Multiple organ failure: clinical and experimental.
The clinical scenario of multiple organ failure (MOF) is reviewed and its frequent correlation with sepsis emphasized. It is hypothesized that MOF is produced by the formation of immune complexes (IC) in response to infection with deposition on organs such as the liver, lung, and kidney. Such immune complexes trap macrophages which can directly damage endothelium. Such a pathologic picture is in keeping with that of MOF. Granular deposits of IgG, IgM, C3, C5, and fibrinogen have been identified in the organs of four patients dying of MOF and sepsis. Similar deposits have been identified using fluorescent antibody stains in the organs of rabbits following cecal perforation. It is hypothesized that sepsis may produce organ failure at a distance from the site of infection via deposits of immune complexes.
D058186:Acute Kidney Injury / Q000276:immunology*; D000818:Animals; D003176:Complement C3 / Q000032:analysis; D004727:Endothelium / Q000276:immunology; D004927:Escherichia coli Infections / Q000276:immunology; D005340:Fibrinogen / Q000032:analysis; D006501:Hepatic Encephalopathy / Q000276:immunology*; D006801:Humans; D007105:Immune Complex Diseases / Q000276:immunology; D007074:Immunoglobulin G / Q000032:analysis; D007678:Kidney Glomerulus / Q000276:immunology; D008099:Liver / Q000276:immunology; D008168:Lung / Q000276:immunology; D011817:Rabbits; D012131:Respiratory Insufficiency / Q000276:immunology*; D012772:Shock, Septic / Q000276:immunology*; D012773:Shock, Surgical / Q000276:immunology
D003176:Complement C3; D007074:Immunoglobulin G; D005340:Fibrinogen