scholarly journals Impact of acute-on-chronic liver failure and decompensated liver cirrhosis on psychosocial burden and quality of life of patients and their close relatives

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Michael Nagel ◽  
Christian Labenz ◽  
Marcus A. Wörns ◽  
J. U. Marquardt ◽  
Peter R. Galle ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Liver Cirrhosis ◽  
Liver Failure ◽  
Chronic Liver ◽  
Chronic Liver Failure ◽  
Psychosocial Burden ◽  
Decompensated Liver Cirrhosis ◽  
Close Relatives

scholarly journals Dysregulated Adaptive Immunity Is an Early Event in Liver Cirrhosis Preceding Acute-on-Chronic Liver Failure

2021 ◽  
Vol 11 ◽  
Author(s):  
Sabrina Rueschenbaum ◽  
Sandra Ciesek ◽  
Alexander Queck ◽  
Marek Widera ◽  
Katharina Schwarzkopf ◽  
...  
Keyword(s):  
T Cells ◽  
Liver Cirrhosis ◽  
Liver Failure ◽  
Cd8 T Cells ◽  
Chronic Liver ◽  
Chronic Liver Failure ◽  
Decompensated Liver Cirrhosis ◽  
Tt Virus ◽  
Adaptive Immune ◽  
Acute Decompensation

IntroductionAcute-on-chronic liver failure (ACLF) is characterized by high levels of systemic inflammation and parallel suppression of innate immunity, whereas little is known about adaptive immune immunity in ACLF. We therefore aimed to characterize the development of the adaptive immune system during the progression of liver cirrhosis to ACLF. Patients with compensated/stable decompensated liver cirrhosis, acute decompensation of liver cirrhosis, or ACLF were recruited from a prospective cohort study. Comprehensive immunophenotyping was performed using high dimensional flow cytometry. Replication of Torque teno (TT) virus was quantified as a marker of immunosuppression. High frequencies of detectable TT virus were observed already in patients with compensated/stable decompensated liver cirrhosis compared to healthy controls (>50% vs. 19%), suggesting relatively early occurrence of immunosuppression in cirrhosis. In line, profoundly reduced numbers of distinct innate and adaptive immune cell populations were observed before ACLF development. These changes were accompanied by parallel upregulation of co-stimulatory (e.g. CD40L, OX40, CD69, GITR, TIM-1) and inhibitory immune checkpoints (e.g. PDPN, PROCR, 2B4, TIGIT) on CD4+ and CD8+ T cells, which again preceded the development of ACLF. On a functional basis, the capacity of CD4+ and CD8+ T cells to produce pro-inflammatory cytokines upon stimulation was strongly diminished in patients with acute decompensation of liver cirrhosis and ACLF.ConclusionImpaired innate and—in particular—adaptive cellular immunity occurs relatively early in the pathogenesis of liver cirrhosis and precedes ACLF. This may contribute to the development of ACLF by increasing the risk of infections in patients with liver cirrhosis.

scholarly journals Plasma cystatin C is a predictor of renal dysfunction, acute-on-chronic liver failure, and mortality in patients with acutely decompensated liver cirrhosis

Hepatology ◽  
2017 ◽  
Vol 66 (4) ◽  
pp. 1232-1241 ◽  
Author(s):  
Daniel Markwardt ◽  
Lesca Holdt ◽  
Christian Steib ◽  
Andreas Benesic ◽  
Flemming Bendtsen ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Liver Failure ◽  
Renal Dysfunction ◽  
Cystatin C ◽  
Chronic Liver ◽  
Chronic Liver Failure ◽  
Decompensated Liver Cirrhosis

scholarly journals Vulnerability to recurrent episodes of acute decompensation/acute-on-chronic liver failure characterizes those triggered by indeterminate precipitants in patients with liver cirrhosis

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0250062
Author(s):  
Hitomi Hoshi ◽  
Po-sung Chu ◽  
Aya Yoshida ◽  
Nobuhito Taniki ◽  
Rei Morikawa ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Liver Failure ◽  
Risk Estimation ◽  
Chronic Liver ◽  
Survival Outcomes ◽  
Chronic Liver Failure ◽  
Acute Decompensation ◽  
History Of ◽  
Insufficient Knowledge

Background Acute decompensation (AD) of liver cirrhosis (LC) and subsequent acute-on-chronic liver failure (ACLF) are fatal and impair quality of life. Insufficient knowledge of the highly heterogeneous natural history of LC, including decompensation, re-compensation, and possible recurrent decompensation, hinders the development and application of novel therapeutics. Approximately 10%-50% of AD/ACLF is reported to be precipitated by any indeterminate (unidentifiable, cryptogenic, or unknown) acute insults; however, its clinical characteristics are unclear. Methods We conducted a single-center observational study of 2165 consecutively admitted patients with LC from January 2012 to December 2019. A total of 466 episodes of AD/ACLF in 285 patients, including their 285 first indexed AD/ACLF, were extracted for analysis. Stratified analyses of different acute precipitants, classified as indeterminate (AD/ACLFIND), bacterial infection (AD/ACLFBAC), gastrointestinal bleeding, active alcoholism, and miscellaneous, were performed. Results AD/ACLFIND was the leading acute precipitant (28%), followed by AD/ACLFBAC (23%). AD/ACLFIND showed better survival outcomes than AD/ACLFBAC (P = 0.03); however, hyperbilirubinemia, hyponatremia, or leukocytosis significantly and uniquely characterized subgroups of AD/ACLFIND with comparable or even worse survival outcomes than those of AD/ACLFBAC. Patients with subsequent AD/ACLF significantly tended to suffer from AD/ACLF with any organ failure in AD/ACLFIND but not in AD/ACLFBAC (P = 0.004, for trend). In competing risk analysis, patients with AD/ACLFIND were significantly more vulnerable to suffer from recurrent episodes of AD/ACLF within 180 days, compared to those triggered by other precipitants (P = 0.04). Conclusions AD/ACLFIND, the leading acute precipitant, also plays a role in subsequent AD/ACLF. An abruptly exacerbating, remitting, and relapsing nature of systemic inflammation underlying AD/ACLF may also be useful for risk estimation.

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