Association of Heparin-Like Effect, Factor VII/XIII Deficiency and Fibrinolysis with Rebleeding Risk in Cirrhosis with Acute Variceal Bleeding.


Journal

Digestive diseases and sciences
ISSN: 1573-2568
Titre abrégé: Dig Dis Sci
Pays: United States
ID NLM: 7902782

Informations de publication

Date de publication:
02 2023
Historique:
received: 11 05 2022
accepted: 31 07 2022
pubmed: 20 8 2022
medline: 10 2 2023
entrez: 19 8 2022
Statut: ppublish

Résumé

Hyperfibrinolysis and coagulation dysfunction may occur in cirrhotic patients with acute variceal bleed (AVB) despite successful endotherapy. To prospectively study the association of endogenous heparinoids and coagulation dysfunction with variceal rebleeding and outcome in cirrhosis. Consecutive patients were assessed with conventional coagulation tests, SONOCLOT™ [(global(gb) and heparinase(h) treated] and factors VII, VIII, XIII, X, tissue plasminogen activator, and plasminogen activator inhibitor ELISA assays in a university hospital. Heparin-like-effect (HLE) was defined as ≥ 20% difference in paired gb/h-SONOCLOT™ traces for activated clotting time (ACT). Of 143 patients screened, 90 (46.4 ± 11.7 years, males 82.2%, ethanol-related 58.8%) were recruited, who bled from esophageal varices (81,90.0%), gastric varices (6,6.6%), or esophageal varices with portal hypertensive gastropathy (3,3.3%). Twenty (21.7%) had early rebleeding, mainly post-variceal ligation ulcer related (70%). Patients who rebled had low Factor XIII [1.6 (1.2-2.1) vs 2.4 ng/ml (2.0-2.8) P = 0.035] and Factor VII (94.1 ± 46.9 vs. 124.0 ± 50.4, P = 0.023). On receiver operating curve analysis, the gbACT > 252 s (sensitivity 86.8%, specificity 76.9%, P < 0.001), hACT > 215 s (sensitivity 71.1%, specificity 70.3%, P < 0.001), and HLE > 50% (sensitivity 69.5%, specificity 70.3%, P = 0.006) predicted rebleeding. Baseline Factor VIII (HR 1.26; 95% CI 1.17-1.34, P < 0.001), low factor VII (HR 0.89; 95% CI 0.76-0.98, P = 0.035), and lysis (HR 1.25, 95% CI 1.17-1.33, P < 0.001) predicted mortality. Endogenous heparinoids at baseline predicted sepsis (HR 1.8; 95% CI 1.4-6.5; P = 0.022), rebleeding events (HR 1.2; 95% CI 1.1-6.3; P = 0.030), and mortality (HR 1.1; 95% CI 1.0-4.6; P = 0.030). Hyperfibrinolysis, Factor VII/XIII deficiency, and HLE are associated with rebleeding after AVB. Trial Registration NCT04111120 available from https://clinicaltrials.gov/ct2/show/NCT04111120 .

Sections du résumé

BACKGROUND
Hyperfibrinolysis and coagulation dysfunction may occur in cirrhotic patients with acute variceal bleed (AVB) despite successful endotherapy.
AIMS
To prospectively study the association of endogenous heparinoids and coagulation dysfunction with variceal rebleeding and outcome in cirrhosis.
METHODS
Consecutive patients were assessed with conventional coagulation tests, SONOCLOT™ [(global(gb) and heparinase(h) treated] and factors VII, VIII, XIII, X, tissue plasminogen activator, and plasminogen activator inhibitor ELISA assays in a university hospital. Heparin-like-effect (HLE) was defined as ≥ 20% difference in paired gb/h-SONOCLOT™ traces for activated clotting time (ACT).
RESULTS
Of 143 patients screened, 90 (46.4 ± 11.7 years, males 82.2%, ethanol-related 58.8%) were recruited, who bled from esophageal varices (81,90.0%), gastric varices (6,6.6%), or esophageal varices with portal hypertensive gastropathy (3,3.3%). Twenty (21.7%) had early rebleeding, mainly post-variceal ligation ulcer related (70%). Patients who rebled had low Factor XIII [1.6 (1.2-2.1) vs 2.4 ng/ml (2.0-2.8) P = 0.035] and Factor VII (94.1 ± 46.9 vs. 124.0 ± 50.4, P = 0.023). On receiver operating curve analysis, the gbACT > 252 s (sensitivity 86.8%, specificity 76.9%, P < 0.001), hACT > 215 s (sensitivity 71.1%, specificity 70.3%, P < 0.001), and HLE > 50% (sensitivity 69.5%, specificity 70.3%, P = 0.006) predicted rebleeding. Baseline Factor VIII (HR 1.26; 95% CI 1.17-1.34, P < 0.001), low factor VII (HR 0.89; 95% CI 0.76-0.98, P = 0.035), and lysis (HR 1.25, 95% CI 1.17-1.33, P < 0.001) predicted mortality. Endogenous heparinoids at baseline predicted sepsis (HR 1.8; 95% CI 1.4-6.5; P = 0.022), rebleeding events (HR 1.2; 95% CI 1.1-6.3; P = 0.030), and mortality (HR 1.1; 95% CI 1.0-4.6; P = 0.030).
CONCLUSIONS
Hyperfibrinolysis, Factor VII/XIII deficiency, and HLE are associated with rebleeding after AVB. Trial Registration NCT04111120 available from https://clinicaltrials.gov/ct2/show/NCT04111120 .

Identifiants

pubmed: 35984611
doi: 10.1007/s10620-022-07656-9
pii: 10.1007/s10620-022-07656-9
pmc: PMC9389477
doi:

Substances chimiques

Factor VII 9001-25-6
Tissue Plasminogen Activator EC 3.4.21.68
Heparin 9005-49-6
Heparinoids 0

Banques de données

ClinicalTrials.gov
['NCT04111120']

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

497-513

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Références

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Auteurs

Madhumita Premkumar (M)

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India. drmadhumitap@gmail.com.

Rohit Mehtani (R)

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Anand V Kulkarni (AV)

Department of Hepatology, Asian Institute of Gastroenterology, Hyderabad, India.

Ajay Kumar Duseja (AK)

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Arka De (A)

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Sunil Taneja (S)

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Virendra Singh (V)

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Nipun Verma (N)

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Jasmina Ahluwalia (J)

Department of Hematology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Kamal Kajal (K)

Department of Anesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Smita Divyaveer (S)

Department of Nephrology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Akash Roy (A)

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Akash Gandotra (A)

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Narender Kalson (N)

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Kushal Kekan (K)

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Harmanpreet Kaur (H)

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Harpreet Kaur (H)

Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

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