SERUM, IONIZED AND INTRACELLULAR MAGNESIUM IN HYPERTENSIVES WITH CIRRHOSIS OF LIVER

Objective: Severe chronic alcohol consumption is known to cause hypomagnesemia and is often associated with arterial hypertension. Many attempts have been done to clarify the nature of the underlying defects. Typical reasons may be a magnesium deficient nutrition, malabsorption, an increased intestinal or sweat excretion, hyperaldosteronism or disorders in catecholamone metabolism, as well as an increased urinary magnesium loss. Some previous studies indicate a magnesium loss in hypertensives with liver disease resulting in tissue depletion of magnesium. Design and method: We studied 15 hypertensive and 15 non-hypertensive alcoholics with cirrhosis of liver. None of the patient was renal insufficient or diabetic. No diuretics, PPI or minerals were taken. Clinical data concerning Age, Sex, BMI or blood pressure values were similar in both groups. 30 patients served as controls. The study was performed in accordance with the declaration of Helsinki. Diagnosis of cirrhosis of liver was performed by liver biopsy. Duration of alcohol abuse was similar in groups. In each patient serum magnesium, erythrocyte magnesium and ionized blood magnesium was measured. Ionized magnesium was measured by a Prime Plus apparatus (Andover, USA). Statistical analysis was performed by ANOVA, values are means+/-s.d. Results: Serum magnesium was measured 0.89+/-0.03 mmo/l in controls, 0.85+/- 0.07 in non-hypertensive liver cirrhosis patients (NHLC) and 0.80+/-0.1 mmo/l in hypertensive patients with cirrhosis of liver (HLC)(p< 0.05). Intracellurar magnesium was 1.76+/+0.12 mmol/l in controls versus 1.38 +/-0.22 in NHLC and 1.25+/-0.15 mmol/l in HCL (p< 0.01). Ionized blood magnesium was 0.62+/-0.7 mmol/l in controls and 0.52 +/- 0.6 mmol/l in all patients with cirrhosis of liver (p< 0.05). Conclusions: The negative magnesium status in serum, intracellular and ionized form in hypertensives with alcohol abuse and cirrhosis of liver is of importance for cardiovascular outcome, morbidity and mortality. A sufficient magnesium supplementation, orally given in a dosage of 300 to 500 mg/d., should be recommended in these patients.