ABSTRACT
OBJECTIVE: Traumatic brain injury (TBI) necessitates reliable biomarkers to improve patient care. This study explored copeptin as a potential biomarker in TBI and its relation to vasopressin (ADH) in such patients. METHODS: A cross-sectional study was conducted on 50 TBI patients. Exclusion criteria included specific medical conditions and recent traumatic events. Copeptin and ADH testing were performed within 30 days post-trauma. Patient data, Glasgow Coma Scale (GCS) scores, imaging results, and the need for surgical intervention were obtained from medical charts. RESULTS: Copeptin levels negatively correlated with GCS scores (ρ = - 0.313, p = 0.027), indicating a potential association with trauma severity. Copeptin levels (mean: 3.22 pmol/L, median 2.027 pmol/L, SD = 3.15) tended to be lower than those found in the normal population, suggesting possible neuroendocrine dysfunction post-TBI. ADH levels (mean: 67.93 pmol/L, median 56.474 pmol/L SD = 47.67) were higher than the normal range and associated with the need for surgery (p = 0.048). Surprisingly, copeptin and ADH levels negatively correlated (r = - 0.491; p < 0.001), potentially due to differences in degradation processes and physiological variations in TBI patients. CONCLUSION: Copeptin shows potential as a predictive biomarker for assessing TBI severity and predicting patient outcome. However, its complex relationship with ADH in TBI requires further investigation. Careful interpretation is needed due to potential variations in excretion dynamics and metabolism. Larger studies on TBI patient cohorts are essential to validate copeptin as a reliable biomarker and improve patient care in TBI.
ABSTRACT
BACKGROUND: Ghrelin is the orexigenic hormone secreted mainly by the stomach. Its involvement in neoplastic development has been studied in gastrointestinal adenocarcinomas. Our paper aims to evaluate the influence of the ghrelin axis in gastrointestinal stromal tumors (GISTs). MATERIALS AND METHODS: The study design included two groups of patients, 46 with gastric GISTs and 30 with obesity. Archived tissue samples were evaluated for the presence of gastritis and H. pylori. Immunohistochemical expression of ghrelin and its receptor (GHS-R) was assessed. RESULTS: All GISTs showed absent immunohistochemical expression for ghrelin, while GHS-R displayed a particular pattern, with notable differences in intensity (p = 0.0256) and percentage of stained cells (p < 0.00001) in the periphery vs. core of tumors. Positive ghrelin expression was lower in the gastric mucosa of the first group compared to the second group (p < 0.001). CONCLUSION: The ghrelin axis can influence GISTs carcinogenesis through activation of GHS-R. A previously described direct autocrine/paracrine mechanism is not supported by our findings.
