Intracellular electrolytes in cardiac failure.

In congestive heart failure (CHF) there are several compensatory mechanisms operating which may influence electrolyte metabolism. The activation of the renin-angiotensin-aldosterone system causes retention of sodium (Na) and losses of potassium (K) and magnesium (Mg). The secondary hyperaldosteronism may give rise to high intracellular Na and low intracellular K through a direct permeability effect on the cell membrane. The Mg deficiency may lead to a further increase of intracellular Na and decrease of intracellular K since Mg is a necessary ion for the function of the Na-K pump. In 297 patients with diuretic treated CHF we found that 42% had hypokalemia, 37% hypomagnesemia and 12% hyponatremia. We also found that 57% had excess muscle Na, 52% had depletion of muscle K and 43% had low muscle Mg. We have also shown that the low muscle K cannot be corrected by K supplementation when there is a concomitant Mg deficiency and that Mg infusions may change the disturbed relation between extra- and intracellular electrolytes towards normal.

Peroral glucose tolerance test. Relation to skeletal muscle electrolytes.

Seventy patients on long-term diuretic therapy for arterial hypertension and/or congestive heart failure were investigated with regard to skeletal muscle electrolytes and the results of a peroral glucose tolerance test. A significant correlation was observed between the muscle content of potassium and the ability to handle a glucose load. Thirty patients underwent a second set of samples six months after the first one, 23 of whom had a reduction of their muscle potassium content relative to the first biopsy. They simultaneously demonstrated a significant impairment of glucose tolerance.

Aggravation of thiamine deficiency by magnesium depletion. A case report.

A patient with Crohn's disease and long-standing diarrhea resulting in a combined thiamine and magnesium deficiency is presented. Despite massive doses of thiamine i.v., the symptoms of thiamine deficiency could not be suppressed until the magnesium deficiency was corrected as well. This case report emphasizes the dependence of thiamine on magnesium for an adequate function in the body.

Plasma and skeletal muscle electrolytes in patients with Crohn's disease.

Plasma and skeletal muscle electrolytes were measured in 13 patients with Crohn's disease, and in an age- and sex-matched reference group. Patients with Crohn's disease demonstrated significantly lower muscle potassium content (p less than 0.01) than did controls. Patients with extensive involvement of the bowel tended to have lower muscle potassium content. The patient population did not differ significantly from the controls with regard to skeletal muscle magnesium content but displayed a far wider range of values. Our results indicate that potassium depletion is present in nonresected patients with Crohn's disease.

Problems with potassium and magnesium in diuretic-treated patients.

Treatment with thiazides and loop diuretics increase the urinary excretion of potassium and magnesium and the body content of these ions are reduced after long-term treatment. The diuretic-induced magnesium deficiency influences the potassium metabolism. Magnesium is a necessary activator of Na-K-ATPase, which supplies the Na-K pump with energy. Lack of magnesium will therefore impair the pumping of sodium out of the cell and of potassium into the cell. The change of the relationship between extra and intracellular potassium may induce cardiac arrhythmias. Certain groups of patients, such as patients on digitalis therapy, patients with secondary hyperaldosteronism, elderly patients with insufficient dietary habits, and heavy drinkers, run an additional risk of developing potassium/magnesium disturbances. In young patients with uncomplicated essential hypertension, the risk is probably very small.

Magnesium deficiency following jejunoileal bypass operations for obesity.

Skeletal muscle biopsies, blood samples, and 24-hour urines, before and after magnesium infusions, were obtained from 12 patients who had undergone jejuno-ileal bypass surgery several years earlier, selected for probable magnesium deficiency on the basis of repeated hypomagnesemia. The patients retained significant amounts of the infused magnesium, and exhibited elevation of low skeletal muscle magnesium and potassium, with concomitant decreases of muscle sodium and chloride. These changes were accompanied by increased urinary calcium and sodium and decreased urinary phosphorus excretion.

Effects on muscle electrolytes of potassium and magnesium infusions, spironolactone medication and operation in a case of primary aldosteronism.

Serum and muscle electrolytes were determined in a case of primary aldosteronism before and after potassium and magnesium infusions as well as spironolactone treatment and following surgery. Repeated potassium infusions resulted in a transient normalization of the muscle potassium (K/m), followed within 3-4 days by a return to the previously low K/m. Magnesium infusions did not give any increase in muscle magnesium (Mg/m). On the contrary, there was a decrease in Mg/m concomitant with a decrease in K/m. Treatment with spironolactone for one month was followed by a normalization of both serum and muscle electrolytes. Following surgery the serum potassium and K/m remained normal, but the serum magnesium (Mg/s) and Mg/m showed a decrease to subnormal values. Despite the initial findings of normal Mg/s and Mg/m as well as excretion of more than 80% of the i.v. magnesium dose, this may indicate that there was a magnesium deficiency in the skeletal pool.

Ventricular extrasystoles and intracellular electrolytes in hypokalemic patients before and after correction of the hypokalemia.

Fifty-four initially hypokalemic patients, 43 of whom were on diuretic treatment, were given potassium supplementation until they showed a repeatedly normal serum potassium level. Muscle specimens obtained by percutaneous biopsy revealed that there were no concomitant increases in muscle potassium content, nor in intracellular potassium concentration, except in the very small group (6 patients) with a muscle magnesium content of greater than or equal to 3.95 mmol/100 g fat free dry solids (FFDS) and an initially lower muscle potassium content (less than or equal to 39.9 mmol/100 g FFDS). ECG, registered for 3 hours on a portable ECG tape recorder before and after correction of the serum potassium level, showed no change in the frequency of ventricular ectopic beats.

Bilateral chylothorax - complication in malignancy.

Bilateral chylothorax is a rare condition caused by traumas and disorders with perforation or destruction of main lymphatics in the thorax leading to lymph leakage. Two patients with bilateral chylothorax are presented one of whom was successfully operated on. Etiology, diagnostics and therapy of this condition are discussed.