scholarly journals Intrarenal Resistance Index as a Prognostic Parameter in Patients with Liver Cirrhosis Compared with Other Hepatic Scoring Systems

Digestion ◽  
2012 ◽  
Vol 86 (4) ◽  
pp. 349-354 ◽  
Author(s):  
M. Götzberger ◽  
J. Singer ◽  
C. Kaiser ◽  
V. Gülberg
Keyword(s):  
Liver Cirrhosis ◽  
Resistance Index ◽  
Scoring Systems ◽  
Prognostic Parameter

Evaluating the effect of midodrine on renal resistance index in patients with liver cirrhosis and ascites

2016 ◽  
Vol 14 (1) ◽  
pp. 19
Author(s):  
HamdyM Moustafa ◽  
KhaledAbdel-Azeem Eid ◽  
AmroM Hassan ◽  
AhmedAbd-Elrady Ahmed
Keyword(s):  
Liver Cirrhosis ◽  
Resistance Index ◽  
Renal Resistance Index

scholarly journals Comparing Mortality Risk Predictive Ability of Different Scoring Systems in Cirrhotic Patients with Bacteremia

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Chi-Chieh Hung ◽  
Yin-Chou Hsu ◽  
Kuo-Hsuan Lin
Keyword(s):  
Liver Cirrhosis ◽  
Mortality Risk ◽  
Predictive Ability ◽  
Scoring Systems ◽  
Meld Score ◽  
Lower Proportion ◽  
Discriminative Ability ◽  
Survivor Group ◽  
Cirrhotic Patients ◽  
Qsofa Score

Patients with liver cirrhosis and bacteremia have substantially higher risk of mortality and morbidity. Our study aimed to investigate scoring systems that can predict the mortality risk in patients with cirrhosis and bacteremia. A single-center, retrospective cohort study was performed among adult patients who visited the emergency department from January 2015 to December 2018. All patients diagnosed with liver cirrhosis and bacteremia were enrolled and divided into survivor and nonsurvivor groups for comparison based on their 30-day in-hospital mortality event. The Pitt bacteremia score (PBS), model for end-stage liver disease (MELD) score, Child–Pugh score, and quick sequential Organ Failure Assessment (qSOFA) score were calculated and compared using the area under the receiver operating characteristic (AUROC) curves. A total of 127 patients (survivor: 86; nonsurvivor: 41) were eligible for this study. Compared with the nonsurvivor group, patients in the survivor group had significantly lower MELD score (22 ± 7 vs. 29 ± 5, p < 0.001 ), lower proportion of high qSOFA (score ≥ 2) (23.3% vs. 51.2%, p < 0.01 ), and high PBS (score ≥ 4) (7.0% vs. 34.1%, p < 0.001 ) category. There was also a significantly different distribution in Child–Pugh classification between the two groups p < 0.01 . The survivor group had significantly lower proportion of acute-on-chronic liver failure (27.9% vs. 68.3%, p < 0.001 ) and fewer number of organ failures p < 0.001 . In comparison of the discriminative ability in mortality risk prediction, PBS (AUROC = 0.83, 95% CI = 0.75–0.90, p < 0.001 ) and MELD scores (AUROC = 0.78, 95% CI = 0.70–0.86, p < 0.001 ) revealed a better predictive ability than Child–Pugh (AUROC = 0.69, 95% CI = 0.59–0.70, p < 0.01 ) and qSOFA scores (AUROC = 0.65, 95% CI = 0.54–0.75, p < 0.01 ). PBS and MELD scores both demonstrated a superior ability of predicting mortality risk in cirrhotic patients with bacteremia.

scholarly journals Evaluation of prognostic scoring systems in liver cirrhosis patients with bloodstream infection

Medicine ◽  
2017 ◽  
Vol 96 (50) ◽  
pp. e8844 ◽  
Author(s):  
Hong Zhao ◽  
Xiuling Gu ◽  
Ruihong Zhao ◽  
Yu Shi ◽  
Jifang Sheng
Keyword(s):  
Liver Cirrhosis ◽  
Bloodstream Infection ◽  
Scoring Systems ◽  
Prognostic Scoring Systems

scholarly journals Mitochondria-targeted antioxidant mitoquinone attenuates liver inflammation and fibrosis in cirrhotic rats

2020 ◽  
Vol 318 (2) ◽  
pp. G298-G304 ◽  
Author(s):  
Saadet Turkseven ◽  
Massimo Bolognesi ◽  
Alessandra Brocca ◽  
Paola Pesce ◽  
Paolo Angeli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Liver Cirrhosis ◽  
Transforming Growth Factor ◽  
Resistance Index ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Liver Inflammation ◽  
Hepatic Oxidative Stress ◽  
Duct Ligation ◽  
Tnf Α

In liver cirrhosis, oxidative stress plays a major role in promoting liver inflammation and fibrosis. Mitochondria dysregulation is responsible for excessive reactive oxygen species production. Therefore, in an experimental model of cirrhosis, we investigated the effect of mitochondria-targeted antioxidant mitoquinone. Liver cirrhosis was induced in Spraque-Dawley rats by common bile duct ligation (CBDL). Mitoquinone (10 mg·kg−1·day−1, oral gavage) or vehicle was administered from 3rd to 28th day after CBDL, when animals were euthanized; liver oxidative stress, inflammation, fibrosis, mitophagy were evaluated; and in vivo and ex vivo hemodynamic studies were performed. In cirrhotic rats, mitoquinone prevented liver inflammation, hepatocyte necrosis, and fibrosis at histological examination; decreased circulating TNF-α, gene expression of transforming growth factor-β1, collagen type 1a1, TNF-α, IL-6, IL-1β, tissue inhibitor of metalloproteinase-1, matrix metalloproteinase (MMP)-2, and MMP-13; and reduced hepatic oxidative stress, as shown by reduced oxidative carbonylation of the proteins, by modulating antioxidants catalase, Mn superoxide dismutase, and Cu/Zn superoxide dismutase. Furthermore, mitoquinone attenuated apoptosis by reducing hepatic protein expression of cleaved caspase-3. A selective removal of dysfunctional mitochondria was improved by mitoquinone, as shown by the increase in Parkin translocation to mitochondria. Treatment with mitoquinone normalized the weight of the spleen; however, it increased portal blood flow and reduced splenic artery intrahepatic resistance, suggesting an effect on resistance index. Mitochondria-targeted antioxidant mitoquinone improves liver inflammation and fibrosis in cirrhotic rats by reducing hepatic oxidative stress, preventing apoptosis, and promoting removal of dysfunctional mitochondria. Therefore, it may represent a promising strategy for the prevention and treatment of liver cirrhosis.

Camel milk and bee honey regulate profibrotic cytokine gene transcripts in liver cirrhosis induced by carbon tetrachloride

2016 ◽  
Vol 94 (11) ◽  
pp. 1141-1150 ◽  
Author(s):  
Kadry Sadek ◽  
Doha Beltagy ◽  
Ebeed Saleh ◽  
Reham Abouelkhair
Keyword(s):  
Liver Cirrhosis ◽  
Carbon Tetrachloride ◽  
Antioxidant Properties ◽  
Resistance Index ◽  
Camel Milk ◽  
Male Rats ◽  
Protective Effects ◽  
Cytokine Gene ◽  
Glucose Levels ◽  
Gene Transcripts

The lack of studies regarding the mechanism of the protective effects of camel milk and bee honey against hepatotoxic compounds led us to perform this study. Thirty-six male rats were divided into two main groups. The first group (n = 9) comprised control non-cirrhotic rats. The rats of the second group (n = 27) were administered carbon tetrachloride (CCl4) by intraperitoneal injection to induce liver cirrhosis. The cirrhotic rats were then divided into three equal subgroups, each comprising nine animals, as follows: (i) cirrhotic rats, (ii) cirrhotic rats treated with camel milk, and (iii) cirrhotic rats treated with camel milk and bee honey. The present findings revealed that CCl4 elevated the activities of liver enzymes, blood glucose levels, non-esterified fatty acids (NEFA) in the serum and glycogen content in the liver. On the other hand, CCl4 significantly decreased phosphorylase activity in the liver tissue and significantly increased carbohydrate intolerance and insulin resistance index (HOMA-IR). Moreover, CCl4 induced a significant increase in oxidative stress, along with increased expression of the profibrotic cytokine genes TNF-α and TGF-β. However, camel milk either alone or in combination with bee honey ameliorated these toxic actions. The antioxidant properties of these protective agents and their effects of downregulating certain procirrhotic cytokine gene transcripts underlie this protection.

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