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- 저자 : ( Yee-kit Tse ) (검색결과 3 건)
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Hepatic Decompensation in Cirrhotic Patients Receiving Antiviral Therapy for Chronic Hepatitis B
( Hye Won Lee ),( Terry Cheuk-fung Yip ),( Yee-kit Tse ),( Grace Lai-hung Wong ),( Beom Kyung Kim ),( Seung Up Kim ),( Jun Yong Park ),( Do Young Kim ),( Henry Lik-yuen Chan ),( Sang Hoon Ahn ),( Vinc 대한간학회 2020 춘·추계 학술대회 (KASL) Vol.2020 No.1
Aims: It is unclear if anti-hepatitis B virus (HBV) treatment can eliminate incident hepatic decompensation. Here we report the incidence and predictors of hepatic decompensation among cirrhotic patients receiving antiviral therapy for chronic hepatitis B. Methods: This is a post hoc analysis of two prospective HBV cohorts from Hong Kong and South Korea. Patients with liver stiffness measurement (LSM) ≥10 kPa and compensated liver disease at baseline were included. The primary endpoint was incident hepatic decompensation (jaundice or cirrhotic complications) with competing risk analysis. Results: 818 patients (mean age, 54.9 years; 519 male [63.4%]) were included in the final analysis. During a mean follow-up of 58.1 months, 32 (3.9%) patients developed hepatic decompensation, among whom 34% were secondary to HCC. Three (0.4%) patients experienced variceal bleeding alone, 27 (3.3%) had non-bleeding decompensation and 13 (1.6%) had more than 2 decompensating events. On multivariable analysis, baseline LSM (adjusted hazard ratio [aHR] 1.03), diabetes (aHR 3.27), platelet (aHR 0.99), and international normalized ratio (aHR 7.99) were independent predictors of hepatic decompensation. 30/506 (5.9%) patients fulfilling the Baveno VI criteria (LSM ≥20 kPa and/or platelet count <150ⅹ10<sup>9</sup>/L) and 2/312 (0.6%) patients not fulfilling the criteria developed hepatic decompensation (P<0.001). Conclusions: Hepatic decompensation is uncommon but not eliminated in patients receiving antiviral therapy for HBV-related cirrhosis, and only a third of decompensating events are secondary to HCC. The Baveno VI criteria, which was originally designed to detect varices needing treatment, can be effectively applied in this population to identify patients at risk of decompensation.
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Huapeng Lin,Grace Lai-Hung Wong,Xinrong Zhang,Terry Cheuk-Fung Yip,Ken Liu,Yee Kit Tse,Vicki Wing-Ki Hui,Jimmy Che-To Lai,Henry Lik-Yuen Chan,Vincent Wai-Sun Wong 대한간학회 2022 Clinical and Molecular Hepatology(대한간학회지) Vol.28 No.1
Background/Aims: We aimed to determine the association between blood urea level and incident cirrhosis, hepatic decompensation, and hepatocellular carcinoma in chronic liver disease (CLD) patients. Methods: The association between blood urea level and liver fibrosis/liver-related events were evaluated on continuous scale with restricted cubic spline curves based on generalized additive model or Cox proportional hazards models. Then, the above associations were evaluated by urea level within intervals. Results: Among 4,282 patients who had undergone liver stiffness measurement (LSM) by transient elastography, baseline urea level had a U-shaped association with LSM and hepatic decompensation development after a median follow-up of 5.5 years. Compared to patients with urea of 3.6–9.9 mmol/L, those with urea ≤3.5 mmol/L (adjusted hazard ratio [aHR], 4.15; 95% confidence interval [CI], 1.68–10.24) and ≥10 mmol/L (aHR, 5.22; 95% CI, 1.86–14.67) had higher risk of hepatic decompensation. Patients with urea ≤3.5 mmol/L also had higher risk of incident cirrhosis (aHR, 3.24; 95% CI, 1.50–6.98). The association between low urea level and incident cirrhosis and hepatic decompensation was consistently observed in subgroups by age, gender, albumin level, and comorbidities. The U-shaped relationship between urea level and LSM was validated in another population screening study (n=917). Likewise, urea ≤3.5 mmol/L was associated with a higher risk of incident cirrhosis in a territory-wide cohort of 12,476 patients with nonalcoholic fatty liver disease at a median follow-up of 9.9 years (aHR, 1.27; 95% CI, 1.03–1.57). Conclusions: We identified a U-shaped relationship between the urea level and liver fibrosis/incident cirrhosis/hepatic decompensation in patients with CLD.
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( Lilian Yan Liang ),( Hye Won Lee ),( Vincent Wai-sun Wong ),( Terry Cheuk-fung Yip ),( Yee-kit Tse ),( Vicki Wing-ki Hui ),( Grace Chung-yan Lui ),( Henry Lik-yuen Chan ),( Grace Lai-hung Wong ) 대한간학회 2021 Clinical and Molecular Hepatology(대한간학회지) Vol.27 No.3
Background/Aims: Serum fibrosis scores comprised of common laboratory tests have high utility to assess severity of liver fibrosis. We aimed to derive and validate a hepatocellular carcinoma (HCC) risk score based on serum fibrosis scores to predict HCC in treatment-naive chronic hepatitis B (CHB) patients. Methods: Fifteen thousand one hundred eighty-seven treatment-naive adult CHB patients were identified to form the training cohort in this retrospective study. Individual fibrosis score was included to construct a new HCC prediction score. The score was externally validated in an independent treatment-naive Korean CHB cohort. Results: 180/15,187 patients (1.2%) in training cohort and 47/4,286 patients (1.1%) in validation cohort developed HCC during a mean follow-up of 52 and 50 months, respectively. The newly developed HCC risk score, Liang score, is composed of gender, age, hepatitis B virus DNA, fibrosis-4 (FIB-4) index, and ranges from 0 to 22. Area under the time-dependent receiver operating characteristic curve of Liang score was 0.79 (95% confidence interval, 0.70-0.89). A cutoff value of nine provided an extremely high negative predictive value of 99.9% and high sensitivity of 90.0% at 5 years in the validation cohort. Patients with Liang score ≤9 had HCC incidence <0.2% per year in both training and validation cohorts, in whom HCC surveillance might be exempted. Conclusion: A novel HCC risk score, Liang score, based on FIB-4 index, is applicable and accurate to identify treatment-naive CHB patients with very low risk of HCC to be exempted from HCC surveillance. (Clin Mol Hepatol 2021;27:499-509)
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