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Purpose: The aim of the present study was to investigate the effect of etanercept (ETA) on histopathological and biochemical changes after traumatic brain injury (TBI) in rats. Materials and Methods: Thirty-six male Wistar albino rats were distributed into three groups (n = 12 each). Control group rats were not subjected to trauma. Trauma group rats were subjected to TBI only. ETA group rats were subjected to TBI plus ETA (5 mg/kg intraperitoneal [i.p.]). The groups were further subdivided into those sacrificed in the hyperacute stage (1 h after TBI) (control-1, trauma-1, and ETA-1 groups) and the acute stage (6 h after TBI) (control-6, trauma-6, and ETA-6 groups). Tissue levels of tumour necrosis factor-alpha, interleukin-1 beta, malondialdehyde, catalase, glutathione peroxidase, and superoxide dismutase were analyzed. Histopathological and ultrastructural evaluations were also performed. Results: i.p. administration of ETA at 1 and 6 h significantly reduced inflammatory cytokine expression, attenuated oxidative stress and lipid peroxidation, prevented apoptosis, and increased antioxidant defense mechanism activity in comparison to trauma group. Histopathological and ultrastructural abnormalities were significantly reduced in ETA-treated rats compared to closed head injury trauma groups. Conclusions: ETA significantly improves neural function and prevents post-TBI histopathological damage in rats.

Background: The aim of our study is to assess the neuroprotective effects of the tumor necrosis factor alpha (TNF-α) inhibitor etanercept (ETA) on histopathological and biochemical changes following spinal cord injury (SCI). Patients and Methods: Fifty-four male Wistar albino rats were randomly assigned into three main groups: The sham, trauma, and ETA group (n = 18 per group). Each of these groups was further divided into three subgroups (n = 6 per subgroup) based on the different tissue sampling times postinjury: 1 h, 6 h, and 24 h. Clip compression model was used for SCI. Rats in the ETA group were treated with 5 mg/kg of ETA immediately after the clip was removed. After 1, 6, and 24 h, the spinal cord was totally removed between the levels T8–T10. Sample tissue was immediately harvested and fixed for histopathological and electron microscopic examination and were analyzed for TNF-α, interleukin-1β (IL-1β), superoxide dismutase (SOD), adenosine deaminase, catalase (CAT), and malondialdehyde levels in both the tissue and serum. Results: The serum and tissue levels of cytokines and enzymes were seen to change after SCI between hyperacute, acute, and subacute stages. Treatment with ETA selectively inhibited TNF-α, and IL-1β expression together with increased levels of antioxidative enzymes (SOD, CAT). Conclusion: Early administration of ETA after SCI may remarkably attenuate neuronal injury by decreasing tissue and serum TNF-α and IL-1β levels, while increasing antioxidative enzymes such as SOD and CAT in subacute and acute stages, respectively.

Severe complications that develop in the early stages in patients with acute leukemia have a mortal course. Bleeding, leukostasis, and less frequently, infections are responsible for early mortality. Hemorrhage is most common in acute leukemia and usually leads to death. Hemorrhage may occur due to chemotherapy or bone marrow transplantation in patients with acute leukemia. Leukocytosis, thrombocytopenia, sepsis, and coagulopathy increase the risk of bleeding. There may be multiple etiologic factors. Subdural or subarachnoid hemorrhage is less common than an intra-axial hemorrhage. The incidence of spontaneous subdural hematoma is higher in patients with leukemia. Although advances in the treatment of platelet transfusion and disseminated intravascular coagulation have decreased the incidence of hemorrhagic complications in patients receiving chemotherapy for acute leukemia, intracranial hemorrhage-related deaths are a significant problem. We discussed the etiology and management of chronic subdural hematoma detected in a two-year-old male patient with Acute Myeloid Leukemia and hyperleukocytosis.