Clinical Experience with Cryosurgery for Advanced Hepatobiliary Tumors

Haddad, F.; Chapman, William C.; Wright, J. Kelly; Blair, Taylor K.; Pinson, C. Wright

doi:10.1006/jsre.1998.5280

Cited by 53 publications

(21 citation statements)

References 20 publications

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“…The significant complications may occur when more than 35% of the liver volume is treated by cryoablation, but ablation of small areas of the liver is usually well tolerated [20,21]. In addition, because patients with multiple liver metastases or tumors of more than 4 cm in diameter have an unfavorable prognosis [22], the numbers and sizes of metastases should be considered.…”

Section: Discussionmentioning

confidence: 99%

Serum cytokine levels in response to hepatic cryoablation

Osada

Imai

Tomita

et al. 2007

Journal of Surgical Oncology

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Section: Discussionmentioning

confidence: 99%

Serum cytokine levels in response to hepatic cryoablation

Osada

Imai

Tomita

et al. 2007

Journal of Surgical Oncology

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“…1 However, complete tumor resection in patients with three or fewer metastatic foci results in a 30% to 35% 5-year survival rate, compared with less than 5% for patients not undergoing resection, 22 in nonrandomized studies. Hepatic tumor ablation with cryoablation and RFA has been applied to patients with unresectable tumors with results that appear to be similar to those of conventional surgical resection, 5,6,12 although most series still have relatively short follow-up and small numbers of patients, and there have been no controlled trials comparing these techniques.…”

Section: Discussionmentioning

confidence: 99%

Hepatic Cryoablation, But Not Radiofrequency Ablation, Results in Lung Inflammation

Chapman

Debelak²,

Pinson³

et al. 2000

Annals of Surgery

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110

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ObjectiveTo compare the effects of 35% hepatic cryoablation with a similar degree of radiofrequency ablation (RFA) on lung inflammation, nuclear factor B (NF-B) activation, and production of NF-B dependent cytokines. Summary Background DataMultisystem injury, including acute lung injury, is a severe complication associated with hepatic cryoablation of 30% to 35% or more of liver parenchyma, but this complication has not been reported with RFA. MethodsSprague-Dawley rats underwent 35% hepatic cryoablation or RFA and were killed at 1, 2, and 6 hours. Liver and lung tissue were freeze-clamped for measurement of NF-B activation, which was detected by electrophoretic mobility shift assay. Serum concentrations of tumor necrosis factor ␣ and macrophage inflammatory protein 2 were measured by enzyme-linked immunosorbent assay. Histologic studies of pulmonary tissue and electron microscopy of ablated liver tissue were compared among treatment groups. ResultsHistologic lung sections after cryoablation showed multiple foci of perivenular inflammation, with activated lymphocytes, foamy macrophages, and neutrophils. In animals undergoing RFA, inflammatory foci were not present. NF-B activation was detected at 1 hour in both liver and lung tissue samples of animals undergoing cryoablation but not after RFA, and serum cytokine levels were significantly elevated in cryoablation versus RFA animals. Electron microscopy of cryoablationtreated liver tissue demonstrated disruption of the hepatocyte plasma membrane with extension of intact hepatocyte organelles into the space of Disse; RFA-treated liver tissue demonstrated coagulative destruction of hepatocyte organelles within an intact plasma membrane. To determine the stimulus for systemic inflammation, rats treated with cryoablation had either immediate resection of the ablated segment or delayed resection after a 15-minute thawing interval. Immediate resection of the cryoablated liver tissue prevented NF-B activation and lung injury; however, pulmonary inflammatory changes were present when as little as a 15-minute thaw interval preceded hepatic resection. ConclusionsHepatic cryoablation, but not RFA, induces NF-B activation in the nonablated liver and lung and is associated with acute lung injury. Lung inflammation is associated with the thawing phase of cryoablation and may be related to soluble mediator(s) released from the cryoablated tissue. These findings correlate the clinical observation of an increased incidence of multisystem injury, including adult respiratory distress syndrome (ARDS), after cryoablation but not RFA.

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“…The use of this method of ablation has been largely abandoned due to a morbidity rate approaching 60%, with the lungs being particularly susceptible to injury (19,32,33,36). In light of the clinical similarities in the lung injury patterns that occur in patients following hepatic cryoablation and prolonged cold ischemia during orthotopic liver transplantation, cryoinjury may represent a form of hepatic I/R injury.…”

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Interleukin-1β is the primary initiator of pulmonary inflammation following liver injury in mice

Glasgow

Ramachandran

Blackwell

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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Hepatic injury can lead to systemic and pulmonary inflammation through activation of NF-κB-dependent pathways and production of various proinflammatory cytokines. The exact mechanism remains unknown, although prior research suggests interleukin-1β (IL-1β) plays an integral role. Cultured murine alveolar macrophages were used to identify an optimized IL-1β-specific short interfering RNA (siRNA) sequence, which then was encapsulated in liposomes and administered intraperitoneally to transgenic HLL mice (5′-HIV-LTR-Luciferase). A 35% hepatic mass cryoablation in HLL and IL-1 receptor 1 knockout mice (IL1R1KO) was performed as a model for liver-induced pulmonary inflammation. IL-1β siRNA pretreatment effectively and significantly reduced circulating IL-1β levels at 4 h post-hepatic injury. IL-6 also was suppressed in mice with impaired IL-1 signaling pathways. NF-κB activation in the noninjured liver of HLL reporter mice pretreated with IL-1β siRNA was found to be reduced compared with controls. Pulmonary NF-κB activity in this group also was diminished relative to controls. C-X-C chemokine levels in the lung remained significantly lower in IL-1 pathway-deficient mice. Similarly, lung myeloperoxidase content was unchanged from baseline at 24 h post-liver injury in IL-1β siRNA-treated animals, whereas all other control groups demonstrated marked pulmonary neutrophilic infiltration. In conclusion, liver injury-induced lung inflammation in this model is mediated predominantly by IL-1β. Knockdown of IL-1β expression before hepatic injury led to significant reductions in both cytokine production and NF-κB activation. This translated to reduced pulmonary neutrophil accumulation. Pretreatment with IL-1β siRNA may represent a novel intervention for preventing liver-mediated pulmonary inflammation.

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Clinical Experience with Cryosurgery for Advanced Hepatobiliary Tumors

Cited by 53 publications

References 20 publications

Serum cytokine levels in response to hepatic cryoablation

Serum cytokine levels in response to hepatic cryoablation

Hepatic Cryoablation, But Not Radiofrequency Ablation, Results in Lung Inflammation

Interleukin-1β is the primary initiator of pulmonary inflammation following liver injury in mice

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