Postoperative delirium is a challenging complication following surgical procedures, in particular in patients with preexisting neurological conditions and elderly people. A recent study has highlighted the role of HMGB1 as a potential mediator in the development of postoperative delirium.
In the context of surgery, HMGB1 is released in response to tissue trauma and acts as a Damage-Associated Molecular Pattern (DAMP) molecule triggering the innate immune response. This response is characterized by activation of immune cells and the release of proinflammatory cytokines.
The connection HMGB1-postoperative delirium revolves around its ability to induce neuroinflammation. Following surgery, an increased level of HMGB1 has been observed: this correlate with the disruption of the blood-brain barrier (BBB) which promotes the diffusion of inflammatory mediators into the brain, contributing to cognitive dysfunction and delirium.
Different researches show how the suppression of HMGB1 can prevent surgery-induced neurocognitive disorders; high plasma levels of HMGB1 have been reported in patients with acute delirium: this reinforce the hypothesis of its involvement in postoperative cognitive disturbances. Targeting HMGB1 might offer new therapeutic strategies for preventing or mitigating postoperative delirium.
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Read the full article about the study: https://www.bjanaesthesia.org/article/S0007-0912(23)00055-7/fulltext