The Role of Anticoagulation in Treating Portal Hypertension

Abstract

Purpose of ReviewTo revise experimental and clinical data supporting a less traditional role of anticoagulation for treating portal hypertension in patients with cirrhosis.Recent FindingsPortal hypertension is the main driver of complications such as ascites, variceal hemorrhage, and hepatic encephalopathy, with inflammation as a key component. The traditional view of cirrhosis as a pro-hemorrhagic condition has recently changed, prothrombotic complications being recognized as frequently as the hemorrhagic ones. Several data indicate a close relationship between inflammation, prothrombotic status, worsening of hepatic fibrosis, and portal hypertension both in animal models and in patients with chronic liver disease. These findings indicate that anticoagulation may represent a potent tool to act on fibrogenesis and therefore consequently to treat portal hypertension. All anticoagulants have good to optimal safety profiles and can be used in patients with advanced chronic liver disease with confidence.SummaryAnticoagulation has a role as a pleiotropic treatment of portal hypertension in cirrhosis.

What's new in portal hypertension?

“…4 The prothrombotic state may result in the worsening of hepatic fibrosis and PH. 5 This hypothesis is supported by the fact that anticoagulation leads to a reduction in hepatic fibrosis and PH.…”

“…A new approach to the pathogenesis of PH which may affect the therapeutic management of this complication, is that the traditional concept of cirrhosis as a pro‐haemorrhagic condition has changed and cirrhosis is now considered to be both a pro‐haemorrhagic and prothrombotic disease . The prothrombotic state may result in the worsening of hepatic fibrosis and PH . This hypothesis is supported by the fact that anticoagulation leads to a reduction in hepatic fibrosis and PH.…”

Direct Oral Anticoagulants in Patients with Liver Disease in the Era of Non-Alcoholic Fatty Liver Disease Global Epidemic: A Narrative Review

“…Experimental and clinical data suggest an association between inflammation, activation of coagulation system and development of hepatic fibrosis and portal hypertension in CLD [57].…”

“…The activation of hepatic stellate cells (HSC) is the key pathogenic mechanism of hepatic fibrogenesis. Experimental animal models support a biological link between coagulation and fibrosis showing that thrombin and FXa can activate HSC [ 62 , 63 ] and, conversely, their inhibition by anticoagulants may prevent or reduce fibrogenesis [ 57 ].…”

“…It was speculated that the protective effect of enoxaparin on liver disease might have been due to an improvement in intestinal microcirculation with secondary reduction in bacterial translocation and thus liver inflammation, rather than by merely preventing PVT [ 65 ]. Few other studies on patients with hepatis B virus (HBV)-related liver fibrosis/cirrhosis or post-liver transplant HCV recurrence-related fibrosis treated with LMWH or warfarin have also shown improved liver function and decreased collagen levels/fibrosis (reviewed in [ 57 ]).…”