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( Eileen L Yoon ),( Eun Jung Ko ),( Jong Eun Yeon ),( Ji Hye Je ),( Yang Jae Yoo ),( Keun Hee Kang ),( Sun Jae Lee ),( Hyun Jung Lee ),( Sang Jun Suh ),( Ji Hoon Kim ),( Yeon Seok Seo ),( Hyun Joon Yi 대한간학회 2013 춘·추계 학술대회 (KASL) Vol.2013 No.1
Background: The modest efficacy, high cost, and significant adverse reactions are the limitations of sorafenib. There have been no reliable serum markers predictive of response to sorafenib. Circulating miRNAs can be ideal biomarkers. We aimed to identify the specific circulating miRNAs prognostic for good response or favorable survival in advanced HCC patients who are scheduled for sorafenib treatment. Methods: On the basis of miRNAs previously reported to be associated with HCC, 6 target miRNAs, miR-21, miR-221, miR-18a, miR-10b*, miR-139-5p, and miR-224 were chosen. Relative expressions were measured by real-time RT-PCR in the sera of 24 HCC patients collected prior to sorafenib treatment. The sera of 25 liver cirrhosis (LC) patients were used as control. The results were validated in the 16 HCC tissue specimens obtained by needle biopsy and various HCC cell lines. Results: All the miRNAs except miR-21 were found to be overexpressed in the sera of HCC patients compared with those of LC patients (P<0.05). In the sera, there was no miRNA which shows significant difference in the relative expression between responder and non-responder group of HCC patients. Among them, circulating miR-10b* was shown to be overexpressed in the worse survivor (Fold change 2.9, P=0.0082). Tissue- based miR-10b* expression in the worse survivor group was down-regulated (Fold change 0.3, P<0.0001). The presence of macrovascular invasion was the only significant predictive factor for longer survival in our HCC patients. Circulating miRNA-10b* expression level was higher in the presence of macrovascular invasion and miR-10b* was also overexpressed in HCC cell lines with invasive tumor characteristics (P<0.001). Conclusions: Circulating miRNAs can overcome the limitation of miRNAs in the tissue obtained by needle biopsy. Serum miR-10b* may affect the invasiveness of HCC and serves as a prognostic biomarker predicting better survival in advanced HCC patients who are treating with sorafenib.
( Eileen L. Yoon ),( Jeong Han Kim ),( Won Hyeok Choe ),( So Young Kwon ),( Won-choong Choi ),( Byung-chul Yoo ) 대한간학회 2016 춘·추계 학술대회 (KASL) Vol.2016 No.1
Aims: Tenofovir (TDF) is a potent agent for chronic hepatitis B (CHB) and TDF monotherapy has been widely accepted for treatment of multi-drug resistance. We aimed to evaluate safety of switching to TDF monotherapy from TDF-based combination therapy. Methods: This is a retrospective study of CHB patients who had been treated with TDF-based combination therapy and switched to TDF monotherapy after achievement of virological response (VR; undetectable HBV DNA by real-time PCR) in Konkuk university hospital and Sanggye Paik Hospital. Results: Total 38 patients were included in this study. Median age was 51 years old and 28 patients were male (73.7%). HBeAg positive patients were 31 (81.6%). Combination types were lamivudine (LMV) plus TDF (19, 50%) and entecavir (ETV) plus TDF (19, 50%). VR duration before switching to monotherapy was median 16.1 months and monotherapy duration was median 7.5 months. Within 6 months, HBV DNA became detectable in 4 patients and one of them was related with poor compliance to antiviral treatment. Excluding one patient with poor compliance, two patients had been treated with LMV plus TDF combination therapy and one patient had been treated with ETV plus TDF combination therapy. Resistance types before combination treatment were LMV only resistance, ETV resistance, and adefovir only resistance each. VR durations of these patients were one month, 13 months and 6 months. Conclusions: Generally, switching to TDF monotherapy from TDF-based combination treatment was safe and effective. Some cases showed that longer consolidation therapy after achievement of VR might be required for safe switching to TDF monotherapy.
( Eileen L. Yoon ),( Tae Yeob Kim ),( Do Seon Song ),( Jin Mo Yang ),( Hee Yeon Kim ),( Chang Wook Kim ),( Young Kul Jung ),( Hyung Joon Yim ),( Soung Won Jeong ),( Sang Gyune Kim ),( Jae Young Jang ) 대한간학회 2018 춘·추계 학술대회 (KASL) Vol.2018 No.1
Aims: To investigate long-term mortality according to the severity of alcoholic hepatitis and the presence or absence of previous acute decompensation (AD) in alcoholic cirrhotic patients with acute deterioration. Methods: A total of 894 alcoholic cirrhotic patients (male 747, mean age 53.1 years) with acute deterioration were prospectively followed up. Severe alcoholic hepatitis (SAH) was defined by a modified discriminant function ≥32. Enrolled patients were divided into 3 groups according to the presence and severity of AH; group1, alcoholic cirrhosis without AH; group2, alcoholic cirrhosis with non-SAH; group3, alcoholic cirrhosis with SAH. AD was defined as: acute development of overt ascites, hepatic encephalopathy, gastrointestinal bleeding, and infection. Results: During follow-up duration (14.3±10.7 months), long-term mortality were higher in patients with group 3 than those in group 1 and 2, but there was no significant difference between group 1 and 2 (group 1, 160/596; group 2, 27/141; group 3, 76/157, P<0.001). Also, in 671 patients who survived for more than 3 months following acute deterioration (long-term survivors), long-term survival curve between groups showed a similar pattern (P=0.004). Interestingly, in group 1, the presence of previous AD negatively affected long-term survival in total and long-term survivors (P<0.001 and P=0.004, respectively). However, in group 3, previous AD negatively affected long-term survival in long-term survivors (P=0.009), but not in total patients (figure 1). Especially in long-term survivors of group 3, previous AD showed hazard ratio of 2.47 (95% confidence interval, 1.16-5.28, P=0.019). Conclusions: Compared with the long-term prognosis of patients with acute deterioration except for AH, that of SAH was poor, but that of non-SAH was similar. However, in patients with acute deterioration except for AH and SAH patients overcoming acute deterioration, the presence of previous AD had a great impact on long-term prognosis. These findings will help to determine the therapeutic plan.
( Eileen L. Yoon ),( Dae Won Jun ),( Sang Bong Ahn ),( Yong Kyun Cho ),( Do Seon Song ),( Jae Yoon Jeong ),( Hee Yeon Kim ),( Young Kul Jung ),( Myeong Jun Song ),( Sung Eun Kim ),( Hyoung Su Kim ),( 대한간학회 2020 춘·추계 학술대회 (KASL) Vol.2020 No.1
Aims: To evaluate the impact of L-carnitine on the improvement of quality of life (QOL) and cognitive function in liver cirrhosis patients with covert hepatic encephalopathy (HE). Methods: We conducted a multi-center, double-blind, randomized, phase III clinical trial in patients with covert HE. A total of 150 covert HE patients were randomized 1:1 to L-carnitine (1 g) or placebo for 24 weeks. Changes in QOL and cognitive function were assessed at 6 months. West Haven criteria, 36- Item Short Form Health Survey (SF-36), psychometric hepatic encephalopathy score (PHES), and the Stroop Test were evaluated in all patients. Results: The L-carnitine supplement improved QOL compared to baseline. PHES scores were improved and normalization rates of minimal HE were increased in the L-carnitine group compared to baseline; however, median PHES scores and normalization rates were not different between the L-carnitine group and the placebo group at Week 24. Assessment of cognitive inhibition via the Stroop test showed significant improvement following 24 weeks of treatment in the L-carnitine group. Model for end stage liver disease scores were increased in the placebo group and significantly decreased in the L-carnitine group. Changes in total carnitine level positively correlated with rate correct scores of the Stroop test in the L-carnitine group. The incidence of adverse events was not different between the treatment groups. Conclusions: L-carnitine supplement was safe and effective for the improvement of QOL and cognitive dysfunction in covert HE patients with liver cirrhosis. (Clinical trial No. KCT0002029)