ABSTRACT
BACKGROUND/AIMS: Endoscopic injection sclerotherapy is in widespread use for patients with esophageal varices. It is well known that pleural effusions are among complications following endoscopic sclerotherapy. However, there are few studies regarding the proportion of patients developing pleural effusions after sclerotherapy. METHODOLOGY: Between August 1991 and September 1998, 575 endoscopic injection sclerotherapies were carried out in 128 patients. Chest radiographs were obtained prior to and 24 hours after all procedures. We also obtained other clinical data from all patients. RESULTS: In total, 17.7% of post-sclerotherapy patients were diagnosed as having small amounts of pleural effusions. Logistic regression revealed pleural effusions after sclerotherapy to be associated with ascites, chest pain for 24 hours, total volume of sclerosant and submucosal injection of more than 4mL of sclerosant. In parallel with injection of an increasing amount of submucosal sclerosant, the proportion of patients with pleural effusion increased. CONCLUSIONS: Pleural effusions were related to ascites, chest pain for 24 hours, total sclerosant volume and submucosal injection of sclerosant.
Subject(s)
Esophageal and Gastric Varices/therapy , Liver Cirrhosis/therapy , Pleural Effusion/etiology , Sclerotherapy/adverse effects , Ascites/etiology , Chest Pain/etiology , Endoscopy/adverse effects , Female , Humans , Injections/adverse effects , Logistic Models , Male , Middle Aged , Oleic Acids/administration & dosage , Oleic Acids/adverse effects , Retrospective Studies , Sclerosing Solutions/administration & dosage , Sclerosing Solutions/adverse effectsABSTRACT
BACKGROUND: Activation of both CD4+ T and CD8+ T cells is triggered by the engagement of the T cell antigen receptor (TCR) with MHC/peptide complexes on antigen-presenting cells. This process also requires other molecular interactions, which transmit co-stimulatory signals to these T cells. To ensure an effective immune response, distinct T cell subsets may additionally employ unique mechanism(s) for efficient activation. RESULTS: We here show that mutant CD8+ T cells lacking the IFN-alpha/beta signalling components are hyporesponsive to antigen stimulation in vitro. We further show that IFN-alpha/beta-mediated signals are required for induction of the chemokines IP-10/I-TAC and their common receptor, CXCR3, and in turn provide evidence that CXCR3-mediated signals indeed function in the activation and proliferation of CD8+ T cells, particularly for the CD44low naive phenotype cells. CONCLUSION: The CXCR3 chemokine system is regulated by IFN-alpha/beta in CD8+ T cells, and it is critical for the efficient cell activation. The present study therefore reveals a novel role of the IFN-alpha/beta-CXCR3 signalling cascade in CD8+ T cell activation.