A Possible Role for Iron Ions in Organ Injury

Abstract

The multiple organ dysfunction syndrome (MODS) remains a leading cause of mortality following injury and other serious illnesses. While the pathophysiology of MODS is as complex as the affected organs are diverse, several threads bind the processes together. First, inflammation is prominent in the microvasculature of affected organs. Second, this inflammation does not appear to require a local stimulus; remote injury is often sufficient to precipitate the syndrome. Third, the injury need not be specific; direct trauma, ischemia/reperfusion and infection can substitute for one another in precipitating the descent into MODS. In this brief review, we consider the data relating iron metabolism and overload to MODS and suggest that iron in local excess can precipitate inflammation via apoptosis of the microvascular endothelium and smooth muscle, amplifying end organ ischemia.

Gold is for the mistress — silver for the maid — Copper for the craftsman cunning at his trade. “Good!” said the Baron, sitting in his hall, “But Iron, cold iron, is master of them all.”

Rudyard Kipling, Cold Iron