Biomedical subjects

E Ryzen

Publications and source records attributed to E Ryzen.

25 records · Page 2Linked to original sources

PubMed1986

TmMg and renal Mg threshold in normal man and in certain pathophysiologic conditions.

The TmMg and renal Mg threshold were assessed in normal subjects and in a number of pathological conditions. The TmMg in normal subjects was 1.4 mg/100 ml glomerular filtrate (GF) 1.73 m2 and numerically equalled the renal Mg threshold of 1.4 mg/100 ml. No significant difference was seen in patients with primary hyperparathyroidism or hypoparathyroidism. Patients with familial hypocalciuric hypercalcemia, however, tended to have an elevated renal Mg threshold. Investigation of 3 patients with idiopathic renal Mg wasting demonstrated a normal TmMg but reduced renal Mg threshold. Urinary Mg excretion was also assessed in normomagnesemic alcoholic patients. Retention of a parenterally administered Mg load and renal Mg retention were significantly greater than normal despite normal serum Mg concentrations. These data suggest that determination of TmMg and renal Mg threshold may provide useful information in understanding Mg homeostasis in normal subjects and in disorders which may result in abnormal Mg metabolism.

Calcium↗

PubMed1985

Magnesium deficiency in a medical ICU population.

The serum magnesium level was measured in 94 consecutive patients admitted to the medical ICU of Los Angeles County/University of Southern California Medical Center over a 2-month period. Sixty-five percent of patients with serum creatinine concentrations of 1.1 mg/dl or less were hypomagnesemic. Of these, one third had hypocalcemia that was corrected with magnesium supplementation. Physicians should be alert to the high incidence of magnesium deficiency in critically ill patients.

California↗

PubMed1985

Low serum concentrations of 1,25-dihydroxyvitamin D in human magnesium deficiency.

The effect of magnesium deficiency on vitamin D metabolism was assessed in 23 hypocalcemic magnesium-deficient patients by measuring the serum concentrations of 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] before, during, and after 5-13 days of parenteral magnesium therapy. Magnesium therapy raised mean basal serum magnesium [1.0 +/- 0.1 (mean +/- SEM) mg/dl] and calcium levels (7.2 +/- 0.2 mg/dl) into the normal range (2.2 +/- 0.1 and 9.3 +/- 0.1 mg/dl, respectively; P less than 0.001). The mean serum 25OHD concentration was in the low normal range (13.2 +/- 1.5 ng/ml) before magnesium administration and did not significantly change after this therapy (14.8 +/- 1.5 ng/ml). Sixteen of the 23 patients had low serum 1,25-(OH)2D levels (less than 30 pg/ml). After magnesium therapy, only 5 of the patients had a rise in the serum 1,25-(OH)2D concentration into or above the normal range despite elevated levels of serum immunoreactive PTH. An additional normocalcemic hypomagnesemic patient had low 1,25-(OH)2D levels which did not rise after 5 days of magnesium therapy. The serum vitamin D-binding protein concentration, assessed in 11 patients, was low (273 +/- 86 micrograms/ml) before magnesium therapy, but normalized (346 +/- 86 micrograms/ml) after magnesium repletion. No correlation with serum 1,25-(OH)2D levels was found. The functional capacity of vitamin D-binding protein to bind hormone, assessed by the internalization of [3H]1,25-(OH)2D3 by intestinal epithelial cells in the presence of serum was not significantly different from normal (11.42 +/- 1.45 vs. 10.27 +/- 1.27 fmol/2 X 10(6) cells, respectively). These data show that serum 1,25-(OH)2D concentrations are frequently low in patients with magnesium deficiency and may remain low even after 5-13 days of parenteral magnesium administration. The data also suggest that a normal 1,25-(OH)2D level is not required for the PTH-mediated calcemic response to magnesium administration. We conclude that magnesium depletion may impair vitamin D metabolism.

Calcifediol↗

PubMed1985

Serum protein binding of 1,25-dihydroxyvitamin D: a reevaluation by direct measurement of free metabolite levels.

Using the technique of centrifugal ultrafiltration isodialysis to measure the free concentration of 1,25-dihydroxyvitamin D [1,25-(OH)2D], we determined the affinity of serum proteins for 1,25-(OH)2D both by Scatchard analysis (increasing ligand concentration at fixed binding site concentrations) and by a novel analysis in which the binding site concentrations were varied (serial dilution) at fixed ligand concentrations. The high affinity binding constant in serum for 1,25-(OH)2D was 3.7 X 10(7) M-1 by Scatchard analysis and 4.2 X 10(7) M-1 by serial dilution analysis. Human serum albumin had a much lower affinity for 1,25-(OH)2D (5.4 X 10(4) M-1). When vitamin D-binding protein (DBP) was selectively removed from serum by an actin affinity column, the affinity of the remaining serum proteins for 1,25-(OH)2D was that of albumin. Postulating a two-site model (DBP and albumin) for transport of 1,25-(OH)2D in serum and incorporating the estimated affinity constants of DBP and albumin for this metabolite, we calculated that 85% of total circulating 1,25-(OH)2D is transported in blood bound to DBP in normal individuals (0.4% is free and 14.6% is bound to albumin). In patients with liver disease, 73% is bound to DBP (1.1% is free and 25.9% is bound to albumin). Using this same two site model, we found a reasonable correlation (r = 0.612; P less than 0.001) between the measured free 1,25-(OH)2D level and the calculated free 1,25-(OH)2D level in serum based on albumin and DBP concentrations in 16 normal subjects and 16 patients with liver disease. These results confirm the concept that although DBP is the principal protein carrier of 1,25-(OH)2D in serum, albumin is a major secondary carrier, especially in patients with low DBP levels.

Adult↗

PubMed1985

Intravenous etidronate in the management of malignant hypercalcemia.

The treatment of hypercalcemia remains a common problem in the management of many patients with cancer. We have used intravenously administered etidronate disodium as a therapy for hypercalcemia in 26 patients with malignant disease. Patients with persistent hypercalcemia despite adequate hydration and a serum creatinine level less than or equal to 1.5 mg/dL were allowed on study. Treatment consisted of intravenously administered etidronate disodium at 7.5 mg/kg/day in 250 mL of saline infused over two hours on 1, 2, 3, or 4 consecutive days. The serum calcium level in 19 (73%) of 26 patients returned to the normal range with a mean response time of 3 +/- 2 days. Similar response rates were seen in patients with a variety of tumors, including breast cancer, non-small-cell lung cancer, and multiple myeloma. Intravenously administered etidronate appears to be safe and effective therapy for hypercalcemia in patients with malignant disease.

Adult↗

PubMed1985

Hypercalcemia in leprosy.

We report a case of hypercalcemia in a patient with leprosy. Aminoterminal parathyroid hormone and 25-hydroxy-cholecalciferol concentrations were suppressed. Urinary hydroxyproline concentrations were elevated. There was no evidence of malignancy. The hypercalcemia resolved with corticosteroid therapy.

Arthritis, Rheumatoid↗

PubMed1985

Parenteral magnesium tolerance testing in the evaluation of magnesium deficiency.

Magnesium deficiency is a common clinical condition, frequently present even with normal serum magnesium (S-Mg) concentrations. We have studied retention of a low-dose (0.2 mEq/kg lean body weight), intravenously administered magnesium load in 6 hypomagnesemic patients and 18 normomagnesemic alcoholics as compared with 16 normal subjects. Both normomagnesemic and hypomagnesemic subjects retained significantly greater amounts of the administered magnesium than did the normal subjects. In patients who were restudied following parenteral magnesium repletion, retention of the magnesium load normalized. We conclude that increased retention of a magnesium load is a more sensitive index of magnesium deficiency than is the S-Mg concentration, and suggest that low-dose magnesium tolerance testing be used more frequently as a clinical tool in the evaluation of states of normomagnesemic magnesium deficiency.

Adult↗