Soluble ST2 Plasma Concentrations Predict Mortality in HBV‐Related Acute‐on‐Chronic Liver Failure

Lei, Ziying; Mo, Zhishuo; Zhu, Jianyun; Pang, Xiaoyan; Zheng, Xingrong; Wu, Zhebin; Wang, Ke; Li, Xinhua; Xie, Dongying; Gao, Zhiliang

doi:10.1155/2015/535938

Cited by 21 publications

(26 citation statements)

References 48 publications

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“…Results of IHC staining for IL‐33 were similar to the findings of previous reports . IL‐33 staining was concentrated in the nuclei of vascular endothelial cells and sinusoidal endothelial cells in areas of inflammation.…”

Section: Discussionsupporting

confidence: 87%

“…Previous studies have concluded that sST2 may be a useful biomarker for cardiovascular disease and inflammation, for example, heart failure and sepsis . In addition, serum sST2 levels predict mortality in HBV‐related acute‐on‐chronic liver failure . In our study, we found the sST2 level to be significantly increased in serum of patients with AIH compared with that of patients with PBC and HCs.…”

Section: Discussionsupporting

confidence: 60%

“…Moreover, the evaluation of dynamic changes in sST2 levels in HBV acute‐on‐chronic liver failure showed that serum sST2 levels increased over time in patients who died during follow‐up but decreased in those who survived. In addition, serum sST2 levels correlated with disease severity, as assessed by total bilirubin (TB), prothrombin time (PT), and the Model for End‐Stage Liver Disease score . In a mouse model in which acute hepatitis was induced by the administration of either CCl 4 or concanavalin A (ConA), IL‐33 was clearly expressed in vascular and sinusoidal endothelial cells in CCl 4 ‐induced mice but was strongly expressed in hepatocytes in ConA‐induced mice .…”

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confidence: 99%

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Interleukin‐33/ST2‐Mediated Inflammation Plays a Critical Role in the Pathogenesis and Severity of Type I Autoimmune Hepatitis

Abe¹,

Takahashi²,

Fujita³

et al. 2019

Hepatol Commun

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Interleukin (IL)‐33 was recently described as a new member of the IL‐1 family; members of this family have proinflammatory activity. IL‐33 and its soluble receptor ST2 (sST2) have been implicated in the pathogenesis of autoimmune diseases. This study investigated serum IL‐33 and sST2 in type I autoimmune hepatitis (AIH) and the relationship of these molecules with clinical and pathologic parameters. Subjects included 65 patients with AIH who were diagnosed in our hospital. The control population included 17 healthy individuals and 36 patients with primary biliary cholangitis (PBC). Mean age at AIH diagnosis was 55.5 years, and the male‐to‐female ratio was 6:59. Serum IL‐33 and sST2 levels were significantly higher in patients with AIH than in those with PBC or controls. Importantly, immunohistochemistry revealed high IL‐33 expression in liver sections from patients with AIH. In particular, serum IL‐33 and sST2 levels were significantly higher in acute‐onset AIH than in chronic‐onset AIH. Serum IL‐33 levels were positively correlated with serum total bilirubin (TB), alanine aminotransferase (ALT), and necroinflammatory activity in AIH. We performed multivariate logistic regression analysis and found serum IL‐33 levels to be independent factors for severe activity. Serum sST2 levels were positively correlated with serum TB and ALT and negatively correlated with serum albumin and prothrombin time in AIH. In particular, serum sST2 levels were significantly higher in severe symptoms of AIH. Serum IL‐33 and sST2 levels in patients with AIH responsive to treatment with prednisolone were significantly decreased after treatment. Interestingly, serum IL‐33 level was associated with a significantly increased risk of relapse. Conclusion: IL‐33/ST2 may play an important role in the pathogenesis and severity of AIH and may be a promising target for AIH therapy.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionsupporting

confidence: 60%

mentioning

confidence: 99%

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Interleukin‐33/ST2‐Mediated Inflammation Plays a Critical Role in the Pathogenesis and Severity of Type I Autoimmune Hepatitis

Abe¹,

Takahashi²,

Fujita³

et al. 2019

Hepatol Commun

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“…The complement system is an important part of the immune system in humans, and serum levels of complement C3 and C4 serve an important role in human immunity (34). Serum complement C3 and C4 levels have previously been reported to be reduced in patients with HBV (35). In the present study, the serum levels of complement C3 and C4 were significantly higher in the compensated group compared with the decompensated group at the baseline.…”

Section: Discussionsupporting

confidence: 52%

Effect of entecavir in the treatment of patients with hepatitis B virus-related compensated and decompensated cirrhosis

Gai

Wang

2017

Experimental and Therapeutic Medicine

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Abstract. Chronic hepatitis B virus (CHB) infection is a burden on global healthcare and is associated with a higher risk of serious sequelae, including cirrhosis and hepatocellular carcinoma. The clinical application of entecavir as a treatment for CHB has produced positive outcomes, and so is an attractive form of pharmacological therapy. However, little data exists comparing the safety and efficacy of entecavir for the treatment of hepatitis B virus (HBV)-related compensated, and decompensated cirrhosis, respectively. The aim of the present study was to evaluate entecavir therapy as a treatment for patients with HBV-related compensated and decompensated cirrhosis. A retrospective analysis of 46 compensated patients (compensated group) and 51 decompensated cirrhotic patients (decompensated group) treated with entecavir was conducted. Baseline demographics, clinical outcomes, and adverse events during the treatment were compared. Treatment with entecavir for 96 weeks resulted in significant improvements in serum levels of HBV DNA (P=0.002), albumin (P=0.014), cholinesterase (CHE; P=0.001), HBV DNA negativity rate (P=0.004), Child-Turcotte-Pugh score (P=0.030), alanine aminotransferase normalized rate (P=0.039), and the degree of esophageal varices liver stiffness (P=0.002) in the two groups. However, statistical analysis revealed that the improvements were significantly higher in the compensated group compared with the decompensated group (P<0.05). The complement component (C)3 and C4 levels were also significantly increased in the compensated group compared with the decompensated group at weeks 24, 48 and 96 (P<0.05). In addition, the incidences of hepatocellular carcinoma, upper digestive tract hemorrhage and ascites were significantly higher in the decompensated group compared with the compensated group (P<0.05). In conclusion, treatment with 96-week entecavir therapy produced similar clinical outcomes in compensated and decompensated cirrhotic patients via inhibiting HBV-DNA viral load and recovering complement C3 and C4; however, entecavir exerts a better effect on patients with compensated cirrhosis, and so this therapy may improve the prognosis of such patients.

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“…Elevated concentrations of this decoy receptor might indicate adverse prognosis in hepatocellular carcinoma. 17,18 Since its discovery in 2005, 4 it has become evident that IL-33 is a versatile cytokine that influences the formation and severity of liver disease. The study by Tan et al emphasizes the crucial role of IL-33 in the formation of liver fibrosis.…”

mentioning

confidence: 99%

Interleukin-33 in the pathogenesis of liver fibrosis: alarming ILC2 and hepatic stellate cells

Weiskirchen

Tacke

2016

Cell Mol Immunol

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Soluble ST2 Plasma Concentrations Predict Mortality in HBV‐Related Acute‐on‐Chronic Liver Failure

Cited by 21 publications

References 48 publications

Interleukin‐33/ST2‐Mediated Inflammation Plays a Critical Role in the Pathogenesis and Severity of Type I Autoimmune Hepatitis

Interleukin‐33/ST2‐Mediated Inflammation Plays a Critical Role in the Pathogenesis and Severity of Type I Autoimmune Hepatitis

Effect of entecavir in the treatment of patients with hepatitis B virus-related compensated and decompensated cirrhosis

Interleukin-33 in the pathogenesis of liver fibrosis: alarming ILC2 and hepatic stellate cells

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