Background: Although early balanced blood product resuscitation has improved mortality after traumatic injury, many patients still suffer from inflammatory complications. The goal of this study was to identify inflammatory mediators associated with death and multiorgan system failure following severe injury after patients undergo blood product resuscitation.
Methods: A retrospective secondary analysis of inflammatory markers from the Pragmatic Randomized Optimal Platelet and Plasma Ratios study was performed. Twenty-seven serum biomarkers were measured at 8 time points in the first 72 hours of care and were compared between survivors and nonsurvivors. Biomarkers with significant differences were further analyzed by adjudicated cause of 30-day mortality.
Results: Biomarkers from 680 patients were analyzed. Seven key inflammatory markers (IL-1ra, IL-6, IL-8, IL-10, eotaxin, IP-10, and MCP-1) were further analyzed. These cytokines were also noted to have the highest hazard ratios of death. Stepwise selection was used for multivariate analysis of survival by time point. MCP-1 at 2 hours, eotaxin and IP-10 at 12 hours, eotaxin at 24 hours, and IP-10 at 72 hours were associated with all-cause mortality.
Conclusion: Early systemic inflammatory markers are associated with increased risk of mortality after traumatic injury. Future studies should use these biomarkers to prospectively calculate risks of morbidity and causes of mortality for all trauma patients.
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http://dx.doi.org/10.1016/j.surg.2021.08.060 | DOI Listing |
Alzheimers Dement
December 2024
Columbia University Irving Medical Center, New York, NY, USA.
Background: Genetic studies indicate a causal role for microglia, the innate immune cells of the central nervous system (CNS), in Alzheimer's disease (AD). Despite the progress made in identifying genetic risk factors, such as CD33, and underlying molecular changes, there are currently limited treatment options for AD. Based on the immune-inhibitory function of CD33, we hypothesize that inhibition of CD33 activation may reverse microglial suppression and restore their ability to resolve inflammatory processes and mitigate pathogenic amyloid plaques, which may be neuroprotective.
View Article and Find Full Text PDFBackground: Neuroinflammation is a critical factor of Alzheimer's Disease (AD). Dysregulation of complement leads to excessive inflammation, direct damage to self-cells and propagation of injury. This is likely of particular relevance in the brain where inflammation is poorly tolerated and brain cells are vulnerable to direct damage by complement.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Missouri, Columbia, MO, USA.
Background: Despite data showing nutritional interventions high in antioxidant/anti-inflammatory properties (anthocyanin-rich foods such as blueberries/elderberries) may decrease risk of memory loss and cognitive decline, evidence for such effects in mild cognitive impairment (MCI) patients is limited. Therefore, we examined preliminary effects of American elderberry (Sambucus nigra canadensis) juice on cognition and inflammatory markers in MCI patients in a double-blind placebo-controlled trial.
Method: MCI patients (N = 24, M = 76.
Alzheimers Dement
December 2024
University of Georgia, College of Pharmacy, Athens, GA, USA.
Background: Reducing chronic inflammation has been linked to anti-inflammatory foods and may be implicated in treating Alzheimer's disease (AD). Plants produce antioxidants, such as phytochemicals, that appear to reduce the incidence of chronic inflammatory diseases. Phytochemicals may include active substances like polyphenols.
View Article and Find Full Text PDFImmunotherapy
January 2025
Blauvelt Consulting, LLC, Lake Oswego, OR, USA.
Aim: Lebrikizumab is an interleukin (IL)-13 inhibitor that specifically blocks IL-13 signaling. Here, we report the effects of lebrikizumab on asthma serum biomarkers in 2 phase 3 clinical studies.
Methods: LAVOLTA I and LAVOLTA II are replicate, double-blind, placebo-controlled trials with 52-week placebo-controlled treatment periods that evaluated lebrikizumab 37.
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