Magnesium is a cofactor for more than 300 enzymes and the second most abundant intracellular cation in the human body. Magnesium affects many cellular functions such as transport of potassium and calcium ions, modulation of signal transduction and energy metabolism.1
Deficiency of magnesium (measured as tMg) occurs frequently in chronic alcoholism and contributes to the increased incidence of cardiovascular disease and osteoporosis2. Magnesium deficiency in chronic alcoholism is primarily due to renal magnesium wasting and is exacerbated by dietary Mg deprivation, gastrointestinal losses with diarrhea or vomiting as well as the concomitant use of drugs such as diuretics and aminoglycosides.2 Hypomagnesemia is almost always documented through total serum values (tMg), but it has recently become user-friendly to assay the biologically active, ionised fraction (iMg). While ion selective electrodes for the measurement of free magnesium are available, these are not widely deployed for routine clinical use.
Recent data obtained through the use of the noninvasive technology suggest that alcohol induces hypertension, stroke and sudden death via its effects on intracellular iMg, which in turn alter the cellular and subcellular bioenergetics and promote an iCa overload.3 Alcohol ingestion can result in profoundly different actions on the cerebral circulation depending upon dose and physiological state. After the administration of an acute dose of alcohol to the experimental animals, brain iMg dropped rapidly and significantly.4'5 Several studies described a marked deficiency of total and ionized magnesium in chronic alcoholic and lower iMg (not tMg) in the ethanol-containing specimens.67 It was pointed out that the determination of iMg concentration in biological fluids is influenced by several factors, and values may differ when measured with different instruments.7 The observation of magnesium status in health and disease depends on which magnesium fraction is measured.17
In the present study we compared the use of iMg vs tMg in a group of patients with ethanol ingestion and in patients with chronic alcoholism, after a period of abstinence and health controls.
SUBJECTS AND METHODS
Three groups of subjects were examined from February 1st to September 31st, 2004. The first group consisted of 74 healthy individuals, randomly selected, of both sexes, aged between 25 and 50 years, without any clinical or laboratory signs of chronic alcoholism or acute alcohol ingestion.
The second group consisted of 91 specimens with ethanol content, who all had the acute symptoms of ethanol ingestion upon their admission to the emergency department. These patients did not have a diagnosis of chronic alcoholism and we do not know whether they were chronic alcoholics. Blood specimens were taken from these patients aged 21 to 63 years for the routine biochemical analysis at the time of the admission, before the administration of any medication.
The third group consisted of 64 patients aged 22 to 71 years, admitted to the psychiatric hospital with a diagnosis of chronic alcoholism. They were not positive for ethanol. The subjects from the group of chronic alcoholics had a history of alcohol consumption lasting between min. 1 and max. 10 (average 3.38) years. At the time of the study they were abstinent from min. 27 to max. 91 (average 53) days. Blood specimens from these groups were taken for routine clinical and laboratory tests at the end of their hospitalization.
All the procedures have been done in accordance with the permission of the Ethics Committee and the Helsinki Declaration.
Blood was collected in evacuated, coagulation-free blood collection tubes (Venosafe, Terumo, Belgium). The blood samples were analyzed on the day of their receipt in the laboratory (for ethanol and iMg) or stored frozen in sealed tubes until they could be analyzed the next day (tMg). …