Serum alkaline phosphatase and rickets.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T C Stamp.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Plasma levels of 25-hydroxycholecalciferol (25-HCC) were measured by a specific competitive protein-binding assay. Mean levels in both normal London adults and adolescent schoolchildren were 16 ng/ml and the mean level in a group of epileptic patients on high-dosage anticonvulsant therapy was 5 ng/ml, (difference from normals P < 0.001). Two further epileptic patients, with well-marked anticonvulsant osteomalacia, were treated with small doses of 25-HCC during full metabolic balance studies; rapid healing followed administration of 25-HCC by mouth in doses of 10-45 mug daily, which is well below the effective dose range of calciferol in this condition. These findings provided further evidence that anticonvulsant osteomalacia results from hepatic enzyme induction which, by increasing the metabolism of cholecalciferol to inactive compounds, lowers 25-HCC levels in patients whose dietary vitamin D intake and exposure to sunlight are otherwise adequate. Results also indicated that under certain circumstances 25-HCC may have considerably stronger antirachitic potency in man than has hitherto been recognized.
A 23-year-old woman presented with an 11-year history of peripheral joint pains and stiffness slowly progressing to the development of gross calcinosis circumscripta. She had no definite evidence of systemic scleroderma. She was first treated for one year with frequent intravenous sodium EDTA, which increased urinary calcium and enhanced negative calcium balance but did not lessen her calcinosis. She was then treated with probenecid up to 2 g daily and her calcinosis lessened steadily over three years. Plasma levels of both phosphorus and urate fell during this time.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The investigation and treatment of osteomalacia are described in four patients with epilepsy treated with long-term anticonvulsant therapy. It is suggested that drug-mediated enzyme induction may be the mechanism responsible by causing a greatly increased inactivation of vitamin D in these patients.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Fasting serum lipid levels and changes in plasma glucose, fatty acid non-esterified (Nefa), and blood pyruvate levels during intravenous glucose tolerance tests were measured in 13 normal subjects before and one, five, and 15 days after the administration of 1-triiodothyronine (T3) calculated as 6 mug/kg body weight. Significant increases in the mean basal metabolic rate and the mean fasting plasma Nefa level occurred within 10 to 17 hours of a single dose of T3, while a rise in the mean fasting plasma glucose concentration just failed to achieve significance. Fasting concentrations of blood pyruvate and serum triglyceride were unaffected. A significant fall in serum cholesterol levels was produced and lasted at least five days. All other indices returned to normal by five days.During intravenous glucose tolerance tests performed at intervals after T3 administration no change in plasma glucose levels from control values was seen. Mean plasma Nefa and blood pyruvate levels, however, were significantly raised above control values during the early stages of the test 10 to 17 hours after T3. The relationship between these findings and those observed in clinical thyrotoxicosis is discussed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.