Systemic inflammatory response syndrome

Magnesium may have an important role in the inflammatory response. Hypomagnesemia has been shown to be an adverse factor in the survival of critically ill patients. Patients admitted to a medical ward or medical intensive care unit who were hypomagnesemic had approximately twice the mortality rate of similar patients who had normal plasma magnesium levels (lRub.e..iZ.l.l.e.t...a./ 1993). The development of the systemic inflammatory response syndrome following an insult is complex.

There has been much animal work to show that hypomagnesemia leads to a proinflammatory state with increased levels of inflammatory cytokines including interleukins 1 and 6, and tumor necrosis factor-a. Magnesium deficiency also has a membrane oxidant effect, with protein oxidation products being detectable in rat brain and kidney after 3 weeks on a magnesium-free diet. The response to an oxidant stress results in greater membrane lipid peroxidation and reduction in endothelial cell viability in the presence of magnesium deficiency. The effect of magnesium deficiency on the mortality following endotoxin challenge has been evaluated in rats (Salem §L§l 1995). A significant increase in mortality was found in magnesium-deficient rats compared with controls. Magnesium replacement in rats immediately prior to endotoxin improved the survival over other deficient animals. Even when the magnesium was given after the endotoxin challenge, there was a significant improvement in survival. Plasma magnesium concentration rose during sepsis which correlated with cell damage. This rise may explain the lack of association between hypomagnesemia and the sepsis syndrome. However, there is no proof that magnesium replacement improves the survival of patients with the systemic inflammatory response syndrome.

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