P-188Hepatic sinusoidal obstruction syndrome (HSOS) in cStage III gastric cancer patients undergoing neoadjuvant chemotherapy with oxaliplatin: a retrospective cohort study

Introduction: Oxaliplatin containing chemotherapy is known to induce HSOS, which is also expressed by its appearance as “blue liver syndrome”. Although it depends on its severity, HSOS could increase morbidity and mortality in surgical patients (pts) and has been well estimated in colorectal liver metastases treated with FOLFOX. However, there are very few reports which refer to oxaliplatin-induced HSOS in gastric cancer, especially in the neoadjuvant chemotherapy (NAC) setting. Here, we assessed HSOS in cStage III gastric cancer pts treated with NAC SOX regimen (S-1 80-120 mg/day according to BSA for 2 weeks, oxaliplatin 130 mg/m2 on day 1, every 3 weeks, 2 courses). Methods: In pts with cStage III gastric cancer treated with NAC SOX, we retrospectively measured spleen volume (determined by CT volumetric measurements), platelet counts, and ICG retention rate at 15 minutes (ICG-R15) before and after NAC prior to gastrectomy, and graded blue liver macroscopically during gastrectomy to assess the relationship between chemotherapy exposure and hepatic sinusoidal injury. Results: A total of 38 cStage III gastric cancer pts were enrolled: median age 68.9 (40-84), 29 male and 9 female. Spleen volume increased in 29 pts (76.3%): ≧ 30% increase in 8 pts (21.1%) and ≧ 50% increase in 2 pts (5.3%). Macroscopic blue liver was recognized in 23 pts (60.5%). A relationship between increases in spleen volume and macroscopic blue liver was not recognized. Pts with abnormal ICG-R15 values (≧10%) increased after NAC (before vs after NAC, 4 vs 11; P = .035), and platelet counts decreased after NAC (median 24.5 vs 19.6 ×10 4 /μl; P = .0039). Pts with macroscopic blue liver decreased more in liver functional reserve after NAC (a numerical difference of ICG-R15 values before and after NAC, median 4.3 vs 2.1%; P = .163), and in platelet counts (a numerical difference of platelet counts before and after NAC, median -8.3 vs -3.4 ×10 4 /μl; P = .0006). Pts with splenic enlargement ≧ 30% also decreased more in liver functional reserve after NAC (median 8.2 vs 3.0%; P = .063), but did not decrease in terms of platelet counts (median -6.9 vs -6.3; P = 1 ). Conclusion: The present study suggests that HSOS could be caused by just two courses of oxaliplatin-containing NAC in gastric cancer pts and can lead to poor liver functional reserve and thrombocytopenia. Increases in spleen volume might not have been relevant with regards to macroscopic blue liver, but it correlated with a decrease in liver functional reserve. Clinical trial information: UMIN000036139