Studies have suggested that patients with severe head injury, in addition to Glasgow Coma Scale (GCS), reveal high D-dimer levels which are independently associated with increased mortality. In the present review, we analyzed the literature where studies have reported the role of D-dimers as a potential biomarker in stratification and early identification of patients with TBI who are at risk of clinical deterioration, where early intervention can improve overall outcomes. After scrutinizing 246 articles, which were narrowed down to 38 (16 prospective, 9 retrospective, 2 RCTs, 2 case-control, 1 cross-sectional study). All these studies included 7,589 patients, in whom D-dimer was measured at different timings and in different ways. Most studies demonstrated significant changes that could be utilized for prognostication. However, we also observed instances where no significant changes were found. Unfortunately, direct comparisons were hindered by variations in the methods used to measure D-dimer across different outcomes. Limitations included the lack of a substantial number of RCTs, heterogeneity of available data, and the difficulty in summarization of specific cutoff points for D-dimer. Future studies, especially RCTs, should measure D-dimer levels at different times from injury for an accurate assessment of its correlation with outcomes.

Paracetamol (PCM) hepatotoxicity is related to reactive oxygen species (ROS) formation and excessive oxidative stress; natural antioxidant compounds have been tested as an alternative therapy. This study evaluated the hepatoprotective activity of an alcoholic extract of Boswellia ovalifoliolata (BO) bark against PCM-induced hepatotoxicity. BO extract also demonstrated antioxidant activity in vitro, as well as scavenger activity against 2, 2-diphenyl-1-picrylhydrazyl. Administration of PCM caused a significant increase in the release of transaminases, alkaline phosphatase, and lactate dehydrogenase in serum. Significant enhancement in hepatic lipid peroxidation and marked depletion in reduced glutathione were observed after parac intoxication with severe alterations in liver histology. BO treatment was able to mitigate hepatic damage induced by acute intoxication of PCM and showed a pronounced protective effect against lipid peroxidation, deviated serum enzymatic variables, and maintained glutathione status toward control. The results clearly demonstrate the hepatoprotective effect of BO against the toxicity induced by PCM.
Acetaminophen ; adverse effects ; Alkaline Phosphatase ; blood ; Animals ; Antioxidants ; metabolism ; pharmacology ; therapeutic use ; Biphenyl Compounds ; metabolism ; Boswellia ; Chemical and Drug Induced Liver Injury ; drug therapy ; metabolism ; pathology ; Glutathione ; metabolism ; L-Lactate Dehydrogenase ; blood ; Lipid Peroxidation ; drug effects ; Liver ; drug effects ; metabolism ; pathology ; Liver Function Tests ; Male ; Oxidative Stress ; drug effects ; Phytotherapy ; Picrates ; metabolism ; Plant Bark ; Plant Extracts ; pharmacology ; therapeutic use ; Rats, Wistar ; Transaminases ; blood