Disturbance of calcium metabolism by anticonvulsant drugs.
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A survey of calcium metabolism in epileptic patients in a residential centre showed a subnormal serum calcium level in 22.5% of patients and a raised alkaline phosphatase in 29%. Hypocalcaemia was related to high dosage of anticonvulsant drugs, to multiple drug therapy, and to the use of individual anticonvulsant drugs in the following order, with decreasing order of importance: pheneturide, primidone, phenytoin, phenobarbitone. Subnormal serum calcium levels occurred more commonly in patients with a raised liver alkaline phosphatase isoenzyme than in those whose phosphatase was mainly of bone origin.Preliminary results of treatment with calciferol suggested that the disturbance of calcium metabolism was the result of vitamin D deficiency. It is possible that anticonvulsant drugs accelerate the breakdown of vitamin D by liver enzyme induction. (+info)
Tubular reabsorption of calcium in normal and hypercalciuric subjects.
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Tubular reabsorption and excretion of calcium were studied at different levels of filtered calcium by means of calcium infusion in normal and hypercalciuric subjects and in patients with idiopathic nephrolithiasis. Calcium reabsorption and excretion rose linearly with filtered load and in no case was a maximum tubular reabsorptive capacity for calcium reached. No decrease in tubular reabsorption of calcium was found in hypercalciuric as compared with normocalciuric subjects, and no difference in tubular reabsorption was found between patients with idiopathic nephrolithiasis and normal subjects. Calcium excretion and reabsorption calculated from the endogenous creatinine clearance during calcium infusion were virtually identical with the corresponding values calculated from the inulin clearance. (+info)
Study of calcium absorption in man: a kinetic analysis and physiologic model.
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A physical model of calcium absorption was developed from analysis of data obtained on 23 subjects, including 13 patients having a variety of abnormalities of calcium metabolism. The model was tested and found consistent in all subjects studied. This technique provides a quantitative description of the rate of entry of oral dose of (47)Ca into the circulation as a function of time by analysis of serum or forearm radioactivity in response to intravenous and oral administration of (47)Ca. The kinetics of the absorption process as proposed by the model are characterized by an initial delay phase of 15-20 min, by a maximal rate of absorption at 40-60 min after ingestion, and by 95% completion of the absorption within 2(1/2) hr. Partial identification of the physiological counterparts of the model was possible by introduction of the isotope at various levels of the gut. Although the region of the duodenum was found to have the greatest rate of absorption per unit length in normal subjects, it was least responsive to stimulation by parathyroid hormone and suppression by calcium loading. Furthermore, the response of the gut to parathyroid hormone was delayed, whereas the suppression of absorption by intravenous or oral calcium loading was rapid and dramatic. The implications of these observations are discussed. (+info)
Oxalosis in infancy.
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We describe 3 infants with nephrocalcinosis and terminal renal failure. In all 3 there was widespread oxalate deposition: biochemical evidence of primary hyperoxaluria was sought but the presence of severe renal failure and the lack of established normal values for urinary and plasma oxalate and glycollate in infants made this diagnosis difficult to establish. (+info)
Postanesthetic myonecrosis in horses.
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Two horses died of massive myonecrosis following surgery. The hematological, biochemical and pathological changes are described and compared with those previously reported in the literature. (+info)
Bilateral basal ganglia calcifications visualised on CT scan.
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Thirty-eight cases of basal ganglia calcification imaged on computed axial tomography were reviewed. Most cases were felt to represent senescent calcification. The possibility of a vascular aetiology in this group is discussed. A less common group of patients was identified with calcification secondary to abnormalities in calcium metabolism or radiation therapy. Three cases of basal ganglia calcifications were detected in juvenile epileptic patients receiving chronic anticonvulsants. These cases may be related to abnormalities in calcium metabolism and alkaline phosphatase activity. Clinical evidence of basal ganglia abnormality was generally absent demonstrating the preservation of neuronal pathways in most cases. (+info)
Boucher-Neuhauser syndrome associated with hypocalciuric hypercalcemia.
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A 52-year-old woman was diagnosed as having cerebellar ataxia, hypogonadotropic hypogonadism and retinochoroidal degeneration, the so-called, "Boucher-Neuhauser" syndrome proposed by Limber et al (Am J Med Genet 33:409, 1989). In addition, laboratory findings showed the elevation of serum calcium (Ca) levels, low urinary Ca excretion, and exaggerated reabsorption of filtrated Ca (FECa:0.14%), suggesting complication of hypocalciuric hypercalcemia. This is a very rare case of Boucher-Neuhauser syndrome associated with hypocalciuric hypercalcemia. (+info)
Hypercalciuria: lessons from studies of genetic hypercalciuric rats.
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Human idiopathic hypercalciuria (IH) is a common cause of hypercalciuria that contributes to calcium oxalate nephrolithiasis. The disorder is characterized by normocalcemia, increased intestinal Ca absorption, and normal or elevated circulating 1,25(OH)2D3. Intestinal Ca hyperabsorption, which is a source of excess urine Ca excretion, may result from either a primary increase in renal 1,25(OH)2D3 production; a primary, vitamin D-independent defect in enterocyte regulation of Ca transport; or a secondary increase in 1,25(OH)2D3 production in response to a defect in renal tubular Ca reabsorption. Breeding male and female Sprague Dawley rats with spontaneous hypercalciuria has resulted in offspring with hypercalciuria, increased intestinal Ca absorption, and normal serum 1,25(OH)2D3. In male IH rats, vitamin D receptor (VDR) content measured by saturation binding and western blotting revealed a twofold increase in VDR number in the duodenum, kidney cortex, and splenic monocytes. The molecular basis for the increase in VDR appears not to be due to increased VDR gene expression, but may result from increased efficiency of translation of the VDR message or prolongation of the half-life of VDR. Comparable migration of normal and IH intestinal VDR on western blots and of intestinal VDR mRNA on northern blots suggests that the abundant VDR in IH rat intestine is not a mutation of the wild-type VDR. These observations strongly suggest that, in IH rats, normal serum 1,25(OH)2D3 and increased VDR results in increased VDR-1,25(OH)2D3 complexes and enhanced biologic actions of 1,25(OH)2D3, including increased intestinal Ca transport. IH in rats may be the first genetic disorder due to a pathologic increase in the VDR. (+info)