Clinical trials

Trauma triggers a complex immune response intended to eliminate danger signals and restore physiological balance. Early post-traumatic inflammation is primarily initiated by damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs). In patients with severe trauma, dysregulated inflammation increases susceptibility to infection, systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome (MODS), and mortality. The lungs are particularly vulnerable, and excessive inflammatory activation may lead to acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), conditions characterized by increased vascular permeability, alveolar epithelial injury, surfactant dysfunction, and impaired gas exchange. Pro-inflammatory cytokines, activated neutrophils, reactive oxygen species, and proteases contribute to endothelial and epithelial barrier disruption. Recent evidence also suggests that several microRNAs, including miR-126, may play a regulatory role in pulmonary barrier integrity through modulation of tight-junction proteins and PI3K/AKT-related pathways. Although many components of the trauma-related inflammatory response have been described, the relationship between systemic inflammatory severity and impairment of pulmonary gas exchange remains insufficiently defined in clinical settings. This study aims to investigate the correlation between inflammatory severity markers (C-reactive protein, procalcitonin, IL-6, reactive oxygen derivatives, neutrophil-to-lymphocyte ratio, lactate), imaging findings (flow-mediated dilation by ultrasound), clinical parameters (blood pressure, heart rate, urine output, vasoactive medication requirements), pulmonary gas-exchange measurements (arterial blood gases, PaO₂/FiO₂ ratio), and circulating miRNA-126 levels in trauma patients. The findings may help identify biomarkers that better reflect inflammatory burden and the risk of lung dysfunction following trauma.

In cases of meningitis caused by external ventricular catheters (EVDs), which are the most commonly placed intracranial catheters that can lead to central nervous system infection through contamination/colonisation, the diagnosis may not be differentiated by either clinical signs and symptoms or conventional cerebrospinal fluid (CSF) tests. Therefore, due to the limitations in diagnosis and prognostic prediction of EVD-induced meningitis and the high mortality/morbidity rates of the disease, markers with high sensitivity and specificity in post-operative meningitis are needed. Calcitonin gene-related peptide (CGRP), a neuropeptide, has been shown to increase when C or Aδ sensory fibres are damaged or in the presence of inflammation in tissues adjacent to the fibres. CGRP is localised in nociceptive nerve terminals together with another neuropeptide, substance P, which has similar biological effects. There are very few studies investigating how CGRP levels in CSF and serum change in bacterial meningitis. Although it is thought that nociception and neuroimmune interactions affect meningeal antibacterial host defence, that nociceptors signal via CGRP to meningeal immune cells during infection, and that this neuroimmune axis exacerbates bacterial meningitis by weakening host defence, it is not yet clear how CGRP and substance P levels affect disease prognosis. This study will evaluate the utility of CGRP and substance P levels as biomarkers to assess diagnosis and treatment response in patients with post-operative meningitis followed in the intensive care unit.