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The use of magnesium has been reported in many pathological conditions. In kidney diseases it has been evaluated for stone prevention and for treatment of hyperphospataemia. The role of magnesium in stone prevention is poorly defined. Although in vitro studies show that magnesium inhibits calcium oxalate and calcium phosphate crystal growth and aggregation, no beneficial effect of magnesium therapy has been demonstrated in a population of recurrent calcium stone formers.85 More recent data show that in patients who had experienced stone formation, oral magnesium supplements are able to produce a significant reduction in stone recurrences.86

In chronic kidney disease, magnesium has been used experimentally in recent decades as an alternative to calcium-based phosphate binders. O'Donovan etal. used magnesium carbonate in 28 patients for 2 years as a substitute for aluminium hydroxide and found a significant drop in predialysis aluminium levels and controlled serum phosphate levels.87 Other investigators observed the same efficacy but also significant side effects. Thus, though magnesium carbonate is an alternative to calcium-containing binders,88 it is not widely used.

The effect of oral magnesium supplementation has been studied in osteoporosis. In fact, significant reductions in serum and bone magnesium have been described in several studies on post-menopausal women with osteoporosis. Recently, dietary magnesium has been observed to be positively associated with bone mineral density (BMD) in a community-based study in elderly men and women.89 Despite this, epidemiological studies relating magnesium intake to bone mass or rate of bone mass loss have been conflicting. There are few studies on the effect of magnesium supplementation on bone loss. Two recent studies on this subject report conflicting results90,91 thus illustrating the ongoing controversy on the role of magnesium in bone turnover.

One of the pathogenetic mechanisms responsible for sickling in patients with sickle cell anaemia (haemoglobin SS) is the decreased hydration status of the cells. One of the main determinants of cell dehydration is the membrane K+-Cl~ cotransport system, and the magnesium-induced inhibition of this transport system may be beneficial in this disease. A small unblinded and uncontrolled study in patients with haemoglobin SS has shown that oral magnesium supplementation for 6 months can induce a significant reduction in the number of painful crises due to vaso-occlusion.92 A double-blind, placebo-controlled study is in progress to evaluate the effect of magnesium pido-late on adult and paediatric cases of haemoglobin SS disease.

Magnesium is also supposed to have a role in affective disorders as it seems to influence several systems related to the pathophysiology of depression (see Ref. 93 for review). The action of magnesium to reduce hypothalamus-pitui-tary-adrenocortical system activity is suggestive of its possible use as a mood stabilizer and controlled studies are warranted to test its clinical efficacy.

Magnesium also has a possible role in the treatment of migraine. A recent small controlled trial showed no beneficial effect in the magnesium group94 and even if it is suggested that the effectiveness of magnesium is related to plasma magnesium levels, there is still insufficient evidence to support its use in migraine.

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