Sepsis and multiple organ failure

Cytokines involved include interleukin-1 (endogenous pyrogen), tumour necrosis factor and interleukin-6. Released from the patient’s own white blood cells, these contribute to the patient’s pyrexia and hypermetabolic state. While production of mediators is needed to combat infection, an excessive or prolonged activation of such cellular and humoral mediator pathways is thought to contribute to the development of multiple organ failure (MOF) in patients with major sepsis.