Biomedical subjects
Publications and source records attributed to R Kitzes.
A case of hypermagnesemia associated with pheochromocytoma is described. A further increase in serum Mg was observed with initiation of beta-blocking therapy. Unilateral adrenalectomy normalized serum Mg levels.
A group of 8 patients with essential hypertension and 12 patients with recurrent renal calcium stones were treated with 50 mg hydrochlorothiazide daily for a period of 3-10 years. Serum, erythrocyte, lymphocyte, skeletal muscle, bone and urine Mg were found to be within the normal range. In the intravenous Mg load test, all patients retained a normal percentage of the loading dose of Mg. Long-term thiazide therapy does not appear to lead to Mg depletion.
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8 young, untreated, hypomagnesemic patients with a recent onset of high-renin essential hypertension, were treated with 750 mg Mg oxide daily. Only functional (vasospastic) lesions were observed in their retinal vessels. After 3 months of therapy, despite no significant change in blood pressure, complete reversal of the retinal changes was observed. The retinal vascular changes could be attributable to vasospasm secondary to hypomagnesemia since serum Mg levels normalized during treatment.
A rise in free fatty acids (FFA) and a concomitant decrease in serum magnesium levels were found soon after acute myocardial infarction (AMI) in a group of 5 patients. Magnesium and FFA returned to normal levels within 3 days. No changes in serum FFA and magnesium levels were found in the postinfarction period in 5 patients who were under treatment with propranolol during the time they developed AMI. The linear model, magnesium = f(time, FFA), was investigated according to the stepwise regression-forward selection system. It was found that the magnesium level in AMI is best predicted by the FFA level (inverse correlation). In the period of 0-72 h after infarction, an inverse linear correlation was found to exist between the FFA level and the period of time after infarction.
Lymphocyte Mg concentration was measured in 2 patients with congestive heart failure, on long-term diuretic treatment, and was found to be lower than normal. The patients exhibited prolonged Q-Tc intervals on ECG analysis. During treatment with Mg sulfate, the Q-Tc interval normalized as the lymphocyte Mg approached control values. An Mg-sparing diuretic was added to the therapeutic regimen.
41 episodes of anginal attacks were promptly terminated by a bolus of Mg sulfate administered intravenously in 15 patients with variant angina. Pretreatment with parenterally administered Mg sulfate in four of these patients prevented further attacks.
Seven patients with congestive heart failure receiving long-term diuretic treatment (more than three years) experienced idionodal tachycardia in the presence of apparently normal serum digoxin levels. Intravenous bolus administration of magnesium (Mg) sulfate, followed by intramuscular Mg repletion, abolished the digitalis-toxic arrhythmia. The finding of decreased lymphocyte Mg and potassium contents proved the existence of cellular Mg depletion associated with normal serum Mg levels in five patients and with hypomagnesemia in the other two. Decreased cellular Mg content with normal serum Mg level predisposes to digitalis-toxic arrhythmias.
A case of pseudogout associated with low values of magnesium and alkaline phosphatase activity in the synovial fluid is presented. The low magnesium concentration is believed to cause the low alkaline phosphatase activity, since adding magnesium in vitro raised the activity to normal. The reason for the low magnesium concentration in the synovial fluid remains unclear.
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Total and ionized plasma Mg levels and cortical and trabecular bone Mg concentration were determined in five untreated nonalcoholic cirrhosis patients with ascites and edema. The high peripheral renin activity and serum aldosterone proved the existence of secondary aldosteronism in these patients. Total plasma Mg and trabecular bone Mg were within normal limits. A decreased absolute level and percentage of ionized plasma Mg were found without hypoalbuminemia, and cortical bone Mg concentration was decreased. Ionized plasma Mg concentration correlated closely with cortical bone Mg concentration when the levels of bone and plasma Mg were below normal.
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Larger and more perfect crystals in bone mineral from osteoporotic women have been described using biophysical methods. In search of the cause of this change, both chemical analysis and infrared spectrophotometry were used on iliac crest bone biopsies from 19 postmenopausal osteoporotic women. These women had each had a vertebral crush fracture and had a urinary hydroxyproline: creatinine ratio greater than 0.012. Lower than normal trabecular bone magnesium content and larger and more perfect crystals in trabecular bone mineral identified on infrared spectrophotometry were found in 16 out of the 19 women. Magnesium deficiency was confirmed by Thoren's magnesium load test in this subgroup of 16. Higher than normal bone magnesium content and smaller and less perfect crystals in bone mineral were found in five postmenopausal uremic women tested.
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Explore the source record for details and available documents.