Articles: treatment.
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Background: Acute respiratory distress syndrome (ARDS) is a serious pathological process with high mortality. Ferroptosis is pivotal in sepsis, whose regulatory mechanisms in sepsis-induced ARDS remains unknown. We aimed to determine key ferroptosis-related genes in septic ARDS and investigate therapeutic traditional Chinese medicine. ⋯ Conclusions: Ferroptosis-related genes of IL1B , MAPK 3, and TXN serve as potential diagnostic genes for sepsis-induced ARDS. Sea buckthorn may be therapeutic medication for ARDS. This study provides a new direction for septic ARDS treatment.
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In recent years, it has become apparent that fibrinolytic dysfunction and endotheliopathy develop in up to 40% of patients during the first hours following thermal injury and are associated with poor outcomes and increased resuscitation requirements. Rapidly following burn injury, the fibrinolytic system is activated, with activation generally greater with increased severity of injury. Very high plasma concentrations of plasmin-antiplasmin complex (marker of activation) have been associated with mortality. ⋯ Here we review the incidence and effects of these responses after burn injury and explore mechanisms and potential interactions with the early inflammatory response. Available data from burn and nonburn trauma suggest that the fibrinolytic, endothelial, and inflammatory systems interact extensively and that dysregulation in one may exacerbate dysregulation in the others. This raises the possibility that successful treatment of one may favorably impact the others.
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Anesthesia and analgesia · Jan 2025
Association Between Preoperative Anemia and Cognitive Function in a Large Cohort Study of Older Patients Undergoing Elective Surgery.
The etiology of anemia has tremendous overlap with the disease states responsible for cognitive decline. We used data from a perioperative database of older adults undergoing elective surgery with anesthesia to (1) examine relationships among preoperative anemia blood markers, preoperative screeners of cognitive function, and chronic disease status; and (2) examine the relationship of these factors with operative outcomes. The primary goal of this study was to investigate the association between preoperative anemia blood markers and cognition measured by a preoperative cognitive screener. Secondary goals were to (1) examine the relationship between preoperative anemia blood markers and chronic disease states (ie, American Society of Anesthesiologists [ASA] and frailty), and (2) investigate the relationship of preoperative anemia blood markers and cognition with operative outcomes (ie, discharge disposition, 1-year mortality, number of surgical complications, length of hospital stay, and length of intensive care unit [ICU] stay). ⋯ In this first medicine study, we established relationships among anemia, preoperative markers of frailty and cognition, and chronic disease states in a large cohort of older patients undergoing elective surgery in a large tertiary medical center. We found that anemia, cognitive vulnerability, and chronic health disease states predicted death within 1 year of surgery, and that these preoperative factors negatively contribute to surgical outcomes such as time in the ICU, length of hospital stay, nonhome discharge, and 1-year mortality. The World Health Organization (WHO) and many academic medical societies have urged the adoption of patient blood management (PBM) disciplines, yet anemia is not routinely optimized as a preoperative risk factor. Given the well-defined association between preoperative anemia and postoperative morbidity and mortality, performing elective surgery on an untreated anemic patient should be considered substandard care. With established safe and effective treatment regimens, iron deficiency anemia is a modifiable preoperative risk factor that should be addressed before elective surgery.
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Treatment of patients who present with poor clinical condition is often postponed until neurological improvement is observed. Despite previous studies, it is still unclear how survivors perceive their quality of life (QoL). This study aimed to evaluate self-perceived QoL in patients with aneurysmal subarachnoid hemorrhage who present with poor clinical condition, as defined by World Federation of Neurosurgical Societies (WFNS) grades 4 to 5, compared with those who present in more favorable clinical condition (WFNS 1-3). ⋯ High-grade WFNS patients rated their QoL as satisfactory, with only a marginal 5-point difference on a 100-point scale compared with low-grade WFNS patients. In addition, almost three-quarters of high-grade WFNS survivors achieved a favorable outcome. Given that a subset of patients, despite presenting with a poor clinical condition, still achieve a favorable outcome, these findings reinforce our perspective advocating for early and comprehensive treatment.
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Osteoarthritis (OA) is a highly prevalent and disabling joint disease, characterized by pathological progressive joint deformation and clinical symptoms of pain. Disease-modifying treatments remain unavailable, and pain-mitigation is often suboptimal, but recent studies suggest beneficial effects by inhibition of the voltage-gated sodium channel Na V 1.7. We previously identified compound 194 as an indirect inhibitor of Na V 1.7 by preventing SUMOylation of the Na V 1.7-trafficking protein, collapsin response mediator protein 2. ⋯ We found that the monoiodoacetate model induced (1) increased pain-like behaviors and calcium responses of glutamatergic neurons in the parabrachial nucleus after evoked cold and mechanical stimuli, (2) conditioned place aversion to mechanical stimulation, (3) functional weight bearing asymmetry, (4) increased sodium currents in dorsal root ganglia neurons, and (5) increased calcitonin gene-related peptide-release in the spinal cord. Crucially, administration of 194 improved all these pain-related outcomes. Collectively, these findings support indirect inhibition of Na V 1.7 as an effective treatment of OA-related pain through the inhibition of collapsin response mediator protein 2-SUMOylation via compound 194.