autodigestion

Autodigestion is the process by which tissues are digested by their own digestive enzymes. It occurs when lysosomal hydrolases or secreted proteases are released in an uncontrolled manner, or when enzymes are prematurely activated within cells or tissues, leading to self-digestion and tissue damage. This mechanism can contribute to inflammation, necrosis, and loss of organ function in affected areas.

A well-known context is acute pancreatitis, where premature activation of trypsinogen to trypsin within the pancreatic tissue triggers widespread proteolysis and fat necrosis. Autodigestion of the pancreatic parenchyma can extend to surrounding fat and supporting tissues, exacerbating inflammation and systemic complications. Other situations, such as ischemia-reperfusion injury or severe inflammatory states, can involve enzymatic injury from leaked lysosomal enzymes and inflammatory proteases that amplify tissue destruction.

In histology and pathology, autodigestion is sometimes used to describe autolysis, the postmortem breakdown of tissues by endogenous enzymes after death. This is distinct from autophagy, a regulated cellular process in which cells degrade and recycle intracellular components for maintenance and survival.

Clinical relevance of autodigestion lies in its contribution to tissue necrosis and organ dysfunction, particularly in pancreatitis, but analogous enzymatic damage can occur in other organs under severe injury or inflammatory conditions. Understanding autodigestion helps explain patterns of tissue injury and informs approaches to management that aim to limit enzymatic damage and its systemic consequences.