Pro- and antiinflammatory cytokine production after radiofrequency ablation of unresectable hepatic tumors

BACKGROUND: Experience using radiofrequency ablation (REA) for treating unresectable hepatic malignancies is expanding, with promising outcomes and fewer complications compared with cryotherapy. This study examined systemic inflammatory responses after REA as measured by the appearance of postoperative symptoms and cytokine production. STUDY DESIGN: Seventeen patients (11 men, 6 women) aged 40 to 85 years (mean 64.2 years) with unresectable primary and metastatic hepatic tumors underwent REA. Mean liver volume treated with REA was 35.3% +/- 3.6% (SEM) (median 36.8%). Plasma cytokines (tumor necrosis factor-alpha, interleukin [IL]-1beta, IL-Ira, IL-6, IL-8, IL-10, p55, and p75) were measured from anesthesia induction through 48 hours after RFA. Ex vivo whole-blood cytokine production was measured at baseline, 24 hours, and 48 hours after REA. RESULTS: Cytokine and cytokine-receptor production were not notably altered by REA. Ex vivo whole-blood endotoxin stimulation indicated that intrinsic cellular immune function remained intact after treatment, although modest decreases in Stimulated tumor necrosis factor a production were observed 24 to 48 hours after REA. Variceal bleeding, hepatic failure, and death occurred in one patient 30 days after RFA. None of the remaining patients exhibited tachycardia or hypotension. Fevers (greater than or equal to38.5degreesC) developed in three patients during the First 48 hours postoperatively. There was no association between plasma cytokines and postoperative complications. CONCLUSIONS: In contrast to previous reports using cryotherapy, systemic inflammatory responses as measured by increased cytokines were not observed after REA. The cryotherapy-induced "cryoshock" phenomenon was not observed in patients undergoing RFA in our study. We conclude that REA ablation is fundamentally different than cryotherapy and apparently does not stimulate Kupffer and other hepatic macrophages to produce proinflammatory cytokines.