Three main preventive principles against milk fever were evaluated in this literature review, and the efficacy of each principle was estimated from the results of controlled investigations. Oral calcium drenching around calving apparently has a mean efficacy of 50%-60% in terms of milk fever prevention as well as prevention of milk fever relapse after intravenous treatment with calcium solutions. However, some drenches have been shown to cause lesions in the forestomacs. When using the DCAD (dietary cation-anion difference) principle, feeding rations with a negative DCAD (measured as (Na + K)-(Cl + S)) significantly reduce the milk fever incidence. Calculating the relative risk (RR) of developing milk fever from controlled experiments results in a mean RR between 0.19 and 0.35 when rations with a negative versus positive DCAD are compared. The main drawback from the DCAD principle is a palatability problem. The principle of feeding rations low in calcium is highly efficient in milk fever prevention provided the calcium intake in the dry period is kept below 20 g per day. Calculating the relative risk (RR) of developing milk fever from controlled experiments results in a very low mean RR (between 0 and 0.20) (daily calcium intake below versus above 20 g/d). The main problem in implementing the low-Ca principle is difficulties in formulating rations sufficiently low in calcium when using commonly available feeds. The use of large doses of vitamin D metabolites and analogues for milk fever prevention is controversial. Due to toxicity problems and an almost total lack of recent studies on the subject this principle is not described in detail. A few management related issues were discussed briefly, and the following conclusions were made: It is important to supply the periparturient cow with sufficient magnesium to fulfil its needs, and to prevent the dry cows from being too fat. Available information on the influence of carbohydrate intake, and on the effect of the length of the dry period and prepartum milking, is at present insufficient to include these factors in control programmes. (+info)
Changes in cellular composition during magnesium deficiency.
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Mg deficiency increased the water content of the liver, kidney, heart and thigh muscle in the rat and decreased the proportion of nitrogen in the dry matter of the same tissues. Changes in the concentration of metals also occurred. 2. Cellular fractional indicated that the Mg and K depleted in liver occurred primarily in the heavy-mitochondrial and microsomal fractions respectively. The calcification of liver and kidney was due to preferential deposition of Ca in the heavy-mitochondrial fraction. 3. The proportion of cellular nitrogen present in the heavy-mitochondrial and microsomal fractions was markedly decreased in the liver and kidney of the Mg-deficient rats, and the proportion in the supernatant fraction increased. 4. Electron microscopy revealed that the cross-sectional areas of liver cells and all their mitochondria were decreased in Mg deficiency. The number of mitochondrial per cell was decreased even more severely and the average area of a mitochondrion was greater in deficient rats than in control animals. 5. The significance of these observations is discussed in relation to the location of the primary metabolic disturbance during Mg deficiency. (+info)
Recent advances in molecular genetics of hereditary magnesium-losing disorders.
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Recent advances in molecular genetics in hereditary hypomagnesemia substantiated the role of a variety of genes and their encoded proteins in human magnesium transport mechanisms. This knowledge on underlying genetic defects helps to distinguish different clinical subtypes and gives first insight into molecular components involved in magnesium transport. By mutation analysis and functional protein studies, novel pathophysiologic aspects were elucidated. For some of these disorders, transgenic animal models were generated to study genotype-phenotype relations and disease pathology. This review will discuss genetic and clinical aspects of familial disorders associated with magnesium wasting and focuses on the recent progress that has been made in molecular genetics. Besides isolated renal forms of hereditary hypomagnesemia, the following disorders will also be presented: familial hypomagnesemia with hypercalciuria and nephrocalcinosis, hypomagnesemia with secondary hypocalcemia, Ca2+/Mg2+-sensing receptor-associated disorders, and disorders associated with renal salt-wasting and hypokalemic metabolic alkalosis, comprising the Gitelman syndrome and the Bartter-like syndromes. (+info)
Serum magnesium aberrations in furosemide (frusemide) treated patients with congestive heart failure: pathophysiological correlates and prognostic evaluation.
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OBJECTIVES: To determine the prevalence of hypomagnesaemia and hypermagnesaemia, to discern various factors associated with abnormal serum magnesium, and to estimate prognostic significance of serum magnesium aberrations in patients with congestive heart failure. DESIGN: Observational study. SETTING: Medical department of a university hospital (tertiary referral centre). PATIENTS: 404 consecutive patients admitted with congestive heart failure as one of the diagnoses and previously treated with furosemide (frusemide) for at least three months. MAIN OUTCOME MEASURES: Clinical, biochemical, and electrocardiographic variables were analysed with respect to serum magnesium aberrations. Following discharge, mortality rates, including sudden death, were registered. RESULTS: Hypomagnesaemia was found in 50 patients (12.3%) and 20 (4.9%) were hypermagnesaemic. Female sex (p < 0.04), diabetes mellitus (p < 0.006), hypocalcaemia (p = 0.03), hyponatraemia (p < 0.05), malignant disease (p = 0.05), and high fever (p = 0.05) were statistically associated with hypomagnesaemia. Renal failure, severe congestive heart failure, and high dose furosemide treatment (> 80 mg/day) were associated with hypermagnesaemia (p < 0.001, p = 0.05, and p < 0.03, respectively). Hypermagnesaemic patients were older and weighed less. On follow up (median duration 43 months), 169 (41.8%) died, with 22 (13%) sudden deaths. Mortality was highest with hypermagnesaemia, lowest with normomagnesaemia, and intermediate with hypomagnesaemia. After adjustment for renal failure, old age, and severity of congestive heart failure, hypomagnesaemia but not hypermagnesaemia emerged as being significantly associated with shorter survival (p = 0.009). No statistical association was found between sudden death and magnesium concentrations. CONCLUSIONS: While hypermagnesaemia seems to represent a prognostic marker only, hypomagnesaemia appears to have an adverse pathophysiological effect. The subgroup of patients at risk for hypomagnesaemia requires frequent serum magnesium determinations and magnesium replacement for as long as hypomagnesaemia persists. (+info)
Magnesium deficiency: effect on bone mineral density in the mouse appendicular skeleton.
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BACKGROUND: Dietary magnesium (Mg) deficiency in the mouse perturbs bone and mineral homeostasis. The objective of the present study was to evaluate bone mineral density of the femur in control and Mg-deficient mice. METHODS: BALB/c mice aged 28 days at study initiation were maintained on a normal or Mg deficient (0.0002% Mg) diet, and at time points 0, 2, 4 or 6 weeks bones were harvested for bone mineral density analysis. Peripheral quantitative computed tomography (pQCT) was used to assess the trabecular metaphyseal compartment and the cortical midshaft. RESULTS: Although mean total bone density of the femoral midshaft in Mg deficient mice did not differ significantly from controls throughout the study, the trabecular bone compartment showed significantly decreased mineral content after 4 (p < 0.001) and 6 weeks (p < 0.001) of Mg depletion. CONCLUSIONS: This study demonstrates the profound effect of Mg depletion on the trabecular compartment of bone, which, with its greater surface area and turnover, was more responsive to Mg depletion than cortical bone in the appendicular skeleton of the mouse. (+info)
Effect of fluoride on the mobilization of skeletal magnesium and soft-tissue calcinosis during acute magnesium deficiency in the rat.
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To investigate the effect of fluoride on the mobilization of skeletal magnesium and on kidney calcification during magnesium depletion, male Holtzman rats were fed a magnesium-sufficient diet (400 ppm of magnesium) and drinking water containing either 0, 50 or 100 ppm of fluoride for a 20-day period prior to the initiation of magnesium deficiency. The high fluoride regimen resulted in a 100-fold increase in the fluoride content of the skeleton. On day 20 magnesium depletion was initiated by feeding the animals a diet containing 12 ppm of magnesium. Over a 4-week period of magnesium deprivation, a 26% decrease of the total magnesium in the humeri was observed. Fluoride exerted a significant effect in retarding the mobilization of skeletal magnesium. Four weeks of magnesium deficiency was associated with a decreased rate of skeletal mineral accretion and with an increase in the kidney calcium content. The decreased rate of mineral accretion was accentuated by the administration of fluoride during the deficiency state. While fluoride exerted an initial protective effect on calcinosis of the kidneys, the overall effect of the administration of fluoride during magnesium deficiency was to promote calcification of the kidneys rather than to prevent it. (+info)
Magnesium deficiency in African-Americans: does it contribute to increased cardiovascular risk factors?
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African-Americans are known to be disproportionately impacted by many chronic diseases such as diabetes, hypertension, cardiovascular, and renal disease. Lower levels of dietary and serum magnesium have been associated with an increased prevalence of hypertension, insulin resistance, and diabetes. Studies suggest a greater prevalence of occult magnesium deficiency among African-Americans compared to other populations. This increased prevalence of hypomagnesemia may contribute to increased insulin resistance leading to accelerated atherosclerosis and premature death. Trials that correct magnesium status/levels among African-Americans, whether through dietary intervention or direct magnesium replacement/supplementation need to be completed to characterize this relationship more completely. (+info)
Optical quantal analysis reveals a presynaptic component of LTP at hippocampal Schaffer-associational synapses.
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The mechanisms by which long-term potentiation (LTP) is expressed are controversial, with evidence for both presynaptic and postsynaptic involvement. We have used confocal microscopy and Ca(2+)-sensitive dyes to study LTP at individual visualized synapses. Synaptically evoked Ca(2+) transients were imaged in distal dendritic spines of pyramidal cells in cultured hippocampal slices, before and after the induction of LTP. At most synapses, from as early as 10 min to at least 60 min after induction, LTP was associated with an increase in the probability of a single stimulus evoking a postsynaptic Ca(2+) response. These observations provide compelling evidence of a presynaptic component to the expression of early LTP at Schaffer-associational synapses. In most cases, the store-dependent evoked Ca(2+) transient in the spine was also increased after induction, a novel postsynaptic aspect of LTP. (+info)