Long-term survival by etiology.

<p>The median survival was significantly longer in HCV-related HCC patients than in HBV-related HCC patients. (2.17 vs. 1.34 years, <i>P</i><0.01).</p

Characteristics of study population.

<p>Abbreviation: HBV, hepatitis B virus; HCV, hepatitis C virus; S.D, standard deviation; INR, international normalized ratio; AJCC/mUICC, American Joint Committee on Cancer/International Union Against Cancer; BCLC, Barcelona Clinic Liver Cancer; TACE, transarterial chemoembolization; TACI, transarterial chemoinfusion.</p><p>*These 3 patients received ¹⁶⁶holmium injection therapy. Values are expressed as mean ± standard deviation, median (quartile), or no (%).</p>†<p>BCLC stage and performance status was not collected at the time of data collection. Hence, BCLC stage was re-coded (staged) by authors with Child-Pugh class, tumor size, tumor number and presence of portal vein invasion and extrahepatic spread, without performance status.</p><p>Characteristics of study population.</p

Adjusted difference in the survival between hepatitis B virus and hepatitis C virus related hepatocellular carcinoma by subgroup.

<p>Abbreviation: HBV, hepatitis B virus; HCV, hepatitis C virus; CI, confidence interval; NR, not reached. In each adjusted model, hepatitis B was used as reference for hepatitis C and following variables were adjusted: age, gender, Child-Pugh class, AJCC/mUICC stage, and initial treatment modality.</p><p>Adjusted difference in the survival between hepatitis B virus and hepatitis C virus related hepatocellular carcinoma by subgroup.</p

The age-specific incidence rates of hepatocellular carcinoma (HCC) by the etiology (A), by gender in HBV-related HCC (B) and by gender in HCV-related HCC (C).

<p>The annual incidence rates of HBV-related HCC peaked in the 50–59 age group, while the annual incidence rates of HCV-related HCC kept gradually increasing until age ≥70 s. Similar trend was observed after stratified by gender, although the peak mean annual incidence rates was observed in the 50–59 in men and in the 60–69 in women in HBV-related HCC (B). Diamonds (♦) and triangles (▴) represent for HBV and HCV-related HCC in (A), men and women in (B) and (C), respectively.</p

Survival by etiology.

<p>Abbreviation: HBV, hepatitis B virus; HCV, hepatitis C virus. HR, hazard ratio. Model 1  =  crude hazard ratio, Model 2  =  adjusted for age, gender, Model 3  =  Model 2 + Child-Pugh class and AJCC/mUICC stage, Model 4  =  Model 3 + initial treatment modality.</p><p>Survival by etiology.</p

Comparison of prognostic factors between hepatitis B virus- and hepatitis C virus-related hepatocellular carcinoma.

<p>Abbreviation: HBV, hepatitis B virus; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; HR, hazard ratio.</p><p>Comparison of prognostic factors between hepatitis B virus- and hepatitis C virus-related hepatocellular carcinoma.</p

Oral Valganciclovir as a Preemptive Treatment for Cytomegalovirus (CMV) Infection in CMV-Seropositive Liver Transplant Recipients

<div><p>Objectives</p><p>Cytomegalovirus (CMV) infections in liver transplant recipients are common and result in significant morbidity and mortality. Intravenous ganciclovir or oral valganciclovir are the standard treatment for CMV infection. The present study investigates the efficacy of oral valganciclovir in CMV infection as a preemptive treatment after liver transplantation.</p><p>Methods</p><p>Between 2012 and 2013, 161 patients underwent liver transplantation at Samsung Medical Center. All patients received tacrolimus, steroids, and mycophenolate mofetil. Patients with CMV infection were administered oral valganciclovir (VGCV) 900mg/day daily or intravenous ganciclovir (GCV) 5mg/kg twice daily as preemptive treatment. Stable liver transplant recipients received VGCV.</p><p>Results</p><p>Eighty-three patients (51.6%) received antiviral therapy as a preemptive treatment because of CMV infection. The model for end-stage liver disease (MELD) score and the proportions of Child-Pugh class C, hepatorenal syndrome, and deceased donor liver transplantation in the CMV infection group were higher than in the no CMV infection group. Sixty-one patients received GCV and 22 patients received VGCV. The MELD scores in the GCV group were higher than in the VGCV group, but there were no statistical differences in the pretransplant variables between the two groups. AST, ALT, and total bilirubin levels in the GCV group were higher than in the VGCV group when CMV infection occurred. The incidences of recurrent CMV infection in the GCV and VGCV groups were 14.8% and 4.5%, respectively (P=0.277).</p><p>Conclusion</p><p>Oral valganciclovir is feasible as a preemptive treatment for CMV infection in liver transplant recipients with stable graft function.</p></div

Rates of CMV reinfection after preemptive treatments.

<p>Relapsed secondary CMV infection rates in the intravenous GCV and in the oral VGCV groups were 14.8% and 4.5%.</p

Baseline characteristics.

<p>^*Initial alphafetoprotein level was missing in 38 patients.</p><p>^†Of the 160 patients with distant metastasis, 33 patients (20.6%) had concomitant nodal metastasis.</p><p>Baseline characteristics.</p

Baseline characteristics of patients with and without CMV infection.

<p>CMV, cytomegalovirus; BMI, body mass index; MELD, model for end-stage liver disease; DDLT, deceased donor liver transplantation; ICU, intensive care unit</p><p>Baseline characteristics of patients with and without CMV infection.</p