Although these two scenarios might under- or overestimate the tru

Although these two scenarios might under- or overestimate the true bleeding incidences, both should be uncommon without seriously biasing our analysis, thanks to the easy accessibility and high coverage of the universal

health insurance in Taiwan.35 Furthermore, the comprehensiveness of NHIRD allows adjustment for various confounders in this research. Patients with liver cirrhosis constituted a unique subpopulation BGJ398 datasheet among all patients with PUB, and therefore were unsurprisingly different from their controls in several baseline characteristics, including H. pylori status, comorbidities, ulcerogenic drugs, and propranolol use. However, the compatible results from the multivariate Cox modeling and stratified analyses affirmed that these unmatched confounders

were appropriately accounted for. Of note, the association between antisecretory drugs and risk of recurrent PUB should be cautiously interpreted. In Taiwan, these medications cannot be prophylactically prescribed and are reimbursed only in patients with endoscopically proven peptic ulcers or erosive esophagitis, with drug duration confined within 4 months in most cases (up to 1 year in those with Los Angeles grade C/D esophagitis or poorly Selleckchem ALK inhibitor healed marginal ulcers on partially resected stomach). As a result, their use actually served as a surrogate marker for a proven UGI pathology documented during the observation period. Finally, the sample size of our cohort mitigated the concern for unmeasured confounders. Existence of any unmeasured factor that could have distorted the analysis was improbable, since it would have

to be either strongly linked to both cirrhosis and elevated rebleeding risk, or would have to be very common. How to reduce the recurrence rate of peptic ulcers remains unknown and scantly investigated in patients with liver cirrhosis. Although H. pylori eradication is unequivocally effective in preventing peptic ulcer recurrence in the general population,36 such effectiveness is not established in patients with cirrhosis.32, 37 Similarly, it has not been determined whether antisecretory maintenance lowers this website the long-term recurrence rate of ulcer bleeding in patients with cirrhosis. The efficacy of acid suppression in patients with cirrhosis appears questionable in that these patients are characterized by marked gastric hypoacidity,38 hence gastric acid may not play a crucial role in their ulcerogenesis. In light of the distinct ulcerogenic mechanism in patients with cirrhosis, agents that sustain reduction of portal pressure may be effective in decreasing ulcer bleeding. We uncovered concomitantly in this study that use of propranolol was linked to protection against recurrent PUB (adjusted HR, 0.78; 95% CI, 0.73-0.84).

Although these two scenarios might under- or overestimate the tru

Although these two scenarios might under- or overestimate the true bleeding incidences, both should be uncommon without seriously biasing our analysis, thanks to the easy accessibility and high coverage of the universal

health insurance in Taiwan.35 Furthermore, the comprehensiveness of NHIRD allows adjustment for various confounders in this research. Patients with liver cirrhosis constituted a unique subpopulation Wnt activation among all patients with PUB, and therefore were unsurprisingly different from their controls in several baseline characteristics, including H. pylori status, comorbidities, ulcerogenic drugs, and propranolol use. However, the compatible results from the multivariate Cox modeling and stratified analyses affirmed that these unmatched confounders

were appropriately accounted for. Of note, the association between antisecretory drugs and risk of recurrent PUB should be cautiously interpreted. In Taiwan, these medications cannot be prophylactically prescribed and are reimbursed only in patients with endoscopically proven peptic ulcers or erosive esophagitis, with drug duration confined within 4 months in most cases (up to 1 year in those with Los Angeles grade C/D esophagitis or poorly find more healed marginal ulcers on partially resected stomach). As a result, their use actually served as a surrogate marker for a proven UGI pathology documented during the observation period. Finally, the sample size of our cohort mitigated the concern for unmeasured confounders. Existence of any unmeasured factor that could have distorted the analysis was improbable, since it would have

to be either strongly linked to both cirrhosis and elevated rebleeding risk, or would have to be very common. How to reduce the recurrence rate of peptic ulcers remains unknown and scantly investigated in patients with liver cirrhosis. Although H. pylori eradication is unequivocally effective in preventing peptic ulcer recurrence in the general population,36 such effectiveness is not established in patients with cirrhosis.32, 37 Similarly, it has not been determined whether antisecretory maintenance lowers selleck chemicals llc the long-term recurrence rate of ulcer bleeding in patients with cirrhosis. The efficacy of acid suppression in patients with cirrhosis appears questionable in that these patients are characterized by marked gastric hypoacidity,38 hence gastric acid may not play a crucial role in their ulcerogenesis. In light of the distinct ulcerogenic mechanism in patients with cirrhosis, agents that sustain reduction of portal pressure may be effective in decreasing ulcer bleeding. We uncovered concomitantly in this study that use of propranolol was linked to protection against recurrent PUB (adjusted HR, 0.78; 95% CI, 0.73-0.84).

Only total CK-18 assays differentiated patients with minimal stea

Only total CK-18 assays differentiated patients with minimal steatosis (<10% hepatic fat accumulation) from those with more hepatic fat (>10% steatosis). All three assays distinguished patients with steatosis from healthy controls. A selective analysis of the NAFLD subgroup demonstrated that the total CK-18 assays reliably CH5424802 concentration differentiated patients with mild NAFL from healthy or real-life controls, whereas the M30 assay could

not. The total CK-18 assays were more sensitive (100% versus 75%) and specific (80% versus 70%) than the M30 ELISA for discriminating between NAFL and NASH. The better classification of NAFL/NASH by the total CK-18 assays was not a byproduct of superior fibrosis staging because the fibrosis severity was similar (generally low) in these patients. Although the NASH patients tended to have higher ALT levels than the NAFL patients, a regression analysis revealed that total CK-18 levels predicted NASH independently of ALT levels, whereas cleaved CK-18 levels did not. The aggregated data demonstrate that a noninvasive measure of various types of hepatocyte death (total CK-18) is a better biomarker of related liver pathology than a test that merely reflects apoptotic severity

(cleaved CK-18). This finding has a number of fundamental Y 27632 implications. First, it supports the concept that dying liver epithelial cells provide key fibrosis stimuli. Completely dead hepatocytes have long been implicated in the pathogenesis of liver fibrosis because of increased fibrogenic activity selleck chemical in hepatic stellate cells that have phagocytosed apoptotic hepatocytes.3 More recent data show that dying (but viable) liver epithelial cells produce and release soluble factors that promote liver fibrosis. Diverse insults that sensitize hepatocytes to death (e.g., an infection

with hepatitis C virus,4 an exposure to agents that induce endoplasmic reticulum stress,5 or an inhibition of autocrine viability factors6) induce them to generate damage-associated molecules. These include hedgehog ligands, which are morphogens stimulating wound-healing mechanisms that promote myofibroblastic cell outgrowth, immune cell infiltration, and the accumulation of liver epithelial progenitors (with fibrogenic activity).7, 8 It is thus not surprising that an assay with improved sensitivity and specificity for detecting hepatocyte death would provide better sensitivity and specificity for responses that are triggered by all dying hepatocytes (and not simply a subset of dead cells). Second, the latter concept raises the intriguing possibility that dying hepatocytes promote hepatic steatosis (rather than vice versa as currently believed). This possibility is supported by evidence showing that hepatic steatosis occurs transiently in remnant livers after partial hepatectomy, which is another process stimulating wound-healing responses to promote liver regeneration.

Only total CK-18 assays differentiated patients with minimal stea

Only total CK-18 assays differentiated patients with minimal steatosis (<10% hepatic fat accumulation) from those with more hepatic fat (>10% steatosis). All three assays distinguished patients with steatosis from healthy controls. A selective analysis of the NAFLD subgroup demonstrated that the total CK-18 assays reliably buy Small molecule library differentiated patients with mild NAFL from healthy or real-life controls, whereas the M30 assay could

not. The total CK-18 assays were more sensitive (100% versus 75%) and specific (80% versus 70%) than the M30 ELISA for discriminating between NAFL and NASH. The better classification of NAFL/NASH by the total CK-18 assays was not a byproduct of superior fibrosis staging because the fibrosis severity was similar (generally low) in these patients. Although the NASH patients tended to have higher ALT levels than the NAFL patients, a regression analysis revealed that total CK-18 levels predicted NASH independently of ALT levels, whereas cleaved CK-18 levels did not. The aggregated data demonstrate that a noninvasive measure of various types of hepatocyte death (total CK-18) is a better biomarker of related liver pathology than a test that merely reflects apoptotic severity

(cleaved CK-18). This finding has a number of fundamental selleckchem implications. First, it supports the concept that dying liver epithelial cells provide key fibrosis stimuli. Completely dead hepatocytes have long been implicated in the pathogenesis of liver fibrosis because of increased fibrogenic activity this website in hepatic stellate cells that have phagocytosed apoptotic hepatocytes.3 More recent data show that dying (but viable) liver epithelial cells produce and release soluble factors that promote liver fibrosis. Diverse insults that sensitize hepatocytes to death (e.g., an infection

with hepatitis C virus,4 an exposure to agents that induce endoplasmic reticulum stress,5 or an inhibition of autocrine viability factors6) induce them to generate damage-associated molecules. These include hedgehog ligands, which are morphogens stimulating wound-healing mechanisms that promote myofibroblastic cell outgrowth, immune cell infiltration, and the accumulation of liver epithelial progenitors (with fibrogenic activity).7, 8 It is thus not surprising that an assay with improved sensitivity and specificity for detecting hepatocyte death would provide better sensitivity and specificity for responses that are triggered by all dying hepatocytes (and not simply a subset of dead cells). Second, the latter concept raises the intriguing possibility that dying hepatocytes promote hepatic steatosis (rather than vice versa as currently believed). This possibility is supported by evidence showing that hepatic steatosis occurs transiently in remnant livers after partial hepatectomy, which is another process stimulating wound-healing responses to promote liver regeneration.

7B) Additionally, we determined that this difference was not the

7B). Additionally, we determined that this difference was not the result of decreased hepatocyte death and passive HMGB1 release by determining supernatant levels of lactate dehydrogenase (LDH) and β-actin (Fig. 7B). The effect of GSI-IX mw the JNK inhibitor on HMGB1 release in vivo after I/R was also investigated. Efficacy of the JNK inhibitor was first confirmed by decreased phosphorylation of c-Jun, compared to vehicle control, on western blotting analysis (Fig. 7C). With administration of the inhibitor given before I/R, there was a significant decrease in serum levels of HMGB1 after I/R (Fig. 7D). We, again, confirmed that this decrease in HMGB1 was not solely the result of decreased hepatocellular

injury with JNK inhibition by determining that sALT learn more levels were unchanged at 3 hours of reperfusion (Supporting Fig. 3), in addition to histologic analysis (data not shown). The p38 inhibitor, SB203580, was also studied both in vitro and in vivo similar to the JNK inhibitor. With administration of the p38 inhibitor before hypoxia exposure in vitro and before I/R in vivo, there was no inhibitory effect noted on HMGB1 release (data not shown), suggesting that p38 does not play a major role in TLR4-mediated HMGB1 release. Therefore, it seems that activation of JNK, but not p38, is required

for the extracellular release of HGMB1, both after hypoxic stress in vitro and I/R in vivo. Hepatic I/R is dependent on the pattern recognition receptors

(PRRs) to sense and initiate the sterile inflammatory response. Although the central role of the PRR, TLR4, in this process had been previously demonstrated,5, 6 the role of TLR4 on individual cell types, specifically, parenchymal versus NPC, during the sterile inflammatory response was conflicted. Therefore, in this study, we describe the novel use of Cre-loxP technology to knock out TLR4 in HCs, myeloid cells, and DCs and elucidate their individual role in I/R injury. The key and novel findings include the following: (1) Both HC and myeloid cell TLR4 is required for maximal I/R-associated injury; (2) DC TLR4−/− worsens injury after I/R and is associated with decreased IL-10 expression; (3) HCs are a major source of circulating see more HGMB1 after I/R; (4) HCs respond to hypoxia with increased phosphorylation of MAP kinases (JNK and p38) in a TLR4-dependent fashion; and (5) hypoxia-induced HMGB1 release from HCs is dependent on the function of JNK. Previous work to define the function of TLR4 on individual cellular populations was limited to the use of chimeras. Although we have shown that there was not a significant difference in hepatic I/R-induced injury with lack of TLR4 on non-BM-derived cells, there was a trend toward an effect and others have subsequently shown that both BM and non-BM-derived populations have a role in mediating I/R injury.

7B) Additionally, we determined that this difference was not the

7B). Additionally, we determined that this difference was not the result of decreased hepatocyte death and passive HMGB1 release by determining supernatant levels of lactate dehydrogenase (LDH) and β-actin (Fig. 7B). The effect of this website the JNK inhibitor on HMGB1 release in vivo after I/R was also investigated. Efficacy of the JNK inhibitor was first confirmed by decreased phosphorylation of c-Jun, compared to vehicle control, on western blotting analysis (Fig. 7C). With administration of the inhibitor given before I/R, there was a significant decrease in serum levels of HMGB1 after I/R (Fig. 7D). We, again, confirmed that this decrease in HMGB1 was not solely the result of decreased hepatocellular

injury with JNK inhibition by determining that sALT screening assay levels were unchanged at 3 hours of reperfusion (Supporting Fig. 3), in addition to histologic analysis (data not shown). The p38 inhibitor, SB203580, was also studied both in vitro and in vivo similar to the JNK inhibitor. With administration of the p38 inhibitor before hypoxia exposure in vitro and before I/R in vivo, there was no inhibitory effect noted on HMGB1 release (data not shown), suggesting that p38 does not play a major role in TLR4-mediated HMGB1 release. Therefore, it seems that activation of JNK, but not p38, is required

for the extracellular release of HGMB1, both after hypoxic stress in vitro and I/R in vivo. Hepatic I/R is dependent on the pattern recognition receptors

(PRRs) to sense and initiate the sterile inflammatory response. Although the central role of the PRR, TLR4, in this process had been previously demonstrated,5, 6 the role of TLR4 on individual cell types, specifically, parenchymal versus NPC, during the sterile inflammatory response was conflicted. Therefore, in this study, we describe the novel use of Cre-loxP technology to knock out TLR4 in HCs, myeloid cells, and DCs and elucidate their individual role in I/R injury. The key and novel findings include the following: (1) Both HC and myeloid cell TLR4 is required for maximal I/R-associated injury; (2) DC TLR4−/− worsens injury after I/R and is associated with decreased IL-10 expression; (3) HCs are a major source of circulating selleckchem HGMB1 after I/R; (4) HCs respond to hypoxia with increased phosphorylation of MAP kinases (JNK and p38) in a TLR4-dependent fashion; and (5) hypoxia-induced HMGB1 release from HCs is dependent on the function of JNK. Previous work to define the function of TLR4 on individual cellular populations was limited to the use of chimeras. Although we have shown that there was not a significant difference in hepatic I/R-induced injury with lack of TLR4 on non-BM-derived cells, there was a trend toward an effect and others have subsequently shown that both BM and non-BM-derived populations have a role in mediating I/R injury.

0056) Additionally, female carriers of the CCKAR haplotype C-T-C

0056). Additionally, female carriers of the CCKAR haplotype C-T-C-T (rs2071011-rs915889-rs3822222-rs1800855) had a reduced risk of gallbladder cancer (odds ratio = 0.61, this website 95% confidence interval: 0.43–0.86) compared with those with the G-C-C-A haplotype; the association also remained significant after Bonferroni correction. These findings suggest that variants in the CCKAR gene may influence the risk of gallbladder cancer in women. Additional studies are needed to confirm our findings. “
“Background and Aim:  To investigate

the therapeutic effect of ligustrazine on hepatic veno-occlusive disease (HVOD) induced by Gynura segetum and the possible mechanism of it. Methods:  Female Kunming mice (115) were randomly divided into four groups, gavaged with 30 g/kg per day Gynura segetum (group A), 30 g/kg per day Gynura

segetum + 100 mg/kg per day ligustrazine (group B), 30 g/kg per day Gynura segetum + 200 mg/kg per day ligustrazine (group C) or 30 mL/kg per day phosphate-buffered saline (PBS) (group D). Thirty days later, all of the mice were killed. Blood samples and livers were harvested. Histological changes were evaluated by light microscopy. Liver function learn more was measured, and the expression of tissue factor (TF), early growth response factor-1 (Egr-1) and nuclear factor-KBp65 (NF-KBp65) were determined by reverse transcription-polymerase chain reaction and Western blot. Results:  A total of 24 mice in group A developed HVOD. Compared with the controls, they had increased liver ratio, serum total bilirubin (TBIL), check details direct

bilirubin (DBIL), transaminase and decreased albumin (ALB) (P < 0.05). Administration of ligustrazine improved the clinical signs and biochemistry parameters in a dose-dependent manner. Compared with group A, the expression of TF, Egr-1 and NF-KB p65 decreased in groups B and C (P < 0.05). Conclusion:  Ligustrazine has a therapeutic effect on HVOD, improving clinical manifestations and liver function. The possible mechanism may be that ligustrazine could reduce the expression of TF by downregulating the expression of transcription factors: Egr-1 and NF-KB p65. "
“Background & Aims: Antiviral therapy may eradicate hepatitis C viral replication, but its long-term impact on the reduction of hepatocellular carcinoma (HCC) remains unclear. This large clinical cohort study aimed to evaluate the predictors of sustained virological response (SVR) and assess the efficacy to reduce HCC post-treatment in Taiwanese chronic hepatitis C patients. Methods: This multicenter study enrolled 1778 anti-HCV-positive patients who were treated with peg-interferon plus ribavirin (PR) for 6-12 months. All of the patients were ≧30 years old and seronegative for HBsAg. The treated patients were followed from the date starting PR therapy to the date of HCC diagnosis, death, or the end of 2011, whichever came first.

0056) Additionally, female carriers of the CCKAR haplotype C-T-C

0056). Additionally, female carriers of the CCKAR haplotype C-T-C-T (rs2071011-rs915889-rs3822222-rs1800855) had a reduced risk of gallbladder cancer (odds ratio = 0.61, CT99021 cell line 95% confidence interval: 0.43–0.86) compared with those with the G-C-C-A haplotype; the association also remained significant after Bonferroni correction. These findings suggest that variants in the CCKAR gene may influence the risk of gallbladder cancer in women. Additional studies are needed to confirm our findings. “
“Background and Aim:  To investigate

the therapeutic effect of ligustrazine on hepatic veno-occlusive disease (HVOD) induced by Gynura segetum and the possible mechanism of it. Methods:  Female Kunming mice (115) were randomly divided into four groups, gavaged with 30 g/kg per day Gynura segetum (group A), 30 g/kg per day Gynura

segetum + 100 mg/kg per day ligustrazine (group B), 30 g/kg per day Gynura segetum + 200 mg/kg per day ligustrazine (group C) or 30 mL/kg per day phosphate-buffered saline (PBS) (group D). Thirty days later, all of the mice were killed. Blood samples and livers were harvested. Histological changes were evaluated by light microscopy. Liver function Rucaparib chemical structure was measured, and the expression of tissue factor (TF), early growth response factor-1 (Egr-1) and nuclear factor-KBp65 (NF-KBp65) were determined by reverse transcription-polymerase chain reaction and Western blot. Results:  A total of 24 mice in group A developed HVOD. Compared with the controls, they had increased liver ratio, serum total bilirubin (TBIL), find more direct

bilirubin (DBIL), transaminase and decreased albumin (ALB) (P < 0.05). Administration of ligustrazine improved the clinical signs and biochemistry parameters in a dose-dependent manner. Compared with group A, the expression of TF, Egr-1 and NF-KB p65 decreased in groups B and C (P < 0.05). Conclusion:  Ligustrazine has a therapeutic effect on HVOD, improving clinical manifestations and liver function. The possible mechanism may be that ligustrazine could reduce the expression of TF by downregulating the expression of transcription factors: Egr-1 and NF-KB p65. "
“Background & Aims: Antiviral therapy may eradicate hepatitis C viral replication, but its long-term impact on the reduction of hepatocellular carcinoma (HCC) remains unclear. This large clinical cohort study aimed to evaluate the predictors of sustained virological response (SVR) and assess the efficacy to reduce HCC post-treatment in Taiwanese chronic hepatitis C patients. Methods: This multicenter study enrolled 1778 anti-HCV-positive patients who were treated with peg-interferon plus ribavirin (PR) for 6-12 months. All of the patients were ≧30 years old and seronegative for HBsAg. The treated patients were followed from the date starting PR therapy to the date of HCC diagnosis, death, or the end of 2011, whichever came first.

Aims: To study these parameters in patients with LC in Tajikistan

Aims: To study these parameters in patients with LC in Tajikistan. Methods: There were diagnosed 1374 patients with LC. Survival was assessed according to the Kaplan-Meier method. The mortality risk of cirrhosis complications was analyzed by a time-dependent Cox regression model. Results: The main etiological factors of development of LC were: HBV (49%), HCV (36%) and alcohol (4%). The incidence of viral LC was 23.2, of alcohol-induced LC (ALC) – 1.4 and primary biliary cirrhosis (PBC) – 0.3 per 100 000 of adult populations. Lifetime and 3-year survival rate of patients depend on a phase of

cirrhotic process compensation. The highest 3-years survival rate of patients from the producing PF2341066 moment of this diagnosis was 79% at Child–Pugh grade A vs. 28% at grade C. The cause of death of 89% of patients has been directly related to

complications of cirrhosis. The main reasons of patients death were: hepatic encephalopathy (46.7%), bleeding serve (18.3%), hepatorenal syndrome (12.5%), spontaneous bacterial peritonitis (9.2%) and portal vein thrombosis Quizartinib research buy (2.5%). The prognosis of survival is most unfavorable at hepatic encephalopathy in comparison with other complications of the LC. Presence more than one complication increases probability of death of patients more than 2.5 times. The higher relative risk of death has patients with grade B and C with comparison to grade A. Conclusion: The main etiological factors of LC are HBV and HCV in Tajikistan. The incidence of viral LC does not differ from that in other countries. ALC

and PBC are over 10 and 5 times less frequent that in Russia. Key Word(s): 1. liver cirrhosis; 2. etiological factor; 3. prevalence; 4. survival rate; Presenting Author: DONGYE YANG Additional Authors: TAOFIC MOUNAJJED, SAMARH IBRAHIM, DEBORAHK FREESE, LIZHI ZHANG Corresponding Author: LIZHI ZHANG Affiliations: Central South University; Mayo Clinic Objective: Autoimmune sclerosing cholangitis (ASC) is a poorly understood autoimmune liver disease in selleck chemical childhood which is referred as an overlap syndrome of autoimmune hepatitis (AIH) associated with bile duct disease typical of primary sclerosing cholangitis (PSC). Recently, IgG4-related sclerosing cholangitis (ISC) is recognized in adult population as biliary manifestation of a steroid-responsive multisystem fibroinflammatory disorder in which affected organs are infiltrated with IgG4+ plasma cells. In this study, we sought to evaluate clinicopathological features of ASC and its correlation with IgG4+ plasma cells infiltration.

7 However, whether the findings of improved survival with selecti

7 However, whether the findings of improved survival with selective techniques really correspond to an improved necrotizing capability, reduced liver toxicity, or both has never been elucidated on the basis of histological findings in a sufficiently large Western population. The results of studies published in the Asiatic literature suggest that segmental or subsegmental

TACE has been more effective and has resulted in higher rates of tumor necrosis (64%-83%) than proximal/whole liver TACE (approximately 38%) in historical series.8-11 Even though the efficacy of TACE can be reliably assessed only by the measurement of tumor necrosis during a histological examination of the whole tumor, only three of these series8, 10, 11 included surgically removed nodules, and the histological quantification of necrosis EPZ-6438 involved small sample sizes (11, 12,

and 7 lesions, respectively). However, in the Western literature, the advantages of selective embolization have not been well reported because nonselective TACE has been performed even in recent studies.12 Therefore, the primary aim of this study was to analyze whether a difference exists between selective/superselective and lobar TACE in determining tumor necrosis by a pathological Akt cancer analysis of the whole lesion at the time of transplantation. The secondary aim was to investigate the relationship between see more the tumor size and the capacity of TACE to induce necrosis. CEUS, contrast-enhanced

ultrasonography; CT, computed tomography; HCC, hepatocellular carcinoma; LT, liver transplantation; MC, Milan criteria; MRI, magnetic resonance imaging; PEI, percutaneous ethanol injection; TACE, transarterial chemoembolization. Data were extracted from a prospectively collected database for 118 consecutive patients who had a pretransplant diagnosis of HCC resulting from cirrhosis, underwent LT between January 1, 2003 and December 31, 2009 at the Liver and Multiorgan Transplant Unit of Sant’Orsola-Malpighi Hospital, and were treated with bridging or downstaging procedures. The final study population consisted of 67 patients treated only with TACE (performed exclusively at our tertiary care institution), as outlined in Fig. 1 and Table 1, with 53 patients meeting the Milan criteria (MC) and 14 meeting our downstaging protocol.3, 13 Before undergoing TACE, all patients were assessed (1) to define the degree of liver function by laboratory examinations and (2) to detect and characterize all liver nodules by imaging techniques. The Child-Pugh score and the Model for End-Stage Liver Disease score (the latter according to the formula proposed by Freeman et al.14) were calculated. The patients were staged according to the United Network for Organ Sharing guidelines15 and the integrated Barcelona Clinic Liver Cancer staging system.