Prothrombotic and Inflammatory Markers in Elderly Patients with Non-Alcoholic Hepatic Liver Disease before and after Weight Loss: A Pilot Study.
TAFI
factor VII (FVII)
insulin resistance
non-alcoholic fatty liver disease (NAFLD)
plasminogen activator inhibitor-1 (PAI-1)
protein S
slimming
von Willebrand factor (VWF)
weight loss
Journal
Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588
Informations de publication
Date de publication:
25 Oct 2021
25 Oct 2021
Historique:
received:
13
09
2021
revised:
19
10
2021
accepted:
21
10
2021
entrez:
13
11
2021
pubmed:
14
11
2021
medline:
14
11
2021
Statut:
epublish
Résumé
Non-alcoholic fatty liver disease (NAFLD) is a pathological condition, ranging from fatty liver to chronic steatohepatitis (NASH), liver cirrhosis, and eventually to hepatocellular carcinoma. Recent findings suggest that patients with NAFLD have an increased risk of cardiovascular events and thromboembolism, which is independent of metabolic diseases that are frequently associated with NAFLD, such as diabetes, hyperlipidemia, and obesity. We evaluated 30 NAFLD patients, before and after weight loss. Plasma levels of C-reactive protein (CRP), fibrinogen, plasminogen activator inhibitor-1 (PAI-1), von Willebrand factor (VWF), homocysteine, coagulation protein S, Thrombin activable fibrinolysis inhibitor (TAFI), and factor VII (FVII) were assessed to evaluate whether they should be responsible of the prothrombotic state of NAFLD after weight loss. At baseline, patients affected by NAFLD had a significantly higher levels of CRP, fibrinogen, PAI-1, VWF antigen, and FVII levels. After weight reduction, we observed a significant drop of inflammatory and prothrombotic markers, as well as glucometabolic, lipid profile. These findings provide evidence for a link between NAFLD/NASH and thromboembolism. The association seems to be linked with primitive thrombotic state and hypercoagulation due to increased levels of coagulation factors and reduced levels of PAI-1. This hypercoagulation state might explain increased levels of thrombosis and splanchnic thrombosis observed in NASH correlated cirrhosis.
Sections du résumé
BACKGROUND
BACKGROUND
Non-alcoholic fatty liver disease (NAFLD) is a pathological condition, ranging from fatty liver to chronic steatohepatitis (NASH), liver cirrhosis, and eventually to hepatocellular carcinoma. Recent findings suggest that patients with NAFLD have an increased risk of cardiovascular events and thromboembolism, which is independent of metabolic diseases that are frequently associated with NAFLD, such as diabetes, hyperlipidemia, and obesity.
METHODS
METHODS
We evaluated 30 NAFLD patients, before and after weight loss. Plasma levels of C-reactive protein (CRP), fibrinogen, plasminogen activator inhibitor-1 (PAI-1), von Willebrand factor (VWF), homocysteine, coagulation protein S, Thrombin activable fibrinolysis inhibitor (TAFI), and factor VII (FVII) were assessed to evaluate whether they should be responsible of the prothrombotic state of NAFLD after weight loss.
RESULTS
RESULTS
At baseline, patients affected by NAFLD had a significantly higher levels of CRP, fibrinogen, PAI-1, VWF antigen, and FVII levels. After weight reduction, we observed a significant drop of inflammatory and prothrombotic markers, as well as glucometabolic, lipid profile.
CONCLUSION
CONCLUSIONS
These findings provide evidence for a link between NAFLD/NASH and thromboembolism. The association seems to be linked with primitive thrombotic state and hypercoagulation due to increased levels of coagulation factors and reduced levels of PAI-1. This hypercoagulation state might explain increased levels of thrombosis and splanchnic thrombosis observed in NASH correlated cirrhosis.
Identifiants
pubmed: 34768440
pii: jcm10214906
doi: 10.3390/jcm10214906
pmc: PMC8585002
pii:
doi:
Types de publication
Journal Article
Langues
eng
Références
BMC Gastroenterol. 2019 Apr 16;19(1):56
pubmed: 30991959
Haematologica. 2007 Mar;92(3):297-9
pubmed: 17339177
JAMA. 1999 Oct 27;282(16):1547-53
pubmed: 10546694
BMC Endocr Disord. 2021 May 1;21(1):91
pubmed: 33933056
Clin Chem. 1972 Jun;18(6):499-502
pubmed: 4337382
Med Sci Sports Exerc. 1999 Nov;31(11 Suppl):S646-62
pubmed: 10593541
Mol Metab. 2021 Nov;53:101262
pubmed: 34082137
J Hepatol. 2014 Jul;61(1):148-54
pubmed: 24657400
Thromb Res. 2021 Feb;198:139-150
pubmed: 33340925
Diabetes Res Clin Pract. 2021 Jul;177:108873
pubmed: 34051282
Case Rep Gastrointest Med. 2017;2017:5236918
pubmed: 29379656
Ann Hepatol. 2009 Oct-Dec;8(4):346-52
pubmed: 20009134
J Diabetes Investig. 2021 Nov;12(11):1934-1941
pubmed: 34132491
Diagnostics (Basel). 2020 Nov 07;10(11):
pubmed: 33171865
Med Sci Sports Exerc. 2011 Aug;43(8):1575-81
pubmed: 21681120
Liver Int. 2020 May;40(5):1111-1120
pubmed: 32090434
Medicine (Baltimore). 2020 Dec 11;99(50):e23660
pubmed: 33327353
Intern Emerg Med. 2012 Jun;7(3):237-42
pubmed: 21249470
J Clin Med. 2021 May 29;10(11):
pubmed: 34072487
Am J Gastroenterol. 2017 Feb;112(2):274-281
pubmed: 27801884
Arterioscler Thromb Vasc Biol. 1996 Mar;16(3):381-5
pubmed: 8630663
BMC Cardiovasc Disord. 2021 May 19;21(1):244
pubmed: 34011282
Circ J. 2013;77(2):281-92
pubmed: 23328449
Semin Thromb Hemost. 2009 Apr;35(3):277-87
pubmed: 19452403
World J Gastroenterol. 2020 Mar 28;26(12):1231-1241
pubmed: 32256013
J Hepatol. 2009 Oct;51(4):682-9
pubmed: 19464747
Int J Mol Sci. 2020 Jul 23;21(15):
pubmed: 32717871
Thromb Res. 2020 May;189:77-87
pubmed: 32192995
Thromb Haemost. 1997 Jul;78(1):656-60
pubmed: 9198234
Lancet Gastroenterol Hepatol. 2021 Jul;6(7):578-588
pubmed: 33961787
Semin Thromb Hemost. 2010 Feb;36(1):41-8
pubmed: 20391295
Gastroenterology. 2001 Jul;121(1):131-9
pubmed: 11438502
Z Gerontol Geriatr. 2008 Jun;41(3):208-16
pubmed: 18327696
Gastroenterology. 2012 Jun;142(7):1592-609
pubmed: 22656328
Hepatology. 2006 Oct;44(4):865-73
pubmed: 17006923