Endogenous heparin‐like activity detected by anti‐Xa assay in infected cirrhotic and non‐cirrhotic patients

Abstract

Background: Bacterial infections have been proposed as a trigger for portal hypertensive bleeding in cirrhotic patients. Endogenous low molecular weight heparinoids have been previously detected in vitro by heparinase‐modified thromboelastography, but it is not known what type of heparinoids they are. The aim of this study was to assay anti‐Xa concentrations to detect heparin activity in infected cirrhotics in vivo. Methods: We evaluated 30 cirrhotic patients (15 with bacterial infection, 15 not infected) and 9 non‐cirrhotic patients with bacterial infection. The anti‐Xa assay was performed at the start of infection in all patients and after resolution of infection in 8 cirrhotics (5 to 10 days after starting antibiotics); thromboelastography (native and heparinase I‐modified TEG) was performed in a subgroup of 11 cirrhotic patients with infection, 8 cirrhotics without infection and 8 non‐cirrhotics with infection. Results: Anti‐Xa activity was detected in 9 of the 15 infected cirrhotics (60%) and only in 1 of 15 non‐infected cirrhotics (6.7%) (P < 0.01). In the infected cirrhotic patients, a heparinase effect was shown in the heparinase I‐modified TEG: k time (P < 0.01), α‐angle (P < 0.01) and r time (P = 0.05), with no effect in the non‐infected cirrhotics. Four of 9 (44%) infected non‐cirrhotics were positive with the anti‐Xa assay. Conclusion: In cirrhotic patients, bacterial infections modify haemostasis by producing endogenous heparin‐like substances which can inhibit the activated clotting factor X (factor Xa). In infected non‐cirrhotics, anti‐Xa activity can also be found.