Increased Liquefactive Necrosis Formation After Transarterial Chemoembolization Combined with Molecular Targeted Agents Plus Immune Checkpoint Inhibitors for Hepatocellular Carcinoma

Abstract

Purpose

In clinical practice, we found some of the patients who received transarterial chemoembolization (TACE) with molecular targeted agents (MTGs) plus immune checkpoint inhibitors (ICIs) for hepatocellular carcinoma (HCC) had obvious liquefactive necrosis formation within the tumor and some even progressed to a liver abscess, which seems more frequent than patients who received other treatments. Thus, we aim to identify this condition and analyze the potential risk factors.

Patients and Methods

Medical records of 72 consecutive patients with intermediate (BCLC B) and advanced (BCLC C) HCC who received TACE plus MTGs combined with (n=30) or without (n=42) ICIs were reviewed. Liquefactive necrosis formation was defined as the presence of obvious liquefactive necrosis within the tumor that required intervention.

Results

The liquefactive necrosis rate was higher in the TACE+MTGs+ICIs group than in the TACE+MTGs group (30% vs 4.8%, P=0.006). Moreover, 18.2% (2/11) of the patients with liquefactive necrosis within the tumor had a bacterial infection. We then take the binary logistic regression analysis model to identify the predictors of liquefactive necrosis formation, and which showed the tumor size (P=0.006, OR=1.355, 95% CI: 1.090–1.684), alpha-fetoprotein level (P=0.036, OR=6.745, 95% CI: 1.130–40.262) and treatment modality (P=0.015, OR=11.717, 95% CI: 1.617–84.887) were the independent risk factor for liquefactive necrosis formation within the tumor.

Conclusion

Patients with HCC who received TACE combined with MTGs plus ICIs have increased liquefactive necrosis formation, and the larger tumor size and higher alpha-fetoprotein level were associated with more liquefactive necrosis formation within the tumor.

Keywords:

• liver cancer
• transarterial chemoembolization
• molecular targeted agents
• immune checkpoint inhibitors
• liquefactive necrosis

Acknowledgments

This work was funded by grants from the National Natural Science Foundation of China [81873917] and China Health Promotion Foundation [XM_2018_011_0006_01].

Disclosure

The authors report no conflicts of interest in this work.