Portal vein intimal thickening in patients with cirrhosis is associated with indicators of portal hypertension

Abstract

Background

The exact pathophysiology of portal vein thrombosis (PVT), a common complication of cirrhosis, remains largely unknown. We previously found that cirrhotic PVT consists of fibrotic intimal thickening of the portal vein wall rather than of true fibrin-rich thrombus. We hypothesized that this intimal thickening of portal vein is secondary to portal hypertension and/or to local inflammatory responses.

Objectives

To investigate the portal vein intimal thickness in cirrhotic patients, and its relationship with clinical and laboratory parameters associated with portal hypertension and inflammation.

Methods

The intimal thickness of right and left portal branches was measured in hilar liver samples from 232 cirrhotic patients without PVT who underwent liver transplantation. The relation between intimal thickness and pretransplant clinical variables was studied with linear regression. Computed tomography scans of 25 patients prior to liver transplantation were reanalyzed for portal vein and portal hypertension related characteristics.

Results

Median right intimal thickness was 129 (1-300 [IQR]) μm; median left intimal thickness was 112 (1-230) μm, and there was a correlation between the intimal thickness of the right and left branches in individual patients (r = 0.30, P < .001). Intimal thickness of the portal vein was associated with a history of variceal bleeding, hepatic encephalopathy or ascites, etiology of disease, and statin use. Other factors, including duration of liver disease, presence of infection, or radiological characteristics were not significantly associated with intimal thickness.

Conclusion

Intrahepatic portal vein intimal thickness is highly variable in patients with cirrhosis, but relatively consistent between right and left portal branches. The association between intimal thickness and history of variceal bleeding suggests that portal hypertension may contribute to initiation of intimal thickening, and consequently to the development of PVT.