{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T11:07:20Z","timestamp":1779188840165,"version":"3.51.4"},"reference-count":35,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T00:00:00Z","timestamp":1772323200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T00:00:00Z","timestamp":1772323200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Int Med Res"],"published-print":{"date-parts":[[2026,3]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>In the pathogenesis of the post-injury period following nonpenetrating traumatic brain injuries (TBIs; post-TBIs), pathological metabolic changes in the oxidative status are important, as a complete understanding of their interactions can explain the concept of how oxidative metabolic\u2013related differences develop, thereby supporting effective treatment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This case\u2013control study included 63 patients (mean age\u2009\u00b1\u2009SD, 36.19\u2009\u00b1\u200911.4 years) in the post-TBI group and 32 healthy controls. Participants were tested for creatine kinase, adenosine triphosphate, and adenosine diphosphate levels using enzyme-linked immunosorbent assays and for pyruvate and lactate levels using a spectrophotometric method according to standard manufacturer protocols.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>This study found abnormally decreased adenosine triphosphate and adenosine diphosphate levels in the general nonpenetrating post-TBI group versus controls. The median total adenosine triphosphate levels were 600.4\u2009\u00b1\u200946.96 in the general clinical group and 745.7\u2009\u00b1\u200949.83\u2009mkmol\/L in controls (p\u2009&lt;\u20090.0001, t\u2009=\u200913.69, 95% confidence interval: 124.0 to 166.5). The median total adenosine diphosphate levels were 247.6\u2009\u00b1\u200933.09 in the general clinical group and 273.9\u2009\u00b131.98\u2009mkmol\/L in controls (p\u2009=\u20090.0004, t\u2009=\u20093.734, 95% confidence interval: 12.20 to 40.26). Compared with controls, elevated creatine kinase levels were found in the general clinical group (p\u2009&lt;\u20090.0001, t\u2009=\u20097.030, 95% confidence interval: \u221239.78 to \u221222.19). The median total creatine kinase (mean\u2009\u00b1\u2009SD) levels were 129.6\u2009\u00b1\u200921.37 in the general clinical group and 98.61\u2009\u00b1\u200919.74\u2009IU\/L in controls. Higher creatine kinase (p\u2009&lt;\u20090.0001, t\u2009=\u20094.779, 95% confidence interval: 13.16 to 32.23) and lower adenosine triphosphate levels (p\u2009&lt;\u20090.001, t\u2009=\u20094.997, 95% confidence interval: \u221270.74 to \u221230.31) were found to be more pronounced after brain contusion compared with those following mild TBIs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Nonpenetrating post-TBIs showed higher creatine kinase levels associated with lower adenosine triphosphate\u2013adenosine diphosphate levels, indicating oxidative dyshomeostasis at 12-month post-injury follow-ups, which could play a pathogenetic role in post-TBIs progression.<\/jats:p>\n                  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