How can we improve the performance of Model for End‐Stage Liver Disease sodium score in patients with hepatitis B virus‐related decompensated liver cirrhosis commencing antiviral treatment?

Kim, Tae Hyung; Ku, Donggyun; Um, Soon Ho; Lee, Yong Sang; Park, Seung Woon; Chang, Jung Mi; Yim, Sun Young; Suh, Sang Jun; Jung, Young Kul; Seo, Yeon Seok; Kim, Ji Hoon; Yim, Hyung Joon; Yeon, Jong Eun; Byun, Kwan Soo; Ahn, Hyonggin

doi:10.1111/jgh.14128

Cited by 7 publications

(6 citation statements)

References 28 publications

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“…The presence of cirrhosis was determined based on liver histology findings, gross findings during surgery, or radiological findings of an irregular liver margin with ascites, varices, or thrombocytopenia (<10 5 cells/mm 3 ), as described previously. 11 Decompensated cirrhosis was characterised by the development of overt clinical signs, including ascites, variceal bleeding, encephalopathy and jaundice. 8 Hepatic encephalopathy was classified according to the West Haven Criteria.…”

Section: Diagnostic Criteria and Definitionmentioning

confidence: 99%

“…NUCs are expected to show an effect even in decompensated cirrhosis, which is an end‐stage liver disease accompanied by serious complications such as ascites, bleeding, encephalopathy and jaundice 8 . However, hepatic decompensation is a critical condition in which patients often experience rapid and fatal deterioration; thus, many patients with HBV‐related decompensated cirrhosis eventually die or undergo emergent liver transplantation (LT) (16%‐24% within 1 year and 30%‐40% within 5 years) even with NUC therapy 9‐11 . In contrast, patients with compensated cirrhosis have a significantly better prognosis, with 1‐ and 5‐year mortality rates of only 0.6% and 3.1% respectively 4,10 …”

Section: Introductionmentioning

confidence: 99%

“…8 However, hepatic decompensation is a critical condition in which patients often experience rapid and fatal deterioration; thus, many patients with HBVrelated decompensated cirrhosis eventually die or undergo emergent liver transplantation (LT) (16%-24% within 1 year and 30%-40% within 5 years) even with NUC therapy. [9][10][11] In contrast, patients with compensated cirrhosis have a significantly better prognosis, with 1-and 5-year mortality rates of only 0.6% and 3.1% respectively. 4,10 Thus, the reversal of the decompensated state, which we have defined as re-compensation, has a very important prognostic implication for patients with HBV-related decompensated cirrhosis who have commenced antiviral treatment.…”

Section: Introductionmentioning

confidence: 99%

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Determinants of re‐compensation in patients with hepatitis B virus‐related decompensated cirrhosis starting antiviral therapy

Kim

Lee

et al. 2021

Aliment Pharmacol Ther

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Summary Background Despite antiviral therapy, liver function often fails to recover in patients with hepatitis B virus (HBV)‐related decompensated cirrhosis. Aim To establish a prognostic model to predict re‐compensation in patients starting potent nucleos(t)ide analogue (NUC) therapy Methods We analysed 311 consecutive patients with HBV‐related decompensated cirrhosis treated with entecavir or tenofovir. The primary outcome was re‐compensation, defined as recovery to a Child–Pugh score of 5. The BC2AID score was developed from a cohort of 152 subjects based on competing risk models and validated in another cohort of 159 subjects. Results Re‐compensation occurred in 57.2% and 66.7% of the subjects in the derivation and validation cohorts, respectively. Six independent predictors for re‐compensation were identified in the derivation cohort and these comprised the BC2AID score: bilirubin ≤5 mg/dL (adjusted sub‐distribution hazard ratio [aSHR] 2.18), absence of severe complications (aSHR 2.78), alpha‐fetoprotein (AFP) ≥50 ng/mL (aSHR 2.54), alanine aminotransferase ≥200 IU/L (aSHR 2.62), international normalised ratio ≤1.5 (aSHR 2.37) and ≤6 months from initial decompensation until initiation of NUCs (aSHR 4.79). In the validation cohort, the area under the receiver operating characteristic curve of the BC2AID score for re‐compensation within 1 year of NUC therapy was significantly higher than that of the Child–Pugh, MELD, MELDNa and BE3A scores (0.813 vs 0.691, 0.638, 0.645 and 0.624, respectively; all P < 0.05). Conclusions Six clinical parameters, including AFP and the timing of antiviral therapy, were combined into a scoring system to accurately predict early re‐compensation in patients with HBV‐related decompensated cirrhosis.

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Section: Diagnostic Criteria and Definitionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Determinants of re‐compensation in patients with hepatitis B virus‐related decompensated cirrhosis starting antiviral therapy

Kim

Lee

et al. 2021

Aliment Pharmacol Ther

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“…The presence of cirrhosis was determined based on liver histology findings, gross findings during surgery, or radiological findings of an irregular liver margin with ascites, varices, or thrombocytopenia (<10 5 cells/mm 3 ) ( Kim et al., 2018 ). Decompensated cirrhosis was characterized by the development of overt clinical signs, including ascites, jaundice, hepatorenal syndrome, hepatic encephalopathy and variceal haemorrhage ( Fontana, 2003 ).…”

Section: Methodsmentioning

confidence: 99%

Ascites re-compensation in HBV-related first decompensated cirrhosis after anti-viral therapy

Zong

Xiong

et al. 2023

Front. Cell. Infect. Microbiol.

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Effective antiviral therapy can significantly improve the long-term prognosis of HBV-related decompensated patients, and re-compensation may be achieved in part of the patients. To explore the re-compensation of ascites after HBV suppression and the risk factors, the clinical outcomes of 196 consecutive patients with HBV-related first decompensated cirrhosis of ascites treated with nucleos(t)ide analogue (NUC) were analyzed retrospectively. Among these patients, the median serum HBV DNA level was 5.0 (IQR, 3.0-6.0) log10 IU/mL before treatment. Most patients were given NUC with high barrier to resistance including ETV (152), TDF (1) and TAF (1). Initial combination of LAM plus ADV and LdT plus ADV was used in 41 patients and 1 patients, respectively. After NUC treatment, the percentage of patients with ascites regression was 77.6%, 81.4%, 70.5%, 93.8%, 80.8% at 12, 24, 36, 48, 60 months, respectively (P<0.001). The distribution of ascites severity showed that the patients’ ascites improved, with the proportion of no ascites and mild ascites gradually increased. The proportion of re-compensation of ascites defined as negative HBV DNA, improved liver function and ascites regression (off diuretics) was 59.7%, 70.0%, 52.3%, 59.4%, 46.2% at 12, 24, 36, 48, 60 months (P<0.001). The rate of ascites regression was higher in viral response (VR) cohort when compared with that in non-VR cohort. Univariate and multivariable analysis showed that level of serum ALT (OR:0.988, 95%CI, p=0.029) and load of serum HBV DNA (OR:0.78895%CI, p=0.044) at baseline were risk factors of re-compensation of ascites. This study demonstrated that antiviral therapy could reverse decompensation of ascites in HBV-related first decompensated cirrhosis and the level of ALT and HBV DNA were risk factors of ascites re-compensation.

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“…The presence of cirrhosis was based on liver histology, gross findings during surgery, or radiological findings of an irregular liver margin with ascites, varices, or thrombocytopenia (<10 5 cells/mm 3 ). [18]…”

Section: Methodsmentioning

confidence: 99%

Comparison of 2 curative treatment options for very early hepatocellular carcinoma

Kim¹,

Chang²,

Um³

et al. 2019

Medicine

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Curative treatments for very early-stage hepatocellular carcinoma (HCC), defined as single HCC with a maximum diameter of <2 cm in patients with well-preserved liver function, consist of surgical resection or radiofrequency ablation (RFA). In this retrospective study, we compared the efficacy of both treatments in 154 patients with very early-stage HCCs who underwent resection or RFA as initial therapy and were followed up for a median of 56.8 months. Propensity score matching analysis was also conducted. Overall survival was comparable between treatment groups (median survival time of 143 vs 97 months for resection and RFA, respectively; P = .132). Resection group; however, demonstrated a significantly lower recurrence rate after initial therapy than RFA group (42.3% vs 65.7%; P = .006) with a longer median recurrence-free survival time (66.7 vs 33.8 months; P = .002), which was confirmed even after matching ( P = .04). In contrast, the recurrence pattern in advanced-stage (9.6% vs 1.0%; P = .01) or incurable recurrences (19% vs 13%; P = .04) was more frequent following resection than RFA. Recurrent lesions were comparatively more curable in RFA group than in resection group (80% vs 54.5%; P = .02). The recurrence of HCC was independently associated with lower serum albumin level ( P = .027), the presence of comorbid diabetes mellitus ( P = .010), and RFA ( P = .034). In conclusion, in patients with very early-stage HCC, surgical resection has achieved significantly better recurrence-free survival than RFA. A closer follow-up is required after resection.

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How can we improve the performance of Model for End‐Stage Liver Disease sodium score in patients with hepatitis B virus‐related decompensated liver cirrhosis commencing antiviral treatment?

Abstract: Ascites and encephalopathy should be considered together with the MELDNa score when predicting short-term mortality and planning liver transplant in patients with decompensated hepatitis B virus-related cirrhosis starting antiviral treatment.

Cited by 7 publications

References 28 publications

Determinants of re‐compensation in patients with hepatitis B virus‐related decompensated cirrhosis starting antiviral therapy

Determinants of re‐compensation in patients with hepatitis B virus‐related decompensated cirrhosis starting antiviral therapy

Ascites re-compensation in HBV-related first decompensated cirrhosis after anti-viral therapy

Comparison of 2 curative treatment options for very early hepatocellular carcinoma

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