Association of endoscopic variceal treatment with portal venous system thrombosis in liver cirrhosis: a case–control study

Abstract

Background: The association of endoscopic variceal treatment (EVT) with portal venous system thrombosis (PVST) in liver cirrhosis is still unclear. Methods: PVST was assessed by contrast-enhanced CT or MRI in 406 cirrhotic patients from our prospective database. Case and control groups, which are defined as patients with and without PVST, respectively, were matched at a ratio of 1:1 according to age, gender, Child-Pugh class, and MELD score. History of EVT was reviewed. Logistic regression analysis was used to identify the risk factors for PVST. Odds ratios (ORs) were calculated. Subgroup analyses were further performed in terms of degree and location of PVST. Results: Overall, 109 patients each were included in case and control groups. The case group had a significantly higher proportion of patients who had undergone EVT than the control group (53.2% versus 18.3%; p < 0.001). In detail, the case group had significantly higher proportions of patients who had undergone EVT for controlling bleeding (45.9% versus 14.7%; p < 0.001), endoscopic variceal ligation (EVL) alone (19.3% versus 9.2%; p = 0.033), and EVL combined with endoscopic cyanoacrylate glue injection (24.8% versus 5.5%; p < 0.001). EVT was independently associated with PVST (OR = 4.258; p < 0.001). In subgroup analyses, EVT remained independently associated with partial PVST (OR = 10.063; p < 0.001), complete PVST/fibrotic cord (OR = 4.889; p = 0.008), thrombosis within main portal vein (OR = 5.985; p < 0.001), and thrombosis within superior mesenteric and splenic veins (OR = 5.747; p < 0.001). Conclusions: EVT may lead to a higher risk of PVST, especially more severe PVST, in liver cirrhosis. Screening for and prophylaxis of PVST after EVT should be further explored.

Case report: Rapid development of acute symptomatic portal vein system thrombosis after endoscopic variceal therapy in a patient with liver cirrhosis

“…Politoske et al ( 6 ) concluded that the incidence of PVT following EVT was similar to that in unselected patients with cirrhosis and portal hypertension. By comparison, accumulative evidence from our group and others have supported EVT as a potential risk factor for the development of PVST in liver cirrhosis ( 7 , 8 ).…”

“…Furthermore, he had imaging evidence before and after EVT, which clearly indicates its impact on acute thrombus extension. Recent evidence also supports a causal effect estimation of EVT, particularly endoscopic sclerotherapy ( 7 ), variceal ligation, and variceal ligation combined with endoscopic cyanoacrylate glue injection ( 8 ), with the risk of PVST. The underlying mechanism of PVST formation after EVT needs to be further explored.…”

“…In our case, it can be proposed that EVT induces an alteration of portal hemodynamics, leading to a transient increase in portal pressure and an increased risk of PVT. However, the correlation between EVT and PVT is still debated among literature ( 6 – 8 ). Our case had been diagnosed with partial PVT which was asymptomatic, but experienced acute symptomatic PVST extending to the SMV within only 2 days after EVT.…”

Understanding the pathogenesis of portal vein thrombosis in liver cirrhosis: We are still on the way

“…Splenectomy, endoscopic variceal treatment, splenic artery embolization, use of nonselective beta-blockers, and higher MELD score at baseline are risk factors contributing to the development of PVT in liver cirrhosis. [10][11][12][13][14] Additionally, the incidence of PVT increases with Child-Pugh score in cirrhotic patients. 1 In this setting, not all of the individual studies included in the meta-analysis by Giri It should also be acknowledged that a proportion of the individual studies included in the meta-analysis by Giri et al are cross-sectional, which cannot establish a cause-effect association.…”

“…However, it should be noted that the development of PVT is multifactorial. Splenectomy, endoscopic variceal treatment, splenic artery embolization, use of nonselective beta‐blockers, and higher MELD score at baseline are risk factors contributing to the development of PVT in liver cirrhosis 10–14 . Additionally, the incidence of PVT increases with Child‐Pugh score in cirrhotic patients 1 .…”