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)

Studies were conducted in a patient with idiopathic hypophosphatemic osteomalacia to delineate the roles of parathyroid hormone (PTH), vitamin D and renal tubular function. A 43-year-old woman presented with progressive skeletal pains resulting in severe incapacity. Workup revealed: hypophosphatemia with a low tubular maximal phosphate reabsorption per glomerular filtrate (TmP/GFR) of 1.05 mg/dl, normocalcemia, hypocalciuria, elevated alkaline phosphatase and glycinuria. PTH and urinary cyclic AMP (UcAMP) were normal, while calcitriol was low. Renal tubular acidosis or other transport defects were not present and no tumor was found. Biopsy was diagnostic for osteomalacia, and the patient responded to 1-alpha OHD3 and phosphate therapy. Hyperparathyroidism was ruled out by 1) normocalcemia persisting after 1-alpha OHD3 and calcium loading and 2) normal PTH and UcAMP challenged by phosphate supplements. Combined calcium and 1-alpha OHD3 administration resulted in hypercalciuria, decreased UcAMP and increased, but not corrected, TmP/GFR. These findings suggest that the osteomalacia was due to hypophosphatemia caused by a renal leak. PTH is only contributory to the phosphaturia. Low calcitriol level contributes to the osteomalacia directly and indirectly through impaired mineral absorption and, therefore, is also responsible for the hypocalciuria.
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PMID:Metabolic studies in a patient with idiopathic hypophosphatemic osteomalacia. 334 50

This study was carried out to evaluate the metabolic consequences of osteosclerotic skeletal metastases of prostatic origin in a homogeneous group of patients. We found significantly increased mean values of serum alkaline phosphatase activity and significantly reduced mean values of serum phosphate, 24-h urinary calcium, fasting calcium excretion and TmP/GFR in cancer patients with respect to age-matched controls. Mean serum immunoreactive parathyroid hormone (iPTH) levels were raised, with two patients showing increased values of the hormone above our normal limits. Our findings indicate that mild secondary hyperparathyroidism is a feature of these patients. However, it cannot be excluded that both the reduced serum phosphate and TmP/GFR values may be related, at least in some cases, to the effects of the tumour itself on tubular reabsorption of phosphate.
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PMID:Biochemical picture accompanying sclerotic bone metastases of prostatic origin. 342 18

The gamma-carboxy glutamic acid (Gla)-containing protein of mammalian bone (BGP, also called osteocalcin) is a 49 amino acid polypeptide containing two to three residues of gamma-carboxyglutamic acid. BGP is synthesized by osteoblastlike cells, and plasma BGP in laboratory animals is derived principally from recently synthesized BGP. These data, taken together with observations that plasma BGP levels are elevated in patients with disorders of high bone turnover, suggest that plasma BGP is a marker of osteoblast activity. Since low bone formation rates may play an important role in the loss of bone mass with age, we have examined the determinants of plasma BGP levels in aging subjects, using a region-specific radioimmunoassay for human BGP based on the synthetic C-terminal peptide hBGP37-49. In 147 carefully screened healthy subjects, aged 23-91, BGP did not change with age, whereas alkaline phosphatase (AP) showed a significant positive correlation (r = 0.30, P less than 0.001). Creatinine clearance (GFR) declined by 0.9 ml/min/yr and correlated with both BGP (r = -0.21, P less than 0.001) and AP (r = -0.21, P less than 0.001). However, correlation of AP with age persisted after controlling for GFR. BGP was not correlated with serum PTH, urine Ca/GFR, or urine cAMP/GFR. In 48 patients with known parenchymal renal disease studied for comparison, plasma BGP was increased at a serum creatinine of greater than or equal to 1.8 mg/dl. Our results indicate that plasma BGP, a specific marker of bone metabolism, is not predictably related to age per se. This result is in contrast to the age-related rise in total AP. Subtle changes in renal function can affect plasma BGP levels.
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PMID:Determinants of bone gamma-carboxyglutamic acid-containing protein in plasma of healthy aging subjects. 387 50

A case of vitamin D resistant hypophosphatemic osteomalacia associated with osteosarcoma of the mandible is presented. The patient complained of lumbar, knee and foot pain and muscle weakness of two years' duration. Serum phosphorous was 1.0-1.6 mg/dl, tubular reabsorption of phosphorus was 47 to 58%, TmPO4/GFR was o.7-1.2 mg/dl. Aminoaciduria was noted. Bone biopsy confirmed the diagnosis of osteomalacia. He partially responded to the treatment with 1 alpha()H) D3 and sodium phosphate. After removal of sarcoma of the mandible, symptoms remitted and pertinent laboratory data became normal except serum alkaline phosphatase for more than one year without treatment. It is suggested that an impaired response of the tubule and bone to active vitamin D3, caused in some way by the osteosarcoma might be one of the causes of osteomalacia in this case.
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PMID:Vitamin D resistant hypophosphatemic osteomalacia associated with osteosarcoma of the mandible: report of a case. 627 44

The ratio of maximum rate of renal tubular reabsorption of phosphate to glomerular filtration rate (TmPO4/GFR) was determined in 546 schoolchildren, aged between 6 and 17.9 years, using the nomogram of Walton and Bijvoet.1 TmPO4/GFR correlated with chronological age in girls and boys and in each remained significantly higher than in adults. TmPO4/GFR in the children correlated neither with fasting serum immunoreactive calcitonin and parathyroid hormone levels nor with the urinary cyclic AMP excretion. The study showed a parallel decrease in TmPO4/GFR, excretion of total hydroxyproline and serum alkaline phosphatase activities after puberty, with a significant relationship of both these indices of bone turnover to TmPO4/GFR values. This indicates that the high renal phosphate threshold of children may be an important factor for bone mineralisation by providing high extracellular inorganic phosphate concentrations during normal growth.
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PMID:Renal threshold phosphate concentration (TmPO4/GFR). 628 Jun 22

The effects of continuous administration of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] on mineral and bone metabolism have been examined in the normal mouse. Four doses (0.05-0.25 micrograms/kg/day) of 1,25(OH)2D3 were infused continuously for 4 weeks in 21-day-old intact animals. Mineral and skeletal changes were evaluated by analytical methods and by histomorphometric analysis of endosteal bone formation and resorption parameters. All doses of 1,25(OH)2D3 increased the fractional osteoclastic surface and the osteoclast number in conjunction with increased hydroxyproline excretion. 1,25(OH)2D3 induced a dose-dependent elevation of the calcification rate, reduction of the mean osteoid seam thickness, and shortening of the mineralization lag time. In addition, there was a dose-related increase in the extent of tetracycline double-labeled osteoid surface and a concurrent rise in the fractional osteoblastic surface associated with elevated serum alkaline phosphatase levels. Increased bone formation appeared to have been balanced by increased bone resorption since the trabecular bone volume remained unchanged. Except at the highest dose given, serum calcium and phosphate concentrations remained normal in spite of increased bone mobilization and presumably enhanced intestinal absorption of minerals. Urinary cAMP and TmP/GFR remained normal, suggesting that parathormone secretion was not altered. The results show that continuous 1,25(OH)2D3 infusion in the young mouse produces a dose-dependent stimulation of bone mineralization rate in response to increased osteoclastic bone resorption. The data indicate that 1,25(OH)2D3 can regulate bone turnover as well as mineral homeostasis in the young mouse.
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PMID:Continuous infusion of 1,25-dihydroxyvitamin D3 stimulates bone turnover in the normal young mouse. 668 45

Fifty-six consecutive patients with sarcoidosis, 31 subacute and 25 chronic, were investigated for abnormalities of calcium and phosphate metabolism with particular reference to parathyroid function. No abnormality of serum calcium, phosphate, creatinine or alkaline phosphatase was found. Serum levels of 25-OH cholecalciferol were normal and parathyroid hormone levels were normal in all but one patient. Maximum renal tubular reabsorption capacities for calcium and phosphate (TmCa/GFR, TmP/GFR) in relation to glomerular filtration rate in the fasting state, were abnormal in some patients but this did not correlate with any other abnormality in parathyroid function. There was significant hypercalciuria (greater than 10 mmol calcium per 24 hours) in 7.5% of our patients and this is believed to be due to increased calcium flow.
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PMID:Calcium and phosphate metabolism in sarcoidosis with particular reference to parathyroid function. 725 66

Although women lose 30% of their skeletal mass after the menopause, the mechanism of this loss is uncertain. Clearly estrogen deficiency is important but whether this works only through direct effects on the skeleton is uncertain. To examine these mechanisms further we have evaluated calcium-related metabolic factors in 655 healthy women. Fasting blood samples were collected from all subjects who were up to 35 years past the menopause, and fasting urine and 24-h urine samples were collected in 365 women who were up to 25 years past the menopause. In the first 15 years postmenopause, there was a rise in total plasma calcium due to a rise in albumin. Bone resorption (hydroxyproline creatinine ratio), bone formation (alkaline phosphatase), and the urine calcium creatinine ratio all rose at menopause and remained elevated for the next 25 years. There was a transient further rise in bone resorption for the 10 years following menopause. Neither PTH nor the free calcitriol index changed for the first 10 years following menopause. Ten years past the menopause, although total calcitriol rose, the free calcitriol index fell due to a rise in vitamin D binding protein. PTH began to rise at 15 years past menopause. GFR fell gradually over the 25 years following menopause. Thus following menopause there is an increase in bone turnover and increased urine calcium loss independent of any effect of PTH or calcitriol, suggesting a direct effect of estrogen deficiency on bone and kidney.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of menopause and age on calcitropic hormones: a cross-sectional study of 655 healthy women aged 35 to 90. 757 5

Thirty five children with ambulant JCA were studied to assess the biochemical parameters of bone metabolism. The mean age of the study group was 8.8 +/- 4.1 years and the mean duration of active disease 3.8 +/- 1.3 years. According to the onset of the disease the children belonged to the systemic (7), polyarticular (12) and pauciarticular type (16). All the patients were treated with NSAIDs. In addition the polyarticular group received either gold injections or D-penicillamine and the systemic group, steroids for at least 3 months. Two groups of controls were studied. The first one included fifteen children without chronic arthritis or bone disease and the second, four children who were treated with corticosteroids for a variety of reasons. In the group with systemic JCA Se Pi (1.28 +/- 0.29 mmol/l) and renal phosphate reabsorption (TmP/GFR = 1.07 +/- 0.18) were significantly lower than in the control groups (1.50 +/- 0.19; 1.54 +/- 0.25 mmol/l, p < 0.01 and 1.35 +/- 0.18; 1.29 +/- 0.23 mmol/l GF, p < 0.05). Also lower were serum alkaline phosphatase (58 +/- 16.4 versus 83 /- 24.2 and 80 +/- 15.6 IU/l, p < 0.05), osteocalcin (5.5 +/- 4.7 versus 11.0 +/- 4.5 and 10.0 +/- 5.7 ng/ml, p < 0.05), 25OHD (15.6 +/- 4.9 versus 27.3 +/- 6.2 and 20.6 +/- 9.8 ng/ml, p < 0.001) and 1,25(OH)2D (12.1 +/- 6.0 versus 20.9 +/- 11.0 and 27.6 +/- 3.2 pg/ml, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes of mineral metabolism in juvenile chronic arthritis. 791 12

Heparin therapy may cause osteoporosis. The effects of short-term low-dose heparin are not known. We have studied the effects of short-term heparin administration, twice daily 5000 IU s.c., for 10 days on the biochemical parameters of bone turnover in six healthy male volunteers. No effects were observed on the urinary excretion of hydroxyproline and calcium. Serum levels of cross-linked carboxy-terminal telopeptide of type I collagen (ICTP), a new marker of bone resorption, did not change significantly. A slight but significant decrease in serum alkaline phosphatase was observed. TmP/GFR increased significantly during heparin administration. In all volunteers a uniform increase in serum transaminases appeared which completely reversed after discontinuation of heparin administration. We conclude that short-term low-dose heparin administration does not change biochemical parameters of bone resorption, but has a small significant suppressing effect on serum alkaline phosphatase levels. Heparin administration resulted in a significant but transient increase of serum transaminase levels.
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PMID:Effects of short-term low-dose heparin administration on biochemical parameters of bone turnover. 821 35


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