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. 2018 Jan 1;9(1):13-20.
doi: 10.7150/jca.21460. eCollection 2018.

Inflammatory Response and Toxicity After Pressurized IntraPeritoneal Aerosol Chemotherapy

Affiliations

Inflammatory Response and Toxicity After Pressurized IntraPeritoneal Aerosol Chemotherapy

Hugo Teixeira Farinha et al. J Cancer. .

Abstract

Background: Pressurized Intraperitoneal Aerosol Chemotherapy (PIPAC) is a novel mode of intraperitoneal (IP) drug delivery claiming high IP tissue concentrations with low systemic uptake. The aim was to study inflammatory response and systemic toxicity after PIPAC. Methods: Retrospective monocentric analysis of a consecutive cohort of PIPAC patients between January 2015 and April 2016. Detailed hematological and biochemical analysis was performed the day before surgery and once daily until discharge. Comparative statistics were performed using Mann-Whitney U test and Wilcoxon signed ranked test. Results: Fourty-two consecutive patients underwent a total of 91 PIPAC procedures. Twenty patients received oxaliplatin and 22 cisplatin+doxorubicin (37 vs. 54 procedures). Creatinine, AST and ALT were not significantly altered after PIPAC (p=0.095, p= p=0.153 and p=0.351) and not different between oxaliplatin and cisplatin+doxorubicin regimens (p=0.371, p=0.251 and p=0.288). C-reactive protein (CRP) and procalcitonin (PCT) increased on post-operative day (POD) 2: ∆max 29±5 mg/L (p<0.001) and ∆max 0.05±0.01 μg/L (p=0.005), respectively. Leucocytes increased at POD 1: ∆max 2.2±0.3 G/L (p<0.001). Albumin decreased at POD 2: ∆max -6.0±0.5 g/L (p<0.001). CRP increase correlated positively with Peritoneal Cancer Index (tumor load) (ρ =0.521, p<0.001). Conclusion: PIPAC was followed by a modest and transitory inflammatory response that was commensurate to the disease extent. No hematological, renal or hepatic toxicity was observed even after repetitive administration.

Keywords: Intraperitoneal Chemotherapy; PIPAC; Peritoneal Carcinomatosis; Toxicity.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interest exists.

Figures

Figure 1
Figure 1
Hepato-renal toxicity after Pressurized Intraperitoneal Aerosol Chemotherapy (PIPAC) treatment by chemotherapy regimen (Oxaliplatin vs. Cisplatin and Doxorubicin) n Oxaliplatin, ▲ Cisplatin + Doxorubicin, Bars represent standard error of the mean (SEM), IR (Institutional Reference, U/L) Hepato-renal toxicity after PIPAC treatment by chemotherapy regimen until postoperative day (POD) 4. AST - aspartate aminotransferase, ALT - alanine aminotransferase.
Figure 2
Figure 2
Hepato-renal toxicity after repetitive Pressurized Intraperitoneal Aerosol Chemotherapy (PIPAC) procedures. Hepato-renal toxicity under PIPAC treatment represented by AST, ALT and Creatinine levels. Δ represents Δmax. No significant difference (p<0.05) was found for repetitive PIPAC applications. AST - aspartate aminotransferase, ALT - alanine aminotransferase.
Figure 3
Figure 3
Inflammatory response after Pressurized Intraperitoneal Aerosol Chemotherapy (PIPAC) by chemotherapy regimen. n Oxaliplatin ▲Cisplatin +Doxorubicin. Inflammatory response under PIPAC treatment by chemotherapy regimen until postoperative day (POD) 4. Bars represent standard error of the mean (SEM).
Figure 4
Figure 4
Inflammatory response after repetitive Pressurized Intraperitoneal Aerosol Chemotherapy (PIPAC) procedures. Inflammatory response under PIPAC treatment represented by C-reactive protein at post-operative day (POD) 2, Procalcitonin at POD 2, Leukocytes at POD 1 and Albumin at POD 2. Bars represent standard error of the mean (SEM). Δ represents Δmax. No significant difference was found when inflammatory response was compared before and after different PIPAC applications.
Figure 5
Figure 5
Tumor load and post- Pressurized Intraperitoneal Aerosol Chemotherapy (PIPAC) inflammation. C-reactive protein (CRP) was plotted against the extent of peritoneal disease (measured by the Peritoneal Cancer Index (PCI)).

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