Importance of adequate immunosuppressive therapy for the recovery of patients with “life-threatening” severe exacerbation of chronic hepatitis B

Fujiwara, Keiichi; Yokosuka, Osamu; Kojima, Hiroshige; Kanda, Tatsuo; Saisho, Hiromitsu; Hirasawa, Hiroyuki; Suzuki, Hiroshi

doi:10.3748/wjg.v11.i8.1109

Cited by 29 publications

(43 citation statements)

References 23 publications

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“…Thus, ETV is considered a first-choice therapy for patients with chronic hepatitis B not previously treated with a nucleoside analogue. However, for patients with severe exacerbation of chronic hepatitis B, treatment during the first 2 wk determines their prognosis [9] . The liver cell injury caused by HBV infection is mediated mainly by the response of CD8+ cytotoxic T lymphocytes to small epitopes of HBV proteins, especially the hepatitis B core antigen, present on the surface of liver cells [12] .…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, viral resistance, which is usually followed by a loss of clinical response, a rise in aminotransferase levels and worsening of hepatic histology, is related to mutations in the tyrosinemethionine-aspartate-aspartate (YMDD) motif which occurs in 70%-80% of patients treated continuously for 4-5 years [8] . Recently, the early introduction of highdose corticosteroid was reported to improve the shortterm prognosis of patients with severe exacerbation of chronic hepatitis B [9] . In this report, we describe 2 cases with severe exacerbation of chronic hepatitis B successfully treated with a combination of entecavir (ETV) and corticosteroid.…”

Section: Introductionmentioning

confidence: 99%

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A combination treatment of entecavir and early-phase corticosteroid in severe exacerbation of chronic hepatitis B

Matsumoto

Miyake

Miyatake

et al. 2009

WJG

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Of patients with severe exacerbation of chronic hepatitis B accompanied by jaundice and coagulopathy, 20%-30% have a fatal outcome. In this report, we describe 2 cases of severe exacerbation of chronic hepatitis B with jaundice and coagulopathy who were successfully treated with a combination of entecavir and corticosteroid. In both cases, rapid reductions in serum hepatitis B virus (HBV)-DNA levels were observed, and corticosteroid was stopped after serum HBV-DNA levels became undetectable. Entecavir treatment was continued. Generally, entecavir treatment reduced serum HBV-DNA levels rapidly, although the improvement in liver function was delayed by a few weeks. During this time lag, liver cell injury continued and the disease progressed. Corticosteroid suppressed the excessive host immune response and was useful for stopping progressive deterioration. A combination of entecavir and early-phase corticosteroid may be a useful treatment in severe exacerbation of chronic hepatitis B.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A combination treatment of entecavir and early-phase corticosteroid in severe exacerbation of chronic hepatitis B

Matsumoto

Miyake

Miyatake

et al. 2009

WJG

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“…35 Previous studies suggest that the use of corticosteroids was crucial for preventing liver cell necrosis when used in the early stage of severe hepatitis. 19 Given this, we speculated that the potential direct effect of glucocorticoids on certain inflammatory regulators could be evaluated for better therapeutic efficacy. Previous studies revealed that overwhelming pro-inflammatory cytokines were secreted after the activation of mononuclear macrophages.…”

Section: Discussionmentioning

confidence: 99%

“…16,17 As an optional therapy for ACHBLF, corticosteroid treatment has received much attention. [18][19][20][21] Glucocorticoids suppresses inflammation by controlling and preventing the immune-correlated damages. The upregulation of SOCS1 by corticosteroids has been established both in vivo and in vitro, [22][23][24] which suggests that cortisol may be playing a key role in suppressing cytokine signaling and the associated inflammatory response through SOCS1.…”

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confidence: 99%

Prognoses of patients with acute-on-chronic hepatitis B liver failure are closely associated with altered SOCS1 mRNA expression and cytokine production following glucocorticoid treatment

et al. 2014

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Suppressor of cytokine signaling (SOCS) 1 plays a crucial role in the immune response and might contribute to the prognoses of liver failure treated with glucocorticoid. We recruited 47 acute-on-chronic hepatitis B liver failure (ACHBLF) patients receiving glucocorticoid treatment and 30 healthy controls to determine the potential effects of glucocorticoid on the transcriptional level of SOCS1 in peripheral blood mononuclear cells. On the third and twenty-eighth days of glucocorticoid treatment, SOCS1 expression was negatively correlated with model for end-stage liver disease (MELD) score. Interleukin-6 (IL-6) and tumor-necrosis factor-a (TNF-a) levels were statistically lower, while the SOCS1 transcription level was higher in survivors than non-survivors both in pre-and post-treatment ACHBLF patients. The methylation rate of the SOCS1 promoter in ACHBLF patients was higher than in healthy control patients as determined by methylation-specific polymerase chain reaction. The mRNA level of SOCS1 in methylated promoters was significantly lower than from patients with unmethylated SOCS1 promoters. interferon (IFN)-c-responsive and STAT1-dependent gene expression was higher in survivors and was dramatically decreased with rising expression of SOCS1 after glucocorticoid treatment. Mortality rates were significantly higher in methylated patients than for those without methylation at the end of a 90-day follow-up. Furthermore, we found that five in six surviving patients displayed demethylated SOCS1 on the twenty-eighth day after treatment, while that number was 3 in 10 in the non-survivors. These findings suggested that ACHBLF patients without SOCS1 methylation may have a favorable response to corticosteroid treatment.

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“…7 The increase in hepatitis B viral replication also has been shown to occur in patients taking chemotherapy 9,10 and corticosteroids. 11,12 However, acute pancreatitis that was developed in healthy HBV carriers with spontaneous acute exacerbation of chronic HBV infection is rare.…”

Section: Discussionmentioning

confidence: 99%

Acute Pancreatitis Complicating Spontaneous Acute Exacerbation of Chronic Hepatitis B Virus Infection: Case Report and Review of the Literature

et al. 2009

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Acute pancreatitis may complicate viral hepatitis B, as well as the other causes of viral hepatitis. There have been reports of acute pancreatitis complicating acute exacerbations of chronic hepatitis B virus infection, most of which were related to immunosuppressive treatment or organ transplantation. However, acute pancreatitis complicating spontaneous acute exacerbation of chronic hepatitis B virus infection is rare. We report a case of acute pancreatitis that developed while a spontaneous acute exacerbation of chronic hepatitis B virus infection was underway in a healthy carrier. (Gut and Liver 2009;3:64-66)

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Importance of adequate immunosuppressive therapy for the recovery of patients with “life-threatening” severe exacerbation of chronic hepatitis B

Abstract: The introduction of high-dose corticosteroid can reverse deterioration in patients with "clinically life-threatening" severe exacerbation of chronic hepatitis B, when used in the early stage of illness.

Cited by 29 publications

References 23 publications

A combination treatment of entecavir and early-phase corticosteroid in severe exacerbation of chronic hepatitis B

A combination treatment of entecavir and early-phase corticosteroid in severe exacerbation of chronic hepatitis B

Prognoses of patients with acute-on-chronic hepatitis B liver failure are closely associated with altered SOCS1 mRNA expression and cytokine production following glucocorticoid treatment

Acute Pancreatitis Complicating Spontaneous Acute Exacerbation of Chronic Hepatitis B Virus Infection: Case Report and Review of the Literature

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