Background Hepatic ischemia-reperfusion injury (IRI) is a complex process involving multiple mediators that initiate inflammatory responses, ultimately leading to cell necrosis and apoptosis. During hepatic IRI, various inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), and reactive oxygen species (ROS) exacerbate liver injury. Infliximab is an antibody that neutralizes TNF-α, and suppression of TNF-α activity with infliximab treatment can protect the liver from IRI. Splenectomy also alleviates hepatic IRI by decreasing neutrophil infiltration, reducing the release of ROS into the hepatic sinusoids, and suppressing TNF-α release. This study aimed to evaluate the effects of infliximab on hepatic IRI based on inflammatory responses, oxidative stress, and apoptosis, and to compare these effects with those of splenectomy.
Methods Twenty-four rats were randomly assigned to the following four groups: (1) sham, (2) hepatic ischemia-reperfusion (IR), (3) hepatic IR with 10 mg/kg infliximab, and (4) hepatic IR with splenectomy. Each group consisted of six rats. Hepatic ischemia was induced for 30 minutes, followed by 2 hours of reperfusion injury. Infliximab was administered intraperitoneally 1 hour before surgery and splenectomy was performed immediately before hepatic ischemia.
Results Infliximab and splenectomy downregulated the levels of liver enzymes (aspartate aminotransferase [p<0.001 for all] and alanine aminotransferase [p<0.001 for all]), a prooxidant (malondialdehyde [p=0.006 for infliximab; p<0.001 for splenectomy]), inflammatory cytokines (TNF-α and nuclear factor kappa B [p<0.001 for all]), and an apoptotic mediator (caspase-3 [p=0.005 for infliximab; p=0.004 for splenectomy]) compared with those with hepatic IR alone.
Conclusion Infliximab treatment and splenectomy mitigated hepatic IRI. These protective effects are likely mediated via anti-inflammatory, antioxidative, and antiapoptotic pathways within the pathophysiology of hepatic IRI.
Immune thrombocytopenia (ITP) is a disease in which thrombocytopenia occurs because of immune-mediated platelet destruction and decreased platelet production. Although many pediatric patients with ITP experience spontaneous remission or reach remission within 12 months of first-line therapy, approximately 20% progress to chronic ITP. Patients who do not respond to first-line treatment or experience frequent relapses are of great concern to physicians. This review summarizes recent treatments for second-line treatment of pediatric chronic ITP.
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Beta-Thalassemia with Initial Presentation as Immune Thrombocytopenia: A Case Report Hyun Sik Kang Clinical Pediatric Hematology-Oncology.2023; 30(1): 42. CrossRef