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)

Parameters of mineral metabolism were examined in 6 patients with moderately severe anticonvulsant drug-induced osteomalacia. Compared to 15 matched controls, the patients exhibited significantly reduced serum calcium, inorganic phosphate, and 25-hydroxyvitamin D concentration, elevated serum alkaline phosphatase and immunoreactive parathyroid hormone (iPTH) concentration, reduced intestinal 47Ca absorption, reduced urinary calcium and increased urinary hydroxyproline excretion, and reduced forearm bone mass. Intestinal absorption of vitamin D3 was normal. Following 4 months of treatment with vitamin D3 (4000 units/day), serum 25-OHD concentration was increased to 3 times mean normal values and all parameters except serum iPTH, urinary calcium excretion, and forearm bone mass were returned to levels not significantly different from normal. Serum iPTH concentration was reduced by 39% (P less than 0.05); 24-h urinary calcium excretion rose by 98% (P less than 0.001), and forearm bone mass increased by 5.6% (P less than 0.05). It is concluded that moderate-dose vitamin D3 supplementation is effective in normalizing parameters of mineral metabolism in this disorder, despite evidence of resistance to the biologic effects of vitamin D.
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PMID:Anticonvulsant drug-induced osteomalacia: alterations in mineral metabolism and response to vitamin D3 administration. 22 50

Renal bone disease was assessed for an average of 5.5 years in 9 patients on maintenance haemodialysis. The investigative methods included serial biochemical estimations, radiographic skeletal surveys and quantitative bone histology. Repeated bone mineral analyses and neutron activation analyses of a hand were also performed in order to monitor changes in skeletal calcium content. Before treatment, progressive osteodystrophy was demonstrated by all techniques. Following therapy with the vitamin D analogues, all patients noted symptomatic improvement; serum alkaline phosphatase reverted to normal and serum parathyroid hormone concentrations decreased. Radiographically, subperiosteal erosions healed while the histological features of osteomalacia and osteitis fibrosa were abolished. Both bone mineral and neutron activation analyses indicated that progressive skeletal demineralisation had been halted. However, a sustained increase in the overall mineral content of bone was not demonstrated. Thus, vitamin D therapy although improving the biochemical, radiological, and histological features of renal osteodystrophy may not restore bone mass to osteopenic bone.
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PMID:Renal osteopenia - an assessment of long-term therapy with vitamin D analogues. 23 16

The role of metabolic acidosis in the genesis of renal osteomalacia was investigated by studying bone mineralisation and resorption rates with a combined isotope and balance technique in six patients, before and after the administration of alkali. Correction of blood pH was achieved in five cases and was associated with a significant rise in the bone mineralisation rates and a significant positive trend in the calcium balances. It is suggested that acidosis contributes to the pathogenesis of osteomalacia in renal failure by slowing skeletal mineralisation, possibly by inhibiting bone alkaline phosphatase.
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PMID:Effect of correction of metabolic acidosis on bone mineralisation rates in patients with renal osteomalacia. 23 58

The histological and biochemical response of osteomalacia has been studied in four patients with primary biliary cirrhosis, who were treated with oral 25-hydroxyvitamin D3, 50 microgram daily, or intramuscular vitamin D2, 150,000 units once weekly, for five to 12 months. All patients showed complete histological healing of osteomalacia, despite rapidly deteriorating liver function in three. Plasma 25-hydroxyvitamin D concentrations were low in all patients before treatment, but became normal during either vitamin therapy. Serum calcium and phosphate levels, and urinary calcium excretion were not always reliable in predicting the histological response to treatment. Serum alkaline phosphatase activity decreased in all patients during vitamin D therapy. We conclude that both high-dose parenteral vitamin D2 and oral 25-hydroxyvitamin D3 may be effective in healing osteomalacia associated with primary biliary cirrhosis. Measurement of plasma 25-hydroxyvitamin D levels during vitamin D therapy provides useful information about 25-hydroxylation of the parent vitamin and intestinal absorption of orally administered 25-hydroxyvitamin D3.
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PMID:Treatment of osteomalacia associated with primary biliary cirrhosis with parenteral vitamin D2 or oral 25-hydroxyvitamin D3. 31 47

Six long-term hemodialysis patients with progressive skeletal deterioration during long-term pharmacologic vitamin D2 therapy were treated for six to 12 months with oral 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) to determine its therapeutic effectiveness in vitamin D2-unresponsive osteodystrophy. On bone biopsy, three of the patients had severe osteomalacia and three showed predominant osteitis fibrosa. Previous therapies, including phosphate binders and dialysis schedules, were maintained. The three patients with osteomalacia and the two with osteitis fibrosa showed clinical deterioration. There was no significant change in serum calcium, phosphate, alkaline phosphatase, bone densitometry, immunoreactive parathyroid hormone levels or bone histology. Roentgenograms showed multiple new fractures of ribs and femoral necks in the patients with osteomalacia and increased bone resorption in two of three patients with osteitis fibrosa. 1,25-(OH)2D3 dosage had to be decreased in all patients because of hypercalcemia with a mean tolerated dose of 0.22 microgram/day. In these patients, 1,25-(OH)2D3 was not effective therapy for progressive osteodystrophy unresponsive to pharmacologic vitamin D2.
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PMID:Experience with 1,25-dihydroxycholecalciferol therapy in undergoing hemodialysis patients with progressive vitamin D2-treated osteodystrophy. 38 92

Long-term anticonvulsant drug therapy may lead to abnormalities of calcium metabolism resulting in osteomalacia. The prevalence and severity of altered calcium metabolism was studied in an adult outpatient population of persons with epilepsy receiving anticonvulsant therapy for a minimum of 2 years. Assessment of calcium metabolism was based on serum concentrations of calcium, phosphorus, alkaline phosphatase and 25-hydroxycholecalciferol and of plasma parathyroid hormone, intestinal absorption of isotopic calcium and skeletal bone mineral mass as determined by in vivo neutron activation or x-ray photodensitometry.Thirty-nine patients who had been receiving anticonvulsant therapy for an average of 20 years were studied; none had clinical evidence of metabolic bone disease. Decreased serum calcium concentration was noted in 10%, decreased serum phosphorus concentration in 10% and elevated serum alkaline phosphatase concentration in 44%. The mean serum 25-hydroxycholecalciferol concentration was significantly lower (P < 0.001) than in a control group (11.6 v. 19.6 mg/mL). None of 18 patients studied had an increased plasma concentration of parathyroid hormone, and only 1 of 17 patients had decreased intestinal absorption of isotopic calcium. Bone mineral mass was decreased in 44% of 32 patients studied.It was concluded that long-term treatment with anticonvulsant drugs leads to mild abnormalities of calcium metabolism and decreased bone mineral mass in a substantial percentage of adult outpatients with epilepsy. These abnormalities probably predispose the patients to the development of clinically significant metabolic bone disease.
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PMID:Calcium metabolism in adult outpatients with epilepsy receiving long-term anticonvulsant therapy. 41 65

Serum calcium, inorganic phosphate and alkaline phosphatase, tubular reabsorption of phosphate (TRP) estimation and radiological examination of the skeleton were conducted in 40 cases (18-50 years of age) on anticonvulsant therapy and 20 controls. The epileptic group showed a statistically significant rise in serum alkaline phosphatase and a fall in TRP. In none of the cases, however, was there clinical or radiological evidence of osteomalacia. Biochemical abnormalities were seen mainly in the youngest individuals. It seems that the critical factor for the development of anticonvulsant osteomalacia is the lack of dietary vitamin D/solar exposure or increased body requirement of the vitamin.
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PMID:Occult anticonvulsant osteomalacia in North India. 42 84

Four patients are reported who had Albright's syndrome, hypophosphatemia, and inappropriately low renal tubular reabsorption of phosphate. Three of the patients had radiologic evidence of rickets or osteomalacia, and the fourth had a bone biospy, which showed microradiographic evidence of a previous mineralization defect. Serum parathormone values were elevated before treatment in two patients. Intravenous infusions of calcium in one patient, and of calcium and parathormone in a second patient, showed appropriate target-organ responsiveness. Patients generally showed radiologic improvement of rickets after treatment with large doses of vitamin D, but such treatment failed to restore normal serum values of phosphorus and alkaline phosphatase. It is postulated that a substance elaborated from the dysplastic bone may be interfering with phosphate reabsorption in the renal tubule.
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PMID:Albright's syndrome with rickets. 43 Nov 33

Of 837 epileptics over 16 years of age treated with mono- or combined hydantoin therapy 20.3% showed radiographic signs of anticonvulsant osteomalacia. With the exception of the patients with severe disturbances of the skeletal system no positive correlation was found with duration of therapy. The percentage of moderate bone changes was the highest in the patients treated for 1 to 2 years; the percentage of severe bone changes in the group treated over 10 years. The rate of osteomalacia correlated with the total dose of hydantoin, phenobarbital, or primidone; the correlation with the dose per year was even more evident. The risk of osteomalacia rose distinctly with doses over 3000 equivalent units/year. The patients with combined hydantoin-barbiturate treatment showed a higher risk than those treated with phenytoin alone. The rate of osteomalacia was the highest in the patients aged under 20 years and over 50 years. Males showed a relatively higher rate of osteomalacia than females, they were treated however with a higher dose per year. The chemical parameters blood alkaline phosphatase and 25-hydroxycholecalciferol corresponded to the radiographic signs, whereas calcium and anorganic phosphate showed no correlation. Early routine radiologic and chemical control especially of the epileptic patients with high risk of osteomalacia should be routinely performed in future.
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PMID:[The frequency of adult anticonvulsant osteomalacia in relation to duration of therapy and dosage of anticonvulsants (author's transl)]. 45 43

1. The current status of treatment for osteoporosis at the osteoporosis clinic of the Department of Orthopaedic Surgery, Kobe University School of Medicine is reported. A study was made in these osteoporotic patients to investigate the relationships between pain and x-rays and also between pain and the clinical laboratory findings in this particular disease. 2. When pains in osteoporosis were classified into 4 grades, severity I through severity IV, the more severe pain was found to be associated more frequently with elevated blood levels of alkaline phosphatase. Many of the patients with severe pain tended to show indistinct trabeculation and sclerosis of the upper and lower margins of vertebral bodies on x-rays while some demonstrated looser's zones notably in the ribs. 3. A considerable portion of those patients who were receiving treatment under the diagnosis of osteoporosis were found to have evidence of osteomalacia, a finding pointing to the likelihood of coexistence of osteoporosis and osteomalacia. This possibility should therefore always be kept in mind when dealing with osteoporotic patients.
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PMID:Treatment of osteoporosis--with special reference to the coexistence of osteoporosis and osteomalacia. 46 48


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