Myostatin is associated with the presence and development of acute-on-chronic liver failure

Acute-on-chronic liver failure (ACLF) has been linked to different pathophysiological mechanisms, including systemic inflammation and mitochondrial dysfunction. Sarcopenia has also been proposed as a potential mechanism; myostatin is a key factor inducing sarcopenia. Therefore, this study aimed to e...

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Vydané v:JHEP reports Ročník 5; číslo 8; s. 100761
Hlavní autori: Ruiz-Margáin, Astrid, Pohlmann, Alessandra, Lanzerath, Silke, Langheinrich, Melanie, Campos-Murguía, Alejandro, Román-Calleja, Berenice M., Schierwagen, Robert, Klein, Sabine, Uschner, Frank Erhard, Brol, Maximilian Joseph, Torre-Delgadillo, Aldo, Flores-García, Nayelli C., Praktiknjo, Michael, Macías Rodríguez, Ricardo U., Trebicka, Jonel
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Netherlands Elsevier B.V 01.08.2023
Elsevier
Predmet:
ACLF
cirrhosis
Gastroenterology and Hepatology
liver failure
malnutrition
myostatin
sarcopenia
ACLF
AD
IL
ROC
PhA
MAMC
myostatin
AUC
malnutrition
liver failure
MELD
TST
HGS
OF
CLIF-C
cirrhosis
sarcopenia
handgrip strength
area under the ROC curve
receiver-operating characteristic
triceps skinfold thickness
Chronic Liver Failure – consortium
phase angle
interleukin
mid-arm muscle circumference
model for end-stage liver disease
acute-on-chronic liver failure
organ failure
acute decompensation
ISSN:2589-5559, 2589-5559
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Shrnutí:Acute-on-chronic liver failure (ACLF) has been linked to different pathophysiological mechanisms, including systemic inflammation and mitochondrial dysfunction. Sarcopenia has also been proposed as a potential mechanism; myostatin is a key factor inducing sarcopenia. Therefore, this study aimed to evaluate the association of myostatin levels with the development of ACLF and mortality in patients with cirrhosis. We performed a prospective cohort study, including both outpatient and hospitalized patients with cirrhosis. Clinical, biochemical, and nutritional parameters were evaluated, and the development of acute decompensation (AD) or ACLF during follow-up was recorded. ACLF was defined according to the EASL-CLIF criteria. Receiver-operating characteristic, Kaplan-Meier and Cox regression analyses were performed. A total of 186 patients with the whole spectrum of cirrhosis were included; mean age was 53.4 ± 14 years, mean Child-Pugh score was 8 ± 2.5 and mean MELD score was 15 ± 8. There was a stepwise decrease in myostatin levels from a compensated stage to AD and ACLF. Myostatin correlated positively with nutritional markers and negatively with severity scores. The prevalence of sarcopenia was 73.6%. During follow-up, 27.9% of patients developed AD and 25.8% developed ACLF. Most episodes were grade 2-3, mainly (62.5%) precipitated by infections. The most common organ failures observed were in the liver (63.3%) and the kidney (64.6%). Receiver-operating characteristic analysis yielded <1,280 pg/ml as the best serum myostatin cut-off for the prediction of ACLF. In Kaplan-Meier curves and multivariate analysis, myostatin levels remained independently associated with the incidence of ACLF and survival. There is a progressive decrease in myostatin levels as cirrhosis progresses, demonstrating an association of sarcopenia with the development of ACLF and increased mortality. Myostatin is a muscle hormone, it is decreased in patients with muscle loss and is a marker of impaired muscle function. In this study we show that myostatin levels are decreased in patients with cirrhosis, with lower levels in patients with acute decompensation and acute-on chronic liver failure (ACLF). Low myostatin levels in cirrhosis predict the development of ACLF and mortality independently of liver disease severity and sex. [Display omitted] •Sarcopenia is associated with ACLF development and outcome.•Myostatin is a key myokine involved in the regulation of skeletal muscle.•Myostatin levels are lower in patients with decompensated cirrhosis and ACLF, and positively correlate with nutritional markers.•Low myostatin levels are associated with the development of ACLF and decreased survival.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
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Contributed equally to this work as senior authors.
Contributed equally to this work as first authors.
ISSN:2589-5559
2589-5559
DOI:10.1016/j.jhepr.2023.100761