Cardiopulmonary hemodynamics and C-reactive protein as prognostic indicators in compensated and decompensated cirrhosis

Turco, Laura; García–Tsao, Guadalupe; Magnani, Ilenia; Bianchini, Marcello; Costetti, Martina; Caporali, Cristian; Colopi, Stefano; Simonini, Emilio; Maria, Nicola De; Banchelli, Federico; Rossi, Rosario; Villa, Erica; Schepis, Filippo

doi:10.1016/j.jhep.2017.12.027

Cited by 118 publications

(147 citation statements)

References 38 publications

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“…It not only leads to the development of CSPH and portosystemic collaterals, but is also responsible for sodium and water retention, all of which eventually lead to the development of clinical decompensation . In a stage of further progression of liver disease, systemic hypotension develops, mainly attributed to further vasodilatation and a relative decrease in cardiac output, leading to refractory ascites and hepatorenal syndrome . Systemic hypotension on the one side and clinical immunological events (e.g., systemic inflammation, infections) on the other side lead to impaired organ perfusion and dysfunction, and the development of multiorgan failure in cirrhosis (so‐called acute‐on‐chronic liver failure) .…”

Section: Preclinical Studies In Portal Hypertension (Ph)mentioning

confidence: 99%

“…(12) In a stage of further progression of liver disease, systemic hypotension develops, mainly attributed to further vasodilatation and a relative decrease in cardiac output, leading to refractory ascites and hepatorenal syndrome. (13) Systemic hypotension on the one side and clinical immunological events (e.g., systemic inflammation, infections) on the other side lead to impaired organ perfusion and dysfunction, and the development of multiorgan failure in cirrhosis (so-called acute-on-chronic liver failure). (14) Therefore, the selection of targets could be different in compensated and decompensated cirrhosis depending on the objective of treatment ( Fig.…”

Section: Preclinical Studies In Portal Hypertension (Ph)mentioning

confidence: 99%

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Prioritization of Therapeutic Targets and Trial Design in Cirrhotic Portal Hypertension

et al. 2019

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Portal hypertension (PH) is the main driver of cirrhosis decompensation, the main determinant of death in patients with cirrhosis. PH results initially from increased intrahepatic vascular resistance. Subsequently, increased inflow from splanchnic vasodilation and increased cardiac output lead to a further increase in portal pressure (PP). Reducing PP in cirrhosis results in better outcomes. Removing the cause of cirrhosis might improve PP. However, this is a slow process and patients may continue to be at risk of decompensation. Additionally, for some chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD), etiological treatments are not yet available. Therefore, there is a need to develop better therapies specifically aimed at reducing PP. For over 35 years, the mainstay of such therapy has been the use of nonselective beta‐blockers (NSBBs) that act by reducing portal venous inflow. Recently, many drugs (mainly targeting intrahepatic mechanisms) have shown promise in preclinical and early clinical studies and may act alone or synergistically with NSBBs in reducing PP in cirrhosis. The objective of this position paper is to propose a novel framework for the design of clinical trials (phase 1, 2, and 3) in patients with cirrhosis and PH and to prioritize targets and pharmacological therapies in this setting. We have focused the discussion on patients with compensated cirrhosis. The paper summarizes discussions held at The American Association for the Study of Liver Diseases (AASLD) Industry Colloquium in January 2018, with the participation of clinical and translational investigators, regulatory professionals, and industry partners.

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Section: Preclinical Studies In Portal Hypertension (Ph)mentioning

confidence: 99%

Section: Preclinical Studies In Portal Hypertension (Ph)mentioning

confidence: 99%

Prioritization of Therapeutic Targets and Trial Design in Cirrhotic Portal Hypertension

et al. 2019

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“…However, a percentage of them (albeit low) dies before experiencing a decompensating event either from a nonhepatic cause or because of the development of a superimposed acute injury that is often a bacterial infection . Patients in the decompensated stage have a much higher mortality outcome (median survival is 2 years), and the main driver of death is an inflammatory state leading to worsening vasodilatation/heart function that results in a stage of “further” decompensation characterized by the development of complications (refractory ascites, hyponatremia, recurrent VH, recurrent hepatic encephalopathy [HE]) and/or to worsening liver function (jaundice, encephalopathy, and/or coagulopathy) (Fig. ).…”

Section: Why Bacterial Infections Are Important In Cirrhosis?mentioning

confidence: 99%

Prophylactic Antibiotics in Cirrhosis: Are They Promoting or Preventing Infections?

García–Tsao

2019

Clinical Liver Disease

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“…Univariate and multivariate logistic regression analyses were performed to establish any factors associated with the risk of having a HVPG measurement >16 mmHg, which is a threshold of high mortality risk cirrhosis. [30][31][32][33][34] Age (<55 vs >55), BMI, ascites (yes/no), cirrhosis aetiology (alcoholic or alcoholic + virus vs other), previous bleeding episode (yes/no), pSWE SS measurements, liver steatosis detected at US (yes/no), PTL count (<150 vs >150), spleen diameter (cm), portal flow velocity (cm/sec; <18 vs >18) and Giannini's score (<909 vs >909) were considered as potential predictors of HVPG measurements higher than >16. The variables that resulted statistically significant at univariate analysis were considered for multivariate analysis.…”

Section: Cohortmentioning

confidence: 99%

Assessing spleen stiffness by point shear‐wave elastography: Is it feasible and reproducible in patients with chronic liver disease? Is it useful to predict portal hypertension?

et al. 2019

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Summary Background and aims To assess the feasibility and reproducibility of the spleen stiffness (SS) measurement by point shear‐wave elastography (pSWE) in a cohort of compensated chronic liver disease (CLD) patients [Cohort 1] and to investigate pSWE accuracy to predict clinically relevant portal hypertension (PH) in a consecutive cohort of cirrhotics with endoscopic signs of portal hypertension [Cohort 2]. Methods [Cohort 1]: 186 consecutive CLD patients underwent abdominal ultrasound (US), liver stiffness (LS) and SS measurement by pSWE and transient elastography (TE) and liver biopsy. Inter‐rater agreement of SS (pSWE) was evaluated by intra‐class correlation coefficient (ICC). [Cohort 2]: 80 cirrhotics underwent US, LS and SS (by pSWE and TE), hepatic venous pressure gradient (HVPG) measurement and upper endoscopy. Linear correlations between LS or SS and HVPG and linear regression analysis were performed to establish determinants of HVPG > 16. Results [Cohort 1] SS measurement failure was 3.4% for pSWE and 13.8% for TE. For pSWE the ICC between two independent examiners was 0.74 (95% CI, 0.66‐0.80). [Cohort 2]: SS measurement failure was 2.5% for pSWE and 48% for TE. HVPG and LS did not correlate. Significant correlation was observed between HVPG and SS (r = 0.36, P = .001). At multivariate analysis only the presence of ascites and SS values significantly correlated with HVPG > 16, a threshold of high mortality risk cirrhosis. Conclusions Measuring SS by pSWE is feasible and reproducible in CLD and is applicable in most cirrhosis cases as a promising tool of prognosis and a surrogate marker of the HVPG threshold related to survival‐ and liver‐related outcomes.

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Cardiopulmonary hemodynamics and C-reactive protein as prognostic indicators in compensated and decompensated cirrhosis

Cited by 118 publications

References 38 publications

Prioritization of Therapeutic Targets and Trial Design in Cirrhotic Portal Hypertension

Prioritization of Therapeutic Targets and Trial Design in Cirrhotic Portal Hypertension

Prophylactic Antibiotics in Cirrhosis: Are They Promoting or Preventing Infections?

Assessing spleen stiffness by point shear‐wave elastography: Is it feasible and reproducible in patients with chronic liver disease? Is it useful to predict portal hypertension?

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