Clinical outcomes after interruption of entecavir therapy in HBeAg-negative chronic hepatitis B patients with compensated cirrhosis

Chen, Y. C.; Peng, Cheng‐Yuan; Jeng, Wen–Juei; Chien, Rong‐Nan; Liaw, Yun–Fan

doi:10.1111/apt.13409

Cited by 52 publications

(65 citation statements)

References 38 publications

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“…“Rapid HBsAg decline” at month 6 was defined as ≥0.5 log 10 IU/mL reduction and at month 12 as ≥1 log 10 IU/mL reduction . Cirrhosis was diagnosed by histological findings or repeated ultrasonography findings consistent with cirrhosis, supplemented with clinical features such as varices and thrombocytopenia, as described elsewhere . Those with evidence of other liver disease(s), such as concurrent infection with other virus(es), alcoholic, metabolic or autoimmune liver disease and hepatocellular carcinoma, were excluded.…”

Section: Methodscontrasting

confidence: 73%

Great and rapid HBsAg decline in patients with on‐treatment hepatitis flare in early phase of potent antiviral therapy

Jeng

Chen

Liaw

2017

Journal of Viral Hepatitis

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HBsAg decline during nucleos(t)ide analogue therapy in chronic hepatitis B with lower pretherapy ALT is usually small and slow. This study aimed to investigate why ~10% of such patients showed "rapid HBsAg decline" ≥0.5 log IU/mL by month 6 of therapy. Patients with persistent pretherapy ALT <5X ULN who had qHBsAg at baseline, months 6 and 12 of entecavir or tenofovir therapy were studied. "On-treatment ALT elevation" was defined as >10% increase above baseline to >2X ULN during first 6 months of therapy. Of the 256 patients treated, 51 experienced transient "on-treatment ALT elevation" [group A], including 30 (11.7%) with ALT elevation to 2-5X ULN [group A-1] and 21 (8.2%) flared to >5X ULN [group A-2]. The magnitude of qHBsAg decline and rate of "rapid HBsAg decline" by month 6 was significantly greater and more frequent in group A (-0.446 vs -0.042 log IU/mL; 45.1 vs 8.8%, respectively, P = 0.000) than in the remaining 205 patients without on-treatment ALT elevation (group B), being greatest in patients with hepatitis flare (group A-2: -0.559 log IU/mL and 57.1%, respectively). In patients with therapy ≥2 years, patients with "on-treatment ALT elevation" also showed significantly greater annual HBsAg decline, more frequent to <100 IU/mL and 4 times higher HBsAg seroclearance rate. "On-treatment ALT elevation," especially flare >5X ULN, during entecavir therapy or tenofovir therapy may enhance/accelerate HBsAg decline, suggesting the effect of immune restoration upon potent viral suppression.

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Section: Methodscontrasting

confidence: 73%

Great and rapid HBsAg decline in patients with on‐treatment hepatitis flare in early phase of potent antiviral therapy

Jeng

Chen

Liaw

2017

Journal of Viral Hepatitis

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“…Hepatic decompensation was defined as a severe clinical syndrome with jaundice and prolonged prothrombin time (international normalized ratio ≥1.5) and/or occurrence of ascites/encephalopathy in patients with or without cirrhosis . Cirrhosis was diagnosed by histologic findings (144 patients) or repeated ultrasonography consistent with cirrhosis, supplemented with the presence of varices (29 patients), splenomegaly (47 patients), and/or thrombocytopenia, as described …”

Section: Methodsmentioning

confidence: 99%

Incidence and predictors of hepatitis B surface antigen seroclearance after cessation of nucleos(t)ide analogue therapy in hepatitis B e antigen–negative chronic hepatitis B

et al. 2018

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The incidence of HBsAg seroclearance after stopping Nuc was much higher than that during therapy and highest in patients without virologic and clinical relapse; patients with clinical relapse who remained untreated had a 7.34 times higher incidence of HBsAg clearance than those who received retreatment, suggesting that transient untreated clinical relapse may drive sufficient immune control to functional cure. (Hepatology 2017).

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“…Even the studies that applied APASL recommendations for stopping NUCs in HBeAg‐negative patients had high virological relapse rates, ranging from 54% to 91% during different follow‐up periods …”

Section: Why Nucs Should Not Be Stopped In Hbeag‐negative Patientsmentioning

confidence: 99%

Why not to stop antiviral treatment in patients with chronic hepatitis B

Marciano

Gadano

2018

Liver International

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Treatment of chronic hepatitis B with entecavir or tenofovir leads to viral suppression in almost all patients. However, prolonged or lifelong treatment is necessary. At present, there is no consensus among the three major guidelines for the treatment of chronic hepatitis B on whether or not to stop antiviral treatment. One of the main reasons for this controversy is that virological relapse has been well documented in patients with chronic hepatitis B who stop treatment. Relapse rate is particularly high in patients who are HBeAg-negative when treatment begins, with reported relapse rates of up to 70% 36 months after treatment discontinuation. Moreover, hepatic decompensation, jaundice and death have been described in patients with cirrhosis after treatment discontinuation. The main reason for stopping antiviral treatment is related to cost, however there is no robust evidence to support treatment discontinuation in most patients.

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Clinical outcomes after interruption of entecavir therapy in HBeAg-negative chronic hepatitis B patients with compensated cirrhosis

Abstract: SUMMARY BackgroundLong-term nucleos(t)ide analogues therapy may reduce hepatocellular carcinoma (HCC) in chronic hepatitis B patients with advanced fibrosis or cirrhosis.

Cited by 52 publications

References 38 publications

Great and rapid HBsAg decline in patients with on‐treatment hepatitis flare in early phase of potent antiviral therapy

Great and rapid HBsAg decline in patients with on‐treatment hepatitis flare in early phase of potent antiviral therapy

Incidence and predictors of hepatitis B surface antigen seroclearance after cessation of nucleos(t)ide analogue therapy in hepatitis B e antigen–negative chronic hepatitis B

Why not to stop antiviral treatment in patients with chronic hepatitis B

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