Hepatocellular carcinoma vascularization: From the most common to the lesser known arteries

AbstractHepatocellular carcinoma is the sixth most common cancer throughout the world. It is almost exclusively arterially vascularized, unlike the vascularization of the liver, which has a dual supply with a portal component of 75 to 80% and an arterial component of 20 to 25%. The reference treatment for intermediary stages of the Barcelona (B) classification is hepatic artery chemoembolization. The aim of chemoembolization is to inject the tumor chemotherapy into the artery and then to embolize the artery (or arteries), which supply the tumor. For this, knowledge of the anatomy of the hepatic artery is essential. Approximately 55% of the patients belong to the modal distribution, although numerous anatomical variants exist and must be recognized. In addition, primarily non-hepatic arteries may contribute to the vascularization of some hepatocellular carcinomas. Furthermore, new arterial supplies can be recruited by tumors after surgical or chemoembolization treatments. The aim of this article is to describe the different arteries, which may vascularize hepatocellular carcinomas. These arteries must be looked for, recognized, and reported by the radiologist on cross-section examinations in the pre-treatment assessment

Interleukin-10 release related to cardiopulmonary bypass in infants undergoing cardiac operation

peer reviewedTo evaluate cytokine balance related to cardiopulmonary bypass, we prospectively investigated 11 infants undergoing cardiac operations for congenital heart disease. Proinflammatory cytokines (tumor necrosis factor- α and interleukin-8) and the antiinflammatory cytokine interleukin-10 were measured at multiple time points before, during, and after bypass. Tumor necrosis factor-α and interleukin-8 values were within normal range before the operation. These values increased significantly during bypass, reaching their peaks after protamine administration (tumor necrosis factor-α, 133.6 ± 124.9 pg/ml; mean ± standard deviation; p < 0.005) and 2 hours after termination of the procedure (interleukin-8, 92.1 ± 44.1 pg/ml; p < 0.01). Tumor necrosis factor-α and interleukin-8 equaled normal prebypass values from the first postoperative day on. Interleukin-10 levels were within normal range before the operation and were already significantly increased 10 minutes after initiation of bypass (interleukin-10, 39.4 ± 34.3 pg/ml; p < 0.05). These levels remained elevated throughout the procedure but returned to normal after protamine administration. A second significant release of interleukin-10 occurred from the early postoperative period on, reaching its peak 24 hours after termination of cardiopulmonary bypass (interleukin-10, 351.6 ± 304.0 pg/ml; p < 0.01). Interleukin-10 values were normal on the second postoperative day in all patients. Interleukin-10 kinetics showed an inverse pattern compared with tumor necrosis factor-α and interleukin-8. This difference suggests an interplay between proinflammatory and antiinflammatory cytokines released during and after cardiopulmonary bypass. Interleukin-10 levels measured 4 and 24 hours after bypass strongly correlated with the degree of hypothermia during bypass (Spearman's correlation coefficient, -0.77 [p < 0.01] and -0.89 [p < 0.0005], respectively); these levels did not correlate with duration of bypass and aortic crossclamping, however. This result suggests that besides immunologically mediated production of interleukin-10, hypothermia itself could modulate interleukin-10 production. In conclusion, this study demonstrates interleukin-10 production, in addition to interleukin-8 and tumor necrosis factor-α synthesis, in response to cardiopulmonary bypass in infants. Interleukin-10 could play a protective role by down-regulating proinflammatory cytokine release during and after cardiopulmonary bypass