Effects of branched-chain amino acids supplementation on patients undergoing hepatic intervention: a meta-analysis of randomised controlled trials.

The benefits of branched-chain amino acid (BCAA) administration after hepatic intervention in patients with liver diseases remain unclear. We conducted a systematic review and meta-analysis to evaluate the effects of BCAA on patients undergoing hepatectomy, trans-arterial embolisation and radiofrequency ablation. Relevant randomised controlled trials (RCT) were obtained from PubMed, EMBASE and Cochrane Library databases. A meta-analysis was performed to calculate the pooled effect size by using random-effects models. The primary outcomes were survival and tumour recurrence. The secondary outcomes were hospital stay, nutrition status, biochemistry profile, complication rate of liver treatment and adverse effect of BCAA supplementation. In total, eleven RCT involving 750 patients were included. Our meta-analysis showed no significant difference in the rates of tumour recurrence and overall survival between the BCAA and control groups. However, the pooled estimate showed that BCAA supplementation in patients undergoing hepatic intervention significantly increased serum albumin (mean difference (MD): 0·11 g/dl, 95 % CI: 0·02, 0·20; 5 RCT) at 6 months and cholinesterase level (MD: 50·00 U/L, 95 % CI: 21·08, 78·92; 1 RCT) at 12 months and reduced ascites incidence (risk ratio: 0·39, 95 % CI: 0·21, 0·71; 4 RCT) at 12 months compared with the control group. Additionally, BCAA administration significantly increased body weight at 6 months and 12 months and increased arm circumference at 12 months. In conclusion, BCAA supplementation significantly improved the liver function, reduced the incidence of ascites and increased body weight and arm circumference. Thus, BCAA supplementation may beneficial for selected patients undergoing liver intervention.

Comparing effectiveness and safety of paclitaxel plus raltitrexed vs. paclitaxel alone in second-line palliative chemotherapy for metastatic gastric adenocarcinoma: A randomized phase II clinical trial.

OBJECTIVE: Paclitaxel (P) is a standard second-line chemotherapy in the treatment of advanced gastric cancer. This study compared the clinical outcome of a paclitaxel plus raltitrexed (RP) regimen as second-line treatment in metastatic gastric cancer (MGC) patients. METHODS: An open, randomized, multi-center phase II clinical trial was conducted involving 148 patients who were randomly assigned and treated with RP [raltitrexed (3 mg/m2 on day 1) and paclitaxel (135 mg/m2 on day 1 every 3 weeks)] or P [paclitaxel (135 mg/m2 on day 1 every 3 weeks)] as 2nd-line chemotherapy. The primary endpoint was progression-free survival (PFS). The secondary endpoints were the overall response rate (ORR), overall survival (OS), and safety. RESULTS: PFS had a tendency to be prolonged with RP compared to P (2.7 months vs. 1.7 months; P = 0.148). OS was also prolonged with RP compared to P (10.2 months vs. 6.1 months; P = 0.140). The ORR was equal in the RP and P groups (6.8% and 4.0%; P = 0.72). The disease control rate (DCR) in the RP and P groups was 56.2% and 36.0%, respectively. Grade 3-4 treatment-related adverse events occurred in 36.2% (RP) and 28.2% (P) of patients. Frequent grade 3-4 toxicities for RP and P were neutropenia (11.0% and 4.0%), anemia (1.4% and 4.0%), and thrombocytopenia (1.4% and 5.3%), and all grades of peripheral neurotoxicity (12.3% vs. 17.3%). All grades of hepatic toxicity were demonstrated for the RP and P groups based on elevated aminotransferase levels (27.4% and 14.1%). Subgroup analysis shows if MGC was combined with ascites or peritoneal involvement, the OS of the RP regimen was longer (P = 0.05). CONCLUSIONS: Second-line palliative chemotherapy with RP was shown to prolong the PFS and OS, especially among patients with ascites or peritoneal involvement, which warrants confirmation using larger sample studies.

Liver cirrhosis following oxaliplatin-based adjuvant chemotherapy for rectal cancer.

INTRODUCTION: Oxaliplatin is a third-generation platinum-based antineoplastic drug that is widely used to treat patients with colorectal cancer. Reported adverse reactions include hepatic sinusoidal obstruction syndrome and liver fibrosis, but there are few reports of cirrhosis associated with chemotherapy. In addition, the pathogenesis of cirrhosis remains unclear. CASE REPORT: We report a case of suspected oxaliplatin-induced liver cirrhosis, an adverse reaction that has not been previously reported. MANAGEMENT AND OUTCOME: A 50-year-old Chinese man was diagnosed with rectal cancer and underwent laparoscopic radical rectal cancer surgery. The patient had a history of schistosomiasis, but history and serology showed no evidence of chronic liver disease. However, after five oxaliplatin-based chemotherapy cycles, the patient presented dramatic changes in liver morphology and developed splenomegaly, massive ascites, and elevated CA125 levels. Four months after discontinuing oxaliplatin, the patient's ascites had decreased significantly and CA125 levels declined from 505.3 to 124.6 mU/mL. After 15 weeks of follow-up, CA125 levels decreased to the normal range, and there has been no increase in ascites in this patient. DISCUSSION: Oxaliplatin-induced cirrhosis may be a serious complication and should be discontinued based on clinical evidence.

Low-Cost Predictors for Liver Function and Clinical Outcomes after Sustained Virological Response in Patients with HCV-Related Cirrhosis and Thrombocytopenia.

Background and Objectives: To find low-cost markers that can identify the hepatitis C virus cirrhotic patients that are at risk for long-term severe adverse liver effects (ascites, ascites or upper gastrointestinal bleeding, hepatocellular carcinoma), after treatment. There is established evidence for the benefits of treating hepatitis C virus cirrhotic patients, but there is still some need for clarification concerning the real impact on the long-term evolution after achieving sustained virological response; there is no general consensus in the literature about identifying the patients that do not improve post-treatment. Materials and Methods: Our retrospective analysis investigated the long-term (2 years) evolution of 46 patients with cirrhosis with thrombocytopenia, previously infected with VHC, treated and who obtained an SVR after DAA treatment. Results: Despite the overall improvement, 8.7% patients developed hepatocellular carcinoma and 6.5% patients ascites/upper GI bleeding. We found that FIB-4, MELD and AFP changes at 1 year were the most significant predictors for these outcomes. Additionally, a drop in leukocyte count after 1 year seemed to indicate a risk for hepatocellular carcinoma, but this was not consistent. Conclusions: It might be beneficial to intensify the surveillance for post-treatment adverse liver effects for the patients with these marker changes at 1 year.

Long-term survival and clinical outcomes following direct-acting antiviral (DAA) treatment in HCV decompensated cirrhosis in Brazil: a real-world study.

INTRODUCTION: The outcomes regarding portal hypertension-related complications and infections after HCV cure in decompensated cirrhosis are scarcely reported. We aimed to identify the predictors of survival and to evaluate the frequency of decompensation events of cirrhosis, including hepatocellular carcinoma (HCC), portal hypertension complications and infections in a cohort of decompensated cirrhotic with sustained virological response (SVR) in a real-world scenario. PATIENTS AND METHODS: This was a prospective study in consecutive HCV-infected patients with decompensated cirrhosis who achieved SVR after direct-acting antiviral (DAA) treatment. At baseline, clinical and laboratory data were recorded. Patients were followed until development of outcomes regarding further decompensation, death, or liver transplant. A Cox-regression analysis was performed and survival curves were constructed using the Kaplan Mayer method. RESULTS: One hundred and thirty patients (age 60 ± 9 years, 64% female, 70% genotype 1) were included and followed-up through three years. SVR was associated with a lower prevalence of ascites and an improvement in Child-Pugh and MELD scores. One and three-year probability of transplant-free survival was 93% and 66%, respectively. Variables related to three-years survival were MELD < 11 (HR 1.24, 95% CI 1.13-1.37) and absence of ascites (HR 2.03, 95% CI 0.99-4.13) after the end of treatment (91% versus 37% in patients with ascites and a higher MELD, p < 0.001). CONCLUSIONS: Decompensated cirrhotics with SVR and a low MELD without ascites have an excellent long-term prognosis. On the contrary, those with higher MELD and ascites have a low probability of survival even in the short term and might be evaluated for liver transplantation.

Scrutinizing pathways of nicotine effect on renal Alpha-7 nicotinic acetylcholine receptor and Mitogen-activated protein kinase (MAPK) expression in Ehrlich ascites carcinoma-bearing mice: Role of Chlorella vulgaris.

Nicotine is one of several physiologically stable and active chemicals found in tobacco. The mechanism through which nicotine causes kidney damage is still obscure. As a result, the goal of this research was to investigate how oral nicotine intake can lead to kidney damage. Naturaly occurring superfood green algae are immense supplements help us using extra chemicals during cancer prevalence if the patient is exposed to nicotine. Hence, the mitigating role of Chlorella vulgaris extract (CVE) against nicotine-nephrotoxic impact in Ehrlich ascites carcinoma (EAC)-bearing mice was studied. For this purpose, four groups of Swiss female mice were assigned, nicotine group (NIC) (100 µg/ml/kg), CVE group (100 mg/kg), CVE + Nicotine, and a control group. Renal dysfunction was evaluated by estimating serum biomarkers ofrenal damage. The expression pattern of Nf-KB, MAPK, P53, and α7-nAchR, lipid peroxidation biomarker, and antioxidant enzyme activities were evaluated in kidney tissue. Also, micro-morphometric examination and apoptosis immunohistochemical reactivity of kidney tissue were applied. The obtained results indicated up-regulation of all estimated genes and oxidative stress. Moreover, a significant (P < 0.05) increment in the apoptotic marker Caspase-3 and declined BCL-2 proteins were recorded. In serum, a significant (P < 0.05) elevation of urea, creatinine, TNF-α, IL-1ß, and Kim-1 were evident. Histological investigation reinforced the aforementioned data, revealing structural changes involving the tubules, glomeruli, and interstitium of mice kidneys. CVE may be a strong contender for protecting renal tissue damage since it reduces renal tissue injury and oxidative stress. Cancer patients who regularly use nicotine through direct smoking or second-hand exposure can benefit from CVE usage as a dietary supplement.

Clinical Impact of Oral Intake in Second-line or Third-line Chemotherapy for 589 Patients With Advanced Gastric Cancer: A Retrospective Cohort Study.

OBJECTIVES: Insufficient oral intake in advanced gastric cancer (AGC) limits the use of several drugs. We aimed to determine the oral intake status of patients with AGC during later-line chemotherapy. MATERIALS AND METHODS: We retrospectively evaluated data of patients with AGC who experienced disease progression during first-line chemotherapy administered from January 2012 to December 2018 in a single institution. We defined "insufficient oral intake" as requiring daily intravenous fluids or hyperalimentation. Multivariate logistic regression was performed to identify oral intake-related factors. RESULTS: Among 589 included patients, at disease progression during first-line, second-line, and third-line chemotherapy, 78.3% (461), 53.3% (314), and 30.4% (179) of patients, respectively, exhibited sufficient oral intake. Fourth-line chemotherapy was initiated for 22.2% (131) of patients, with 20.0% (118) exhibiting sufficient oral intake. During second-line and third-line chemotherapy, 11/67 (16%) and 2/39 (5%) patients, respectively, exhibited improvements in oral intake; 85/428 (19.9%) and 70/259 (27.0%), respectively, exhibited deteriorations in oral intake. Factors correlated to deterioration in oral intake during second-line chemotherapy were poor Eastern Cooperative Oncology Group Performance Status (odds ratio, 4.32; P<0.001), moderate or severe ascites (1.96; P=0.045), peritoneal metastasis (2.12; P=0.029), prior palliative surgery (3.41; P=0.003), and high neutrophil-to-lymphocyte ratio (3.09; P<0.001); those correlated to deterioration in oral intake during third-line chemotherapy were poorly differentiated pathology (2.52; P=0.025) and high neutrophil-to-lymphocyte ratio (2.65; P=0.006). CONCLUSION: As later-line chemotherapy is ineffective in improving oral intake in patients with AGC, careful adaptation of regimens is required for patients at risk for impaired oral intake.

Refractory ascites induced by mycophenolate in a pediatric kidney transplant patient.

Common side effects of mycophenolate mofetil (MMF) are diarrhea, leukopenia, and infectious complication. The polymorphisms of enzymes affecting MMF clearance could be related to MMF toxicity, and in vitro study revealed that high MMF levels might cause endothelial dysfunction. A 7-year-old Korean male with end-stage renal disease on peritoneal dialysis due to mesangial proliferative glomerulonephritis received a kidney transplantation (KT) from a deceased donor, and immunosuppressive medications including MMF, tacrolimus, and methylprednisolone were started after KT. The patient developed oliguria immediately after surgery, and therapeutic plasmapheresis was initiated with continuous renal replacement therapy for the possibility of graft dysfunction and nephrotic syndrome relapse. Renal function recovered 4 days later, but the patient developed ascites. Diagnostic paracentesis revealed findings that were interpreted as uncomplicated ascites in cirrhosis, not of renal origin. Abdominal ultrasonography showed increased parenchymal echogenicity without cirrhotic change in the liver. Based on a case report and differential diagnosis, we replaced MMF with azathioprine, and 4 weeks later a sudden increment in urine output was detected. Eleven months after KT, the patient is free from ascites. The UGT2B7 802 polymorphism was tested, and wild-type UGT2B7 802 was detected, which is related to low MMF clearance. The low clearance of MMF by UGT2B7 802 wild-type polymorphism might have led to MMF toxicity affecting endothelial dysfunction. This case suggests that refractory ascites could be induced by MMF, and endothelial damage is a possible mechanism.

Amlodipine Induced Massive Ascites, a Rare Clinical Case.

INTRODUCTION: Calcium channel blockers (CCBs) are commonly used agents in the treatment of hypertension as part of monotherapy or combination therapy. Peripheral edema is the most common side effect that requires discontinuation or replacement of treatment. Some studies in the literature have shown that long-acting dihydropyridine type CCBs lead chylous ascites in peritoneal dialysis patients. However, amlodipine-associated serous ascites cases are not available in the literature. CASE REPORT: In this case report, we describe a rare case of amlodipine induced massive ascites in a 30-year-old male with renal transplantation. CONCLUSION: We aimed to create awareness that pharmacologic causes should be considered in cases of ascites of unknown aetiology.

Eosinophilic Gastroenteritis in an Ulcerative Colitis Patient During Treatment with Tumor Necrosis Factor-alpha Antagonist.

A 45-year-old man with steroid-dependent ulcerative pancolitis was hospitalized with frequent diarrhea, abdominal pain and distension 3 months after induction of golimumab, a tumor necrosis factor-alpha antagonist. Computed tomography showed wall thickening from the stomach to the colon and massive ascites. Peripheral blood test revealed eosinophilia. A large number of eosinophils were observed in the ascites fluid. Although esophagogastroduodenoscopy showed no abnormal findings and colonoscopy showed ulcerative colitis with a Mayo endoscopic subscore of 1, eosinophil infiltration was histologically observed. Based on these findings, we diagnosed him with eosinophilic gastroenteritis and started prednisolone. Consequently, his eosinophil counts and abdominal symptoms dramatically improved.

A mouse model of subacute liver failure with ascites induced by step-wise increased doses of (-)-epigallocatechin-3-gallate.

Acute liver failure is divided into hyperacute, acute and subacute liver failure. Ascites is a common complication of subacute liver failure. Although animal models of acute liver failure have been established, the study of the pathogenesis of subacute liver failure with ascites complication is hampered by the lack of experimental animal model. The present study aimed at providing a mouse model of subacute liver failure with ascites complication. Kunming mice were intraperitoneally injected with (-)-epigallocatechin-3-gallate (EGCG), a redox-active polyphenol from green tea, for 32 consecutive days with step-wise increased dosage. The EGCG treatment resulted in liver failure as evidenced by extensive hepatocyte necrosis observed histologically along with significant elevation of serum alanine aminotransferase, aspartate aminotransferase, total bilirubin and direct bilirubin levels as well as significant reduction of serum albumin. Liver fibrosis was not observed by Masson staining and fibrosis-associated proteins were not increased. The mortality was less than 12% and the survival mice developed noticeable ascites. Hepatic thioredoxin and glutathione systems were activated by the EGCG. These adaptive responses might render most mice tolerable to the EGCG treatment. The EGCG treatment significantly up-regulated renal urea transporter A1 and promoted its trafficking to apical membrane. These alterations, known to increase water reabsorption, may be responsible, at least in part, for the formation of the ascites. Overall, the mice treated with gradually elevated doses of EGCG exhibits some of the features observed in patients with subacute liver failure, especially ascites. This mouse model is a useful tool for investigating the pathogenesis of subacute liver failure with ascites complication.

Altered Expression of Zinc Transporter ZIP12 in Broilers of Ascites Syndrome Induced by Intravenous Cellulose Microparticle Injection.

Ascites syndrome (AS) is a harmful disease in fast-growing broilers characterized by heart failure and serious fluid accumulation in the abdominal cavity. One of the known functions of zinc transporter ZIP12 is an important regulator in pulmonary hypertension (PH) in rat. Whether chicken ZIP12 is involved in the process of AS need to be explored. Here, chicken ZIP12 was sequenced and expression pattern and histological distribution were detected in broilers of AS induced by intravenous cellulose microparticle injection. Phylogenetic analysis showed that ZIP12 was significantly different between chicken and mammalian. The relative mRNA expression level of ZIP12 in the liver and lung in AS and pre-ascites (PAS) groups were significantly higher (P < 0.01) than that in control. The immunohistological staining using rabbit anti-chicken ZIP12 IgG and integrated optical density analysis showed the positive cells of ZIP12 distributed in detected tissues and the expression level of ZIP12 protein increased in AS and PAS groups compared to control. The results will provide the basic data of ZIP12 in the pathological process of AS in broiler chickens and offer an important reference for prevention and control of the disease.

Misery Loves Company: Presenting Symptom Clusters to Urgent Care by Patients Receiving Antineoplastic Therapy.

PURPOSE: The Centers for Medicare & Medicaid Services (CMS) identifies suboptimal management of treatment toxicities as a care gap and proposes the measurement of hospital performance on the basis of emergency department visits for 10 common symptoms. Current management strategies do not address symptom co-occurrence. METHODS: We evaluated symptom co-occurrence in three patient cohorts that presented to a cancer hospital urgent care center in 2016. We examined both the CMS-identified symptoms and an expanded clinician-identified set defined as symptoms that could be safely managed in the outpatient setting if identified early and managed proactively. The cohorts included patients who presented with a CMS-defined symptom within 30 days of treatment, patients who presented within 30 days of treatment with a symptom from the expanded set, and patients who presented with a symptom from the expanded set within 30 days of treatment start. Symptom co-occurrence was measured by Jaccard index. A community detection algorithm was used to identify symptom clusters on the basis of a random walk process, and network visualizations were used to illustrate symptom dynamics. RESULTS: There were 6,429 presentations in the CMS symptom-defined cohort. The network analysis identified two distinct symptom clusters centered around pain and fever. In the expanded symptom cohort, there were 5,731 visits and six symptom clusters centered around fever, emesis/nausea, fatigue, deep vein thrombosis, pain, and ascites. For patients who newly initiated treatment, there were 1,154 visits and four symptom clusters centered around fever, nausea/emesis, fatigue, and deep vein thrombosis. CONCLUSION: Uncontrolled symptoms are associated with unplanned acute care. Recognition of the complexity of symptom co-occurrence can drive improved management strategies.

Pseudoprogression manifesting as recurrent ascites with anti-PD-1 immunotherapy in urothelial bladder cancer.

BACKGROUND: Immunotherapies targeting the PD-1 checkpoint pathway have recently gained regulatory approval in numerous cancer types. With the widespread use of immune checkpoint therapies, varying patterns of responses and immune-related adverse events are being observed. CASE PRESENTATION: In this case, we highlight a patient who developed recurrent, large-volume ascites, while simultaneously having a 49% reduction in peritoneal tumor lesion size by RECIST criteria. Sampling of the fluid revealed high levels of IL-6 and IL-15. Cytology revealed no malignant cells on 4 separate paracenteses over a period of 6 weeks. Cell counts revealed that 45% of cells were lymphocytes, and further analysis was performed by fluorescence-activated cell sorting (FACS). The majority of lymphocytes were CD8+, of which 78% were PD-1+ and 43% were HLA-DR+ indicating an activated phenotype. CONCLUSIONS: In summary, treatment with anti-PD-1 therapy may result in pseudoprogression manifested by ascitic fluid accumulation due to the influx of activated T cells. Since worsening of ascites is typically associated with disease progression, it is important to consider the possibility of pesudoprogression in such patients undergoing therapy with immune checkpoint inhibitors.

Mediation of inflammatory ascites formation induced by macromolecules in mice.

The first 60-min phase of inflammatory ascites formation was studied by intraperitoneally (i.p.) administered macromolecular inducers: yeast cell wall zymosan binds to specific macrophage receptors, polyethyleneimine (PEI) and concanavalin A (ConA), produces non-covalent cross-links on the surface of various cells, while λ-carrageenan may function as a contact activator. Depletion of peritoneal macrophages was performed by overnight pretreatment with diphtheria toxin in transgenic mice, resulting in a significant (p < 0.01) decrease in the induced formation of ascitic fluid. It was shown that induced ascites is mediated partly (PEI, ConA, and carrageenan) or completely (zymosan) by peritoneal macrophages. Inhibition of prostanoid synthesis with indomethacine or of the kallikrein/bradykinin system with aprotinin also produced a significant (p < 0.01) but incomplete inhibition. A slight additivity occurred between the different inhibitory effects. In another series of experiments, the i.p. administration of bradykinin (without a macromolecular inducer) also produced marked ascites, which was not affected by macrophage depletion. The origin of the macrophage-independent part of the induced ascites is best explained by the deformation of the mesothelial cell surface, resulting in signal transfer to the underlying endothelium and the passage of ascitic fluid in the opposite direction. The soluble mediators are represented by prostanoids, bradykinin and other, unidentified agonists.

Intractable ascites associated with mycophenolate in a simultaneous kidney-pancreas transplant patient: a case report.

BACKGROUND: Mycophenolic acid (MPA), either given as an ester pro-drug or as an enteric-coated sodium salt, is the most commonly prescribed anti-proliferative immunosuppressive agent used following organ transplantation and widely applied in immune-mediated diseases. Clinicians are well aware of common adverse reactions related to MPA treatment, in particular diarrhea, leukopenia and infections. Here we report a case of severe, persistent ascites associated with MPA treatment. The otherwise unexplained and intractable ascites, requiring repeated paracenteses for more than 8 months, rapidly ceased with stopping the MPA treatment. To our knowledge this is the first case of severe ascites associated with MPA treatment reported in the scientific literature. CASE PRESENTATION: A 45-year old female with type 1 diabetes mellitus received a simultaneous kidney-pancreas transplant. The surgery was uneventful. However, post-operatively she developed severe transudative ascites requiring in total more than 40 paracenteses treatments draining in the average 2.8 l of ascites fluid. The ascites formation persisted despite exclusion of a surgical complication, fully functioning kidney and pancreas allografts, lack of any significant proteinuria, normalization of circulating albumin levels, intensive use of diuretics and deliberate attempts to increase the intervals between the paracentesis treatments. Various differential diagnoses, including infectious, hepatic, vascular and cardiac causes were ruled out. Nine months after surgery enteric-coated mycophenolate sodium was switched to azathioprine after which ascites completely resolved. When mycophenolate was recommenced abdominal fullness and weight gain reoccurred. The patient had to be switched to long-term azathioprine treatment. More than 1 year post-conversion the patient remains free of ascites. CONCLUSION: MPA is the most widely used antimetabolite immunosuppressive agent. We suggest to consider MPA treatment in the differential diagnosis of severe and unexplained ascites in transplant and non-transplant patients.

Clinical Application of Artificial Ascites in assisting CT-guided Percutaneous Cryoablation of Hepatic Tumors Adjacent to the Gastrointestinal Tract.

This study was to assess the safety and efficacy of artificial ascitetes in assisting CT-guided cryoablation of hepatic tumors adjacent to the gastrointestinal (GI) tract. A total of 84 patients with peripheral hepatic tumors adjacent to the GI tract, who were treated cryoablation, were included in this retrospective study. Of these 84 patients, cryoablation had been performed in 39 patients with 41 peripheral hepatic tumors. These were assisted by induction artificial ascites while 40 patients with 43 peripheral hepatic tumors underwent cryoablation without induction of ascites. The artificial ascites separation success rate, the cryoablation technique effectiveness, local tumor progression and complications were all evaluated. The results showed that the artificial ascites separation success rate for 41 hepatic tumors adjacent to the GI tract was 95% (39/41). Technique effectiveness of group I was achieved in 35 of 43 tumors (81.3%) after follow-up imaging three months after cryoablation. In group II, technique effectiveness was achieved in 39 of 41 tumors after follow-up imaging three months following cryoablation. No major complications were encountered in either of the two groups. Artificial ascites assisting in CT-guided percutaneous cryoablation is a reliable and effective method for the treatment of hepatic tumors adjacent to the GI tract, and it can achieve a fine local control of such tumors.