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)

To define the potential role of subclinical vitamin D deficiency in postmenopausal bone loss, we analyzed the levels of circulating 25-hydroxyvitamin D (25OHD) in 539 midwestern caucasian women screened for osteoporosis. Low 25OHD (less than 38 nmol/L) was found in 49 subjects (aged 52-77 yr). Women with low 25OHD had a reduced vertebral bone density (VBD), assessed by quantitative computed tomography, compared to age-matched controls (P less than 0.001). They also had significantly lower levels of serum calcium and phosphate, lower urinary calcium, higher serum alkaline phosphatase, and, in most cases, increased immunoreactive PTH (iPTH) concentrations, suggesting secondary hyperparathyroidism. Furthermore, only in the low 25OHD group did VBD correlate directly with 25OHD (r = 0.41; P less than 0.01), and inversely with iPTH (r = -0.47; P less than 0.01). Multivariate analyses revealed that iPTH was the major determinant of the observed decrease in VBD. Seasonal variations of serum 25OHD were noted only in the control population; in this group the 25OHD levels also correlated with sunlight exposure (r = 0.48; P less than 0.01), as assessed by an outdoor score. Thus, vitamin D deficiency develops when both the endogenous and exogenous sources are insufficient and contributes to a reduced bone mass in elderly women.
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PMID:Subclinical vitamin D deficiency in postmenopausal women with low vertebral bone mass. 199 17

Several parameters of phosphocalcic metabolism were evaluated in 21 patients with active pulmonary tuberculosis. The serum levels of total calcium, ionic calcium, phosphorus, albumin, magnesium and alkaline phosphatase, and calciuria and calcium/creatinine ratio in 24-hour urine were normal and not change during therapy. The patients with tuberculosis showed a significant reduction in the 250HD concentrations (8.8 +/- 5.2 ng/ml vs 19.2 +/- 10.7 ng/ml; p = 0.002), 1.25(OH)2D (25 +/- 8 pg/ml vs 34 +/- 9 pg/ml; p = 0.002) and parathyroid hormone (intact molecule) (1.9 +/- 0.9 pmol/l vs 5.9 +/- 2.0 pmol/l; p = 0.0001). By contrast, the levels of calcitonin (65 +/- 30 pg/ml vs 36 +/- 17 pg/ml; p = 0.001) and tartrate-resistant acid phosphatase (17.3 +/- 2.3 U/l vs 11.8 +/- 1.8 U/l; p = 0.0001) were increased. There also was a mild increase of vitamin D carrier protein (532 +/- 109 mg/l vs 480 +/- 37 mg/l; p = 0.04). These data are consistent with a partial inhibition of parathyroid hormone, associated with vitamin D deficiency. The inhibition of the axis of parathyroid hormone--1.125(OH)2D resulting from calcium release from the bone is advanced as an explanation. This release might be due to the action on the bone of cytokines produced within the inflammatory process itself. The reduction in 250HD could presumably be related with the lower exposure to sun, which is common in sick persons.
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PMID:[Phosphocalcium metabolism disorders in patients with active pulmonary tuberculosis]. 194 83

Congenital erythropoietic porphyria (CEP) is a rare disorder of heme biosynthesis that results in the production of large quantities of photoactive porphyrins. The clinical syndrome is dominated by extreme photosensitivity with mutilation of light exposed extremities and hemolytic anemia. Bone disease has been occasionally noted, but is not well characterised. We describe a man with CEP who developed bone pain and spinal crush fractures at the age of 22. Skeletal radiographs revealed features typical of other severe hemolytic anemias, but in addition there was loss of the terminal phalanges of the hand as a result of photomutilation. Spinal bone density (assessed by DPA) was reduced and at the hip bone density was at the lower limit of normal. The metacarpal cortical bone density was 2.9 standard deviations below normal. Biochemical and histological studies accelerated bone turnover. Although the serum 250H vitamin D concentration was very low (because of light avoidance) there was no evidence that the bone disease was a consequence of this. Treatment for one year with clodronate and a high transfusion regime was associated with small reductions in serum alkaline phosphatase and urine hydroxyproline excretion, but there was no improvement in bone mineral density. We conclude that CEP has a distinctive osteodystrophy comprising osteolysis of light-exposed extremities and a high turnover type of osteoporosis. Privational vitamin D deficiency may also occur. The effect upon bone of the new therapies for CEP should be considered.
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PMID:The osteodystrophy of congenital erythropoietic porphyria. 206 45

To demonstrate an as yet merely postulated generalized osteopathy in psoriatics, the serum calcium level, the alkaline phosphatase in the serum and the urinary excretion of hydroxyproline were evaluated in 24 patients with Ps and 24 patients with PA. Moreover, the bone bioptates from 25 patients with PA and 10 patients with Ps were examined histologically and measured morphometrically. The investigations provide evidence for the existence of a generalized "latent" osteopathy in terms of an elevated bone turnover rate without loss of bone volume (high turnover remodelling) in both patients with PA as well as those with Ps without arthritis. As a pathogenetically essential factor shared by dermatosis and "osteopathy", latent vitamin D deficiency and/or D hormone resistance is discussed.
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PMID:Studies on psoriatic osteopathy. 206

43 infants taking the same dosage of vitamin D and calcium were investigated. The results showed that vitamin D deficiency rickets (VDR) were still present in some infants when vitamin D was sufficient, because of deficiency of 1,25-dihydroxyvitamin D (1,25-(OH)2D3). Serum calcium, phosphorus, alkaline phosphatase, triiodothyronine (T3), thyroxine (T4), calcitonin (CT), immunoreactive parathyroid hormone (iPTH), and 25-hydroxyvitamin D (25 OHD3) concentrations were compared among infants with normal, VDR of the early and recovering stages. The decompensation of physiological hypocalcemia in infants is probably the real cause of VDR and the decompensation is correlated closely with the development of parathyroid gland. This new concept is raised both at home and abroad. More practical methods for the treatment and prevention of VDR are suggested.
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PMID:[Decompensation of physiologic hypocalcemia in infants inducing vitamin D deficiency rickets]. 216 95

1. Calcitriol (1,25-dihydroxyvitamin D3) concentrations in plasma of humans and pigs with pseudo-vitamin D deficiency rickets type I (PVDRI) have been reported to be significantly lower than in normal subjects and animals. Sometimes, however, calcitriol concentrations are relatively high in these subjects and animals (50-80 pmol/l) and nevertheless clinical symptoms of rickets develop. We have studied whether or not the development of rachitic lesions in piglets with PVDRI is due to altered binding properties of the intestinal calcitriol receptor in addition to the defective renal production of calcitriol. PVDRI piglets with clinical and biochemical symptoms of rickets (hypocalcaemia, increased activity of alkaline phosphatase) and with calcitriol concentrations in plasma of 83.7 +/- 4.2 pmol/l (n = 7) were used. They were compared with unaffected piglets with normal calcitriol concentrations (178.0 +/- 17.7 pmol/l, n = 9). 2. The equilibrium dissociation constant (Kd) of the receptor in the PVDRI piglets (0.31 +/- 0.05 nmol/l) and in control piglets (0.33 +/- 0.05 nmol/l) and the maximum binding capacity (Bmax.) (674 +/- 103 and 719 +/- 122 fmol/mg of protein, respectively) were not different (n = 9). 3. The association rate constant (kass) at 4 degrees C [0.15 x 10(7) and 0.24 x 10(7) (mol/l)-1 min-1] and the dissociation rate constant (kdiss) (0.40 x 10(-3) and 0.48 x 10(-3) min-1; half-life of dissociation = 24.1 and 28.9 h, respectively) were also not different between diseased and control piglets.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies of the porcine intestinal calcitriol receptor in pseudo-vitamin D deficiency rickets type I. 217 64

Vitamin D deficiency leads to secondary hyperparathyroidism initially and then to mild osteomalacia, both of which conditions may be aymptomatic and may predispose to bone fracture. To assess the importance of vitamin D deficiency in predisposing to fractured neck of femur, we studied the vitamin D status, dietary intake and socio-economic characteristics in 69 patients with fractured neck of femur (group A), 28 normal subjects with age above 60 (group B), and 101 normal volunteers (group C). Patients with fractured neck of femor had significantly lower levels of serum 25-hydroxy-cholecalciferol compared with subjects of groups B and C. There is no statistically significant difference in other biochemical parameters, including calcium, phosphate, and alkaline phosphatase. Patients with fractured neck of femur and with 25-hydroxycholecalciferol below 20 ng/mL were characterized by a home-bound and/or institutionalized life-style, smaller living place, and limited access to open space. To conclude, hypovitaminosis D is a common problem among elderly patients with fractured neck of femur in Hong Kong. The fact that such vitamin D deficiency is associated with muscle weakness may contribute to falls, and thus indirectly account for an increased rate of hip fractures over the normal control.
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PMID:Vitamin D status among patients with fractured neck of femur in Hong Kong. 225 13

The histological features of thalassemic bone are imperfectly known, and the roles of bone marrow hyperactivity, iron overload or vitamin D deficiency in the pathogenesis of the disease are not clearly identified. In this study we examined iliac crest biopsies from 17 transfusion-dependent children with homozygous beta-thalassemia and severe radiological skeletal thalassemic changes, including widening of medullary spaces and osteoporosis. Rachitic lesions were not observed. Serum ferritin concentrations were increased in all but one subject. Iron deposits were histochemically detected in bone marrow, at the marrow-bone interface, along cement lines and mineralizing perimeters. Minor changes were present in trabecular bone, and osteomalacia was absent. By contrast, cortical bone exhibited severe changes including fissures and focal mineralization defects. Plasma 25-hydroxyvitamin D (25(OH)D) concentrations measured during the winter (December-May, 6.5 +/- 4.9 ng/ml, mean +/- SD, n = 6) and during the summer (June-November, 13.8 +/- 8.4 ng/ml, n = 9) did not differ from those of age-matched children living in the same country. Seven patients had moderate hypocalcemia but no biological signs suggestive of vitamin D deficiency: all had normal alkaline phosphatase activity, normal or slightly elevated plasma phosphate, only two had low plasma 25(OH)D concentrations and two others supranormal values of plasma immunoreactive parathyroid hormone. These results show that iron overload and vitamin D deficiency do not seem to play an important role in the pathogenesis of thalassemic bone disease, which is characterized by cortical lesions probably related to marrow hyperactivity.
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PMID:Bone disease in children with homozygous beta-thalassemia. 230 56

It is not known if the effects of vitamin D deficiency on chick bone are due to direct actions of the vitamin or if they are secondary to other changes, such as hypocalcemia. Day-old cockerels were fed either a rachitogenic diet containing no Ca (-D-Ca), 1.4% Ca (-D), or 3% Ca (-DHiCa) and given corn oil (-D groups) or vitamin D3 in corn oil (+D and +D-Ca) p.o. for up to 21 days. Radii were harvested and incubated for 6-8 h in a defined medium. Medium samples were taken every 2 h and analysed for Ca, Pi and lactate. Some bones were incubated in a respirometer to measure O2 consumption. Compared to +D, -D birds showed evidence of D deficiency by decreased plasma Ca concentration (35%), bone and body weight (43%) and Ca release from bone (70%) and by histological changes in bone characteristic of rickets. Increases were seen in total and bone alkaline phosphatase activity in plasma (270 and 706%, respectively), Pi release (23%), O2 consumption (23%) and lactate production (52%) by the -D radii. The marked hypocalcemia seen in the -D chicks did not occur in -DHiCa birds. Nevertheless, bone and body weights were decreased in this group and bone lactate production, O2 consumption and total and bone alkaline phosphatase in plasma were increased. Rachitic bone lesions were only partially corrected by the high-Ca diet. Release of Ca and Pi from the -DHiCa bone was not different than from +D radii. Comparing +D-Ca and -D-Ca groups with +D chicks, both were hypocalcemic with decreased bone weight, body weight and bone Ca release, while showing elevated lactate production and Pi release. The only difference between the +D-Ca and -D-Ca groups was a 50% decrease in Ca release by -D-Ca bone. The results suggest that in chicks: (1) some, but not all, of the effects of vitamin D deficiency on bone can be corrected by normalizing plasma Ca and (2) evaluation of the effects of vitamin D deficiency on bone may require hypocalcemia, since some responses are masked by normocalcemia.
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PMID:Interrelationships of vitamin D, bone metabolism and blood calcium concentration in the chick. 253 68

The serum concentration of 25-hydroxyvitamin D level and plasma albumin-adjusted calcium, phosphate, and alkaline phosphatase levels were studied in 200 patients with hip fracture (age range 49-93 years) and 427 elderly subjects living in the community (age range 60-90 years). The mean serum 25-hydroxyvitamin D levels in controls were higher than in temperate countries, but the 25-hydroxyvitamin D concentration was significantly lower in the patients than the controls for all sex and age groups. There was little difference in albumin-adjusted calcium and alkaline phosphatase levels, but the phosphate level was higher in the patients than in the controls. None of the patients with a low 25-hydroxyvitamin D level had a blood picture suggestive of osteopathy resulting from vitamin D deficiency or frank osteomalacia. Hip fracture patients with a low 25-hydroxyvitamin D level were much less ambulant and went outdoors much less frequently than hip fracture patients with a normal vitamin D level. A low vitamin D level was a risk factor for hip fracture in Hong Kong Chinese, and may be prevented by frequent outdoor exposure.
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PMID:Plasma 25-hydroxyvitamin D concentration in patients with hip fracture in Hong Kong. 258 33


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