase. After the discovery of 1,25-dihydroxycholecalciferol, this compound or 1 alpha-hydroxycholecalciferol was applied to the treatment of renal osteodystrophy. In a preclinical study, especially of 1 alpha-hydroxycholecalciferol, nephritogenoside nephritis was the most responsive condition. These active vitamin D preparations are now widely used in patients with chronic renal failure under hemodialysis. Other active vitamin D compounds, such as hexafluoro-1,25-dihydroxycholecalciferol and 22-oxacalcitriol, are also under investigation.
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PMID:History of vitamin D treatment of renal osteodystrophy. 918 58

We hypothesized that fluoride partly acts by changing the levels of circulating calcium-regulating hormones and skeletal growth factors. The effects of oral fluoride on 24 female, Dutch-Belted, young adult rabbits were studied. The rabbits were divided into two study groups, one control and the other receiving about 16 mg fluoride/rabbit/day in their drinking water. After 6 months of fluoride dosing, all rabbits were euthanized and bone and blood samples were taken for analyses. Fluoride treatment increased serum and bone fluoride levels by over an order of magnitude (P < 0.001), but did not affect body weight or the following serum biochemical variables: urea, creatinine, phosphorus, total protein, albumin, bilirubin, SGOT, or total alkaline phosphatase. No skeletal fluorosis or osteomalacia was observed histologically, nor did fluoride affect serum PTH or Vitamin D metabolites (P > 0.4). BAP was increased 37% (P < 0.05) by fluoride; serum TRAP was increased 42% (P < 0.05); serum IGF-1 was increased 40% (P < 0.05). Fluoride increased the vertebral BV/TV by 35% (P < 0.05) and tibial ash weight by 10% (P < 0.05). However, the increases in bone mass and bone formation were not reflected in improved bone strength. Fluoride decreased bone strength by about 19% in the L5 vertebra (P < 0.01) and 25% in the femoral neck (P < 0. 05). X-ray diffraction showed altered mineral crystal thickness in fluoride-treated bones (P < 0.001), and there was a negative association between crystal width and fracture stress of the femur (P < 0.02). In conclusion, fluoride's effects on bone mass and bone turnover were not mediated by PTH. IGF-1 was increased by fluoride and was associated with increased bone turnover, but was not correlated with bone formation markers. High-dose fluoride treatment did not improve, but decreased, bone strength in rabbits, even in the absence of impaired mineralization.
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PMID:Fluoride treatment increased serum IGF-1, bone turnover, and bone mass, but not bone strength, in rabbits. 919 19

Different research methods demonstrated the presence of variable quantities of Vitamin D as well as its metabolites in calcinogenic plants. Most of the experiments indicated that the active component most probably should be the metabolite 1,25 (OH)2D3 linked as a glycoside. By this research it was achieved to evaluate the presence of elements with Vitamin D-like activity in the calcinogenic plants Solanum malacoxylon, Cestrum diurnum, Trisetum flavescens and Nierembergia veitchii by testing different extracts of the above plants by oral application to rachitic chicks within the research model "Strontium added Alimentation". After the oral administration of the extracts, the serum was analysed to determine the level of the elements calcium, phosphorus and alkaline phosphatase. The results gained with chicks demonstrated the presence of substances with Vitamin D-like activity in the 4 plants. Solanum malacoxylon and Cestrum diurnum as well contained substances of hydrosoluble character with elevated activity which was indicated by the significant high levels of calcium and phosphorus combined with a reduced activity of the alkaline phosphatase. This indicated the presence of 1,25 (OH)2D3 in both plants. The hydrosoluble character of the active substance in both plants is most probably explained as a compound of the metabolite 1,25 (OH)2D3, combined as a glycoside in the position O-25 of the molecule. Nierembergia veitchii and Trisetum flavescens contained only minor concentration of elements with hydrosoluble characteristics. The results of the 4 analysed plants were evaluated quantitatively as follows: Solanum malycoxylon--82,800 IU of Vitamin D/kg, Cestrum diurnum--63,200 IU of Vitamin D/kg, Nierembergia veitchii--16,400 IU/kg and Trisetum flavescens 12,000 Vitamin D IU/kg. All concentrations are calcinogenic.
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PMID:[Effects of calcinogenic plants--qualitative and quantitative evaluation]. 949 29

Some studies have suggested that the use of sunscreens to prevent skin cancer may put the population at risk of vitamin D deficiency. We followed 24 sunscreen users and 19 controls over 2 years, including two summers, two winters and a basal period (winter). Vitamin D, parathormone and bone biological markers were evaluated each season. Mean levels of 25-hydroxyvitamin D rose in summer, with the increments being significantly higher for the second year in the control group. Levels decreased in winter in both groups, and were significantly lower in sunscreen users. We did not observe any significant change in parathormone, tartrate resistant phosphatase, total alkaline phosphatase, osteocalcin, urine hydroxyproline or urine calcium. Clinically prescribed sunscreen creams (sun protection factor 15) caused a minor decrease in 25-hydroxyvitamin D levels, which did not induce secondary hyperparathyroidism or an increment in bone biological markers.
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PMID:Clinically prescribed sunscreen (sun protection factor 15) does not decrease serum vitamin D concentration sufficiently either to induce changes in parathyroid function or in metabolic markers. 976 86

Maternal vitamin D deficiency can aggravate development of neonatal hypocalcemia and impair fetal bone growth. Despite abundant sunshine exposure, Arab women have low serum concentrations of 25-hydroxy vitamin D (25-OHD). A study conducted in Al Ain, United Arab Emirates (UAE), compared the vitamin D status of 33 UAE nationals, 25 non-Gulf Arabs (Jordanians, Egyptians, Palestinians, and Lebanese), and 17 Europeans. Serum concentrations of calcium, phosphorus, alkaline phosphatase, and intact parathyroid hormone were not significantly different in these three groups. However, mean serum 25-OHD concentrations were significantly lower among UAE nationals (8.6 ng/ml) and other non-Gulf Arabs (12.6 ng/ml) than in Europeans (64.3 ng/ml) (p 0.0001). The rate of vitamin D insufficiency (5 ng/ml) was 24% among UAE nationals and 12% among non-Gulf Arabs; there were no such cases among Europeans. The ultraviolet ray (UV) exposure score, which weighted sunshine exposure against the magnitude of body coverage with clothing, was significantly higher in European women than in the two Arab groups. There was a positive correlation between total UV exposure score and serum 25-OHD level (r = 0.59425). About 35% of the variation in serum 25-OHD could be explained by the cutaneous skin exposure score. The limited exposure of Arab women's skin to sunlight as a result of their traditional, extensive clothing appears to play an important role in the high frequency of low vitamin D status in this population. Vitamin D supplementation should be considered.
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PMID:Biosocial factors affecting vitamin D status of women of childbearing age in the United Arab Emirates. 981 52

Prevention of secondary hyperparathyroidism (SHPTH) and treatment of the moderate cases by small p.os doses of Vitamin D has not been thoroughly investigated on the long term, while large doses of Vitamin D have been successful in the short term treatment of this entity. We administered calcitriol p.os 0.5-1.0 microgram, according to iPTH levels, after each dialysis session, in 19 patients (group A) for 36 months. They were ten men and nine women, 63 years old (43-81), with iPTH levels > 4N (419 +/- 185 pg/mL). Seven adenomas were found in five of them (group A1). Serum Ca, phosphate (P) and alkaline phosphatase (AP) were measured every 15-30 days. Serum iPTH and aluminum as well as echogram or scanning of the parathyroid glands were checked every 6 months. Ten additional dialysis patients, seven men and three women, 54.5 years old (36-68), non-significantly different to group A in iPTH levels (290 +/- 225 pg/mL) with three adenomas in two of them (group B1) received no calcitriol and served as controls (group B). Calcitriol treatment significantly lowered serum iPTH levels in group A patients (from 419 +/- 185 to 173 +/- 142 pg/mL, p < 0.0001, delta iPTH: -246 +/- 161 pg/mL); iPTH remained stable in group B patients (delta iPTH: +7.9 +/- 116 pg/mL) with an intergroup significant difference at P < 0.0001. All other parameters measured did not show any significant change. No significant correlation of iPTH to Ca, P or AP was found in A. Initial iPTH levels were higher in A1 and B1 patients and decreased by calcitriol in A1 group. Adenomas in A1 patients did not change in number and size in contrast to B1 where new adenomas appeared (5 patients, 10 glands). Small doses of vitamin D lower high iPTH levels and prevent parathyroid gland hyperplasia. Existing hypertrophy is stabilized under calcitriol treatment both morphologically and biologically.
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PMID:Long-term effects of small doses of calcitriol in hemodialysis patients with moderate secondary hyperparathyroidism. 1008 80

A 27-year-old woman with anorexia nervosa since adolescence was referred to our unit for generalized bone pain most severe at the pelvis and an inability to stand. She reported a pelvic fracture diagnosed one year earlier, which had failed to heal. Laboratory tests showed low serum phosphate, normal total serum calcium corrected for serum albumin, and very low urinary calcium excretion. Serum bone alkaline phosphatase and parathyroid hormone levels were elevated, whereas 25-hydroxy-vitamin D was severely decreased. Multiple vertebral and rib fractures were seen on plain radiographs. Radiographic images consistent with osteomalacia were pseudofractures of the left inferior pubic ramus, a bilateral complete fracture of the superior pubic ramus, and a characteristic pseudofracture (Looser zone) in the lateral margin of the right scapula. Vitamin D-deficient osteomalacia with secondary hyperparathyroidism was strongly suspected at this point, but it was decided not to confirm this diagnosis by bone biopsy with histomorphometry and osteoid labeling because of the emotional instability of the patient. Dual-energy X-ray absorptiometry disclosed severe demineralization. After two months on calcium and vitamin D supplements, the bone pain had abated and the patient was able to stand. Serum calcium had increased; serum phosphate, 25-hydroxy-vitamin D, and parathyroid hormone had returned to normal, and the pseudofractures showed evidence of healing. Osteoporosis is a well-known complication of anorexia nervosa. This case shows that osteomalacia can also occur. Vitamin D status should be assessed in patients with long-standing severe anorexia nervosa.
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PMID:Osteomalacia in a patient with severe anorexia nervosa. 1056 80

We examined how cholecalciferol (vitamin D) nutrition affected serum 25-hydroxycholecalciferol (25(OH)D) and 1, 25-dihydroxycholecalciferol (1,25(OH)(2)D). Rats were fed conventional diet (vitamin D, 4.5 IU/g, or 7 nmol/d) or the same diet plus 18 nmol/d of extra vitamin D for 3 wk. The extra vitamin D resulted in greater serum 25(OH)D (51 +/- 3, vs. control of 21 +/- 2 nmol/L), and kidney mRNA for vitamin D receptor [VDR mRNA] (P = 0. 026) and lower serum 1,25(OH)(2)D (72 +/- 16 vs. control of 161 +/- 10 pmol/L, P = 0.001), and parathyroid hormone (PTH) (89 +/- 4 vs. control of 160 +/- 15 ng/L, P = 0.001). Kidney VDR mRNA relative to GAPDH mRNA correlated inversely with serum 1,25(OH)(2)D (r = -0.714, P = 0.006). There were no differences in serum calcium, phosphate, alkaline phosphatase, or weight gain. Experiment 2 compared groups supplemented with 0.2, 2 or 20 nmol/d of vitamin D orally, or 20 nmol/d dermally to see how vitamin D nutrition influenced the response of 1,25(OH)(2)D to changes in diet calcium. Vitamin D did not affect urinary calcium or pyridinoline excretion, serum calcium, phosphate, vitamin D binding protein or alkaline phosphatase. In groups given 20 nmol/d of vitamin D, renal mitochondrial 25(OH)D-1alpha-hydroxylase was lower (P < 0.01) and 25(OH)D-24-hydroxylase was higher (P < 0.05). Higher 25(OH)D concentration was related to proportionally lower 1,25(OH)(2)D at every calcium intake, indicating greater tissue sensitivity to 1, 25(OH)(2)D. We conclude suppression of 1,25(OH)(2)D and PTH, and higher renal VDR mRNA and 24-hydroxylase did not involve higher free 1,25(OH)(2)D concentration or a first pass effect at the gut. Thus, 25(OH)D or a metabolite other than 1,25(OH)(2)D is a physiological, transcriptionally and biochemically active, noncalcemic vitamin D metabolite.
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PMID:Improved cholecalciferol nutrition in rats is noncalcemic, suppresses parathyroid hormone and increases responsiveness to 1, 25-dihydroxycholecalciferol. 1070 88

Vitamin D insufficiency is still a concern in countries where there is no routine food supplementation, such as France. A low vitamin D status is clearly associated with an increased risk of fracture in the elderly, but the long-term consequences of latent vitamin D insufficiency in young people and adults are not known. We fed 26 growing pigs a high calcium diet (1.1%) with a 1000 IU cholecalciferol/kg diet (controls), or without vitamin D (0D) for 4 months. We then analyzed the overall impact of low vitamin D status on osteotropic hormones (calcitriol and immunoreactive parathyroid hormone), plasma markers of bone remodeling (alkaline phosphatase [ALP] activity, carboxyterminal propeptide of type I procollagen [PICP], osteocalcin, hydroxyproline), whole bone parameters (ash content, bending moment), histomorphometry, and the populations of marrow osteoblastic and osteoclastic precursors by ex vivo cultures. The fall in plasma 25-dihydroxyvitamin [25(OH)D] in the 0D pigs indicated severe depletion of their vitamin D stores. However, they remained normocalcemic, were mildly hyperparathyroid after 2 months of vitamin D deprivation, and showed only a slight decrease in plasma calcitriol. The bone mineral content and bending moment of metatarsals decreased and they had increased osteoblastic (+59%, p < 0.05 0D vs. controls) and osteoclastic (+31%, p < 0.1 0D vs. controls) surfaces. This was not paralleled by increased bone turnover, because plasma hydroxyproline and ALP were unchanged and PICP and osteocalcin were decreased. The adherent fraction of bone marrow cells showed a great increase in the number of total stromal colony-forming units (CFU-F; +93%, p < 0.05 0D vs. controls) and in the percent of ALP(+) CFU-F (+58%, p < 0.01 0D vs. controls) in cultures from 0D pigs. More tartrate-resistant acid phosphatase-positive (TRAP(+)) multinucleated cells were generated in cultures of nonadherent marrow cells from 0D pigs, and the area of resorption was 345% greater than in controls. Thus, vitamin D deprivation caused only moderate hormonal changes in growing pigs fed a high-calcium diet, but affected their bone characteristics and greatly enhanced the pool of osteoblasts and osteoclasts by stimulating the commitment of their precursors in bone marrow.
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PMID:In vivo bone metabolism and ex vivo bone marrow osteoprogenitors in vitamin D-deprived pigs. 1077 89

Oncogenic osteomalacia is a rare paraneoplastic syndrome. It is characterized by bone pain, muscle weakness, gait disturbance, fractures and skeletal deformities. Hypophosphatemia, diminished renal phosphate reabsorption, decreased 1,25 dihydroxy Vitamin D and elevated alkaline phosphatase are the biochemical hallmarks of this disorder. Most tumors are of mesenchymal origin. We report the case of a 39-year-old woman with oncogenic osteomalacia caused by osteosarcoma of the right scapula which was unrecognized for several years. She subsequently developed tertiary hyperparathyroidism after treatment with oral phosphate and Vitamin D. This case illustrates that oncogenic osteomalacia may persist for many years before the tumor is discovered. This is because the tumors are frequently very small and are in obscure locations. The uniqueness of this case is the coexistence of hyperparathyroidism and oncogenic osteomalacia. Five other cases have been reported up to date. All patients had received phosphate supplement, ranging from 10 to 14 years prior to their diagnosis. Interestingly, our patient was on the treatment for only 2 years. The proposed mechanism is that exogenous phosphate stimulates parathyroid activity through sequestration of calcium.
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PMID:Development of tertiary hyperparathyroidism after phosphate supplementation in oncogenic osteomalacia. 1085 15


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