[Oral magnesium supplementation to patients receiving diuretics--normalization of magnesium, potassium and sodium, and potassium pumps in the skeletal muscles]. / Peroralt magnesiumtilskud til patienter i diuretisk behandling--normalisering of magnesium, kalium og natrium, kalium-pumper i tvoerstribet muskulatur.

In 76 consecutive patients who had received diuretics for 1-17 years for arterial hypertension or congestive heart failure, muscle concentrations of magnesium, potassium, and sodium-potassium pumps were significantly reduced compared to 31 age- and sex-matched controls. Thirty-six patients with muscle magnesium and/or potassium below the control level received oral magnesium hydroxide supplement for 2-12 weeks (N = 20) or 26 weeks (N = 16). After short term (2-12 weeks) magnesium supplementation muscle parameters were increased, but far from normalized. After magnesium supplementation for 26 weeks, the muscle concentrations of magnesium, potassium and sodium-potassium pumps were normalized in most cases. Oral magnesium supplementation may restore diuretic-induced disturbances in the concentrations of magnesium, potassium and sodium-potassium pumps in skeletal muscle. A supplemental period of at least six months seems required before complete normalization can be expected.

[Pre-eclampsia. Etiology--physiopathology--treatment]. / Praeeklampsi. Aetiologi--patofysiologi--behandling.

Recent observations indicate that pre-eclampsia is a disease, which occurs because of a partially defective maternal immune response against the fetal (paternal) antigen expressed on trophoblast tissue. The resulting defective or insufficient placentation can cause ischaemic changes, which seem to act in a harmful way on the vascular endothelium, initially locally in the utero-placental circulation, but later with universal systemic effects. The resulting endothelial dysfunction and concommitant thrombocyte activation seems to account for an important part of the pathophysiology of pre-eclampsia. Hypertension is presumably a secondary phenomenon. The definitive treatment of pre-eclampsia is delivery, which is always indicated in cases of severe pre-eclampsia after 32 weeks of pregnancy. In milder cases and before 32 weeks it is reasonable to await delivery, if necessary starting anti-hypertensive treatment. Treatment of hypertension has to balance the risks of maternal cerebral complications against the risks of reduced utero-placental bloodflow with resulting intra-uterine growth retardation. Low-dose acetylsalicylic acid treatment could in theory constitute a prophylactic principle, but the results of new, large, well-conducted, randomised trials advise against using such treatment prophylacctically at present. The effect of fish-oil supplements is not yet clarified, whereas mineral supplements such as calcium and magnesium are unlikely to have prophylactic effects on the development of pre-eclampsia, at least not in western industrialized society.

Oral magnesium supplementation restores the concentrations of magnesium, potassium and sodium-potassium pumps in skeletal muscle of patients receiving diuretic treatment.

In 76 consecutive patients who had received diuretics for 1-17 years for arterial hypertension or congestive heart failure, muscle concentrations of magnesium, potassium, and sodium-potassium pumps were significantly reduced compared to 31 age- and sex-matched controls. Thirty-six patients with muscle magnesium and/or potassium below the control level received oral magnesium hydroxide supplement for 2-12 weeks (n = 20) or 26 weeks (n = 16). After short-term (2-12 weeks) magnesium supplementation muscle parameters were increased, but far from normalized. After magnesium supplementation for 26 weeks, the muscle concentrations of magnesium, potassium and sodium-potassium pumps were normalized in most cases. Oral magnesium supplementation may restore diuretic-induced disturbances in the concentrations of magnesium, potassium and sodium potassium pumps in skeletal muscle. A supplemental period of at least 6 months seems to be required before complete normalization can be expected.

Magnesium intake and status and pregnancy outcome in a Danish population.

OBJECTIVE: To investigate the relation between pregnancy outcome and magnesium intake and status. DESIGN: A prospective observational study in which the estimate of nutrient intake and serum samples were obtained before the final outcome of pregnancy was known. A second part of the investigation was a cross-sectional comparison of magnesium status of normal pregnant women and women with certain pathological pregnancies. SETTING: Antenatal clinic associated to the University Clinic of Obstetrics and Gynaecology, University of Aarhus, Denmark. SUBJECTS: 1203 consecutive women in the 30th week gestation were invited to participate in the study, 991 (82.4%) accepted and records for 965 (80.2%) were available for analysis. DATA: Food intake data were collected by a combination of a self administered questionnaire and a structured interview of a dietary history type. Serum samples were obtained from blood withdrawn in the 30th and 37th week gestation. Obstetric data were collected from the midwifery and hospital records. For a second part of the investigation, biopsies from the uterus and the abdominal rectus muscle were obtained from women delivered by caesarean section. RESULTS: In the women with normal pregnancies and in the three groups of pathological pregnancies (pre-eclampsia, SGA-infants and preterm labour) the average magnesium intake was within the range of 200 to 208 mg per 1000 kcal per day (SD 32) and there were no differences between the groups. Neither were differences in serum magnesium observed. Birthweight for gestational age was not influenced by magnesium intake. No differences in magnesium status as assessed by determination of magnesium content in muscle biopsies were found between the normal pregnancies and women with pre-eclampsia, SGA-infants or preterm labour. CONCLUSION: The intake of magnesium seemed adequate, and pre-eclampsia, SGA-infants, or preterm labour did not seem associated with a low dietary intake of magnesium or magnesium deficiency. Routine magnesium supplementation during pregnancy is not recommended for populations of relative good socio-economic status.

[Magnesium and long-term diuretic therapy]. / Magnesium og langvarig diuretikabehandling.

Thiazides and loop diuretics, facilitate the loss of Mg and K resulting in increased excretion in the urine. Although serum-K and serum-Mg values in patients receiving long-term treatment for hypertension or incompensated heart disease usually are normal, muscle-Mg and muscle-K contents are reduced in around 50% of these patients. Mg deficiency increases K loss and K/Mg deficiencies are frequently observed simultaneously. K repletion is often difficult if the accompanying Mg deficiency is not corrected simultaneously. The K/Mg loss from the muscles is accompanied by reduced concentration of Na,K-pumps. These disturbances may produce muscle symptoms, increased sensitivity to digitalis, inhibition of growth and possibly arrhythmias. Evaluation of the K and Mg status during diuretic treatment should be preferentially based on tissue determinations. The muscle biopsy method is rapid, reliable and may reveal conditions of deficiency. In several cases, oral supplements of Mg have proved to be adequate to restore the normal K/Mg status.

Reduced concentrations of potassium, magnesium, and sodium-potassium pumps in human skeletal muscle during treatment with diuretics.

Animal studies have shown that potassium depletion induced by diuretics or potassium deficient fodder leads to a selective decrease in the concentrations of potassium and in the concentration of sodium-potassium pumps in skeletal muscle. In 25 patients who had received diuretics for 2-14 years the mean concentrations of potassium, magnesium, and sodium-potassium pumps were measured in skeletal muscle biopsy specimens and were significantly lower than in those from a group of age matched controls. The reductions in all three variables were significant in those patients receiving diuretics for arterial hypertension as well as in those being treated for congestive heart failure. In 14 patients the mean muscle potassium concentration was below the control range, but only one of those was hypokalaemic (3.4 mmol/l), and 13 were receiving potassium supplements. In 15 patients the mean muscle magnesium concentration was below normal, and the mean muscle potassium and magnesium concentrations showed a linear correlation. In 12 patients in whom the mean muscle potassium concentration was below 80 mumol/g wet weight there was a linear correlation between the cellular potassium:sodium ratio and the concentration of 3H-ouabain binding sites indicating that potassium deficiency also leads to a down regulation of sodium-potassium pumps in human skeletal muscle. In spite of potassium supplements long term treatment with diuretics may lead to potassium and magnesium deficiencies, which are not detectable using the standard methods of serum analysis. The changes in concentrations of electrolytes and sodium-potassium pumps associated with treatment with diuretics may impair muscle function and potassium homoeostasis and interfere with the distribution of digitalis glycosides.