Clinical characteristics and prognostic factors of liver cirrhosis patients with systemic inflammatory response syndrome

Yang, Danhong; Xie, Yangli; Pan, Hongying; Huang, Yicheng; Dai, Yining; Tong, Yongxi; Chen, Meijuan

doi:10.1111/hepr.12886

Cited by 11 publications

(9 citation statements)

References 40 publications

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“…It had been recognized that the severity of portal hypertension and circulatory dysfunction can lead to an increase in levels of biomarkers associated with systemic inflammation (such as WBC and interleukin [IL]‐6) and impaired intestinal integrity (FABP2), of which systemic inflammation may be a key driver of clinical deterioration 24 . Systemic inflammation in cirrhotic patients maximizes the risk of complications, such as VH, 25 hepatic encephalopathy, 26 and increased the mortality rate 27,28 . CRP, the production of which is stimulated by IL‐6 synthesis, is strongly associated with an ongoing systemic proinflammatory response, during which hepatic endothelial dysfunction elevates vasoconstrictor production, leading to deteriorated portal hypertension.…”

Section: Discussionmentioning

confidence: 99%

“…27,28 CRP, the production of which is stimulated by IL-6 synthesis, is strongly associated with an ongoing systemic proinflammatory response, during which hepatic endothelial dysfunction elevates vasoconstrictor production, leading to deteriorated portal hypertension. Turco et al29 demonstrated that CRP could be used to predict the clinical outcomes of both patients with compensated and decompensated cirrhosis.…”

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confidence: 99%

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Predicting the risk of variceal rehemorrhage in cirrhotic patients with portal vein thrombosis: A two‐center retrospective study

Zhang,

Zhong,

Zhong

et al. 2023

J of Digest Diseases

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Background and aimsAlthough portal vein thrombosis (PVT) was considered worsening portal hypertension and leading to poor prognosis, the risk stratification still be unclear. This study was to evaluate its effect on the risk of variceal rehemorrhage, accordingly identify the clinical predictors and develop a competitive risk model utilized for cirrhotic patients with PVT.MethodsCirrhotic patients with and without PVT admitted for variceal hemorrhage were retrospectively included by matching (1:1) for sex, age and etiology from two tertiary centres for 1‐year follow‐up, of which patients with PVT were divided into the training and validation cohort. Cox regression analysis was performed to identify risk factors and therefore develop a competitive risk model, of which the predictive performance and the optimal decision threshold were evaluated by C‐index, competitive risk curves, calibration curves and decision curve analysis.ResultsWe included 398 patients and firstly found that PVT could significantly increase variceal rehemorrhage risk. Then, multivariate Cox regression analysis identified that CTP score (P = 0.013), time course of PVT (P = 0.025), CRP (P < 0.001) and AST (P = 0.039) were independently associated with variceal rehemorrhage, which were incorporated into the competitive risk model, with high C‐index (0.804 and 0.742 of the training and validation cohort, respectively), risk stratification ability and consistency. The optimal decision range of the threshold probability was 0.2–1.0.ConclusionsThis study not only confirmed the harmful effect of PVT on variceal rehemorrhage but also developed a competitive risk model for cirrhotic patients with PVT, which could be conveniently used for clinical decision making.This article is protected by copyright. All rights reserved.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Predicting the risk of variceal rehemorrhage in cirrhotic patients with portal vein thrombosis: A two‐center retrospective study

Zhang,

Zhong,

Zhong

et al. 2023

J of Digest Diseases

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“…Creatinine ≥175 µmol/L, C-reactive protein (CRP) ≥25 mg/L, multisite infection, acute-on-chronic liver failure, and advanced hepatocellular carcinoma were also identified as independent predictors of 90-day mortality in cirrhotic patients with systemic inflammatory response syndrome (commonly known as SIRS). Similarly, another study also demonstrated that a procalcitonin level of ≥1.0 ng/mL can predict the 90-day mortality rate for liver cirrhosis, but only in univariate analysis 28…”

Section: Application Of Pct In Liver Diseasesmentioning

confidence: 95%

Procalcitonin and Liver Disease: A Literature Review

Dong

Wan

Lin

et al. 2018

JCTH

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Procalcitonin (PCT) is a widely used biomarker for the diagnosis of bacterial infections. It is produced by various organs and the liver is considered to be the most important site of production. Severe liver dysfunction has been shown to influence PCT levels. Patients with no sources of infection who have liver disease are observed to have increased serum levels of PCT, thereby reducing the diagnostic utility and value within this particular patient subset. Here, we have summarized the relationship between PCT and liver disease, including liver cirrhosis, liver failure, and liver transplantation.

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“…GALT constitutes the largest lymphoid organ of the body, and its activation in portal hypertensive enteropathy results in the release of several inflammatory mediators. These mediators would be transported by the intestinal lymph nodes to the pulmonary circulation inducing an inflammatory phenotype and later to the systemic circulation [91,118,119].…”

Section: The Reexpression Of the Trophoblastic-yolk Sac-related Phenomentioning

confidence: 99%

The Wound-Healing Portal Hypertensive Response

Aller¹,

Blanco-Rivero²,

Arias³

et al. 2020

Translational Studies on Inflammation

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Portal hypertensive inflammation is associated with chronic liver diseases. The three successive and overlapping systemic inflammatory phenotypes, i.e., neurogenic, immune, and endocrine, which characterize the wound-healing response, are expressed by the portal venous system upon liver injury. The diverse functions of hepatic stellate cells in homeostasis and inflammation indicate the versatile nature of these mesenchymal-derived cells, which could adopt numerous phenotypes according to the interstitial microenvironmental characteristics. Consequently, these inflammatory phenotypes could represent the reexpression of two extraembryonic functional axis, i.e., coelomic-amniotic and trophoblastic-vitelline, whose coupling in the portal system would induce a gastrulation-related phenotype. Therefore, hepatic stellate cells and liver-specific mesenchymal cells could recapitulate and couple these abovementioned extra-embryonic phenotypes during portal hypertension. These hepatic cellular population, thanks to their potential ability to integrate and reexpress functions showing analogies to extra-embryonic functions, display characteristics of stem/progenitor cells. In this way, during the development of portal hypertension, hepatic stellate cells not only could reexpress extra-embryonic functions, but also could adapt themselves in order to induce a gastrulation-related process in the space of Disse. Hence, by understanding the ontogenic interactions between hepatic stellate cells and the host inflammatory response in portal hypertension, it is possible to design effective therapeutic and prophylactic strategies to avoid or reverse wound-like hypertensive response.

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Clinical characteristics and prognostic factors of liver cirrhosis patients with systemic inflammatory response syndrome

Abstract: Cr ≥ 175 µmol/L, CRP ≥ 25 mg/L, multi-site infection, ACLF, and advanced HCC independently predicted a higher rate of 90-day mortality in liver cirrhosis with SIRS.

Cited by 11 publications

References 40 publications

Predicting the risk of variceal rehemorrhage in cirrhotic patients with portal vein thrombosis: A two‐center retrospective study

Predicting the risk of variceal rehemorrhage in cirrhotic patients with portal vein thrombosis: A two‐center retrospective study

Procalcitonin and Liver Disease: A Literature Review

The Wound-Healing Portal Hypertensive Response

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