Saudi Journal of Gastroenterology
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Year : 2014  |  Volume : 20  |  Issue : 5  |  Page : 265-266
Spontaneous resolution of portal vein thrombosis in cirrhosis: Where do we stand, and where will we go?


Xijing Hospital of Digestive Diseases, Fourth Military Medical University, No. 127 Changle West Road, Xi'an, 710032, China

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Date of Web Publication25-Sep-2014
 

How to cite this article:
Qi X, Yang Z, Fan D. Spontaneous resolution of portal vein thrombosis in cirrhosis: Where do we stand, and where will we go?. Saudi J Gastroenterol 2014;20:265-6

How to cite this URL:
Qi X, Yang Z, Fan D. Spontaneous resolution of portal vein thrombosis in cirrhosis: Where do we stand, and where will we go?. Saudi J Gastroenterol [serial online] 2014 [cited 2019 Jul 22];20:265-6. Available from: http://www.saudijgastro.com/text.asp?2014/20/5/265/141680


It is being gradually recognized that portal vein thrombosis (PVT) is negatively associated with the prognosis of cirrhosis. [1],[2] But the standard treatment algorithm remains lacking. [3] Anticoagulation, which is a widely available treatment option for venous thromboembolism, is also employed for the management of PVT in cirrhotic patients. [4] Retrospective case series demonstrated a relatively low risk of anticoagulation-related bleeding and a high rate of portal vein recanalization after anticoagulation, [3],[4] which provided the preliminary support for the use of anticoagulation in cirrhosis with PVT. However, the clinicians are very cautious of the potential bleeding secondary to anticoagulation, because cirrhosis itself has a bleeding tendency.

In the dilemma of whether or not anticoagulation therapy should be employed, the investigators would rather pay more attention to the natural history of PVT in cirrhosis in the absence of any interventions. To our knowledge, spontaneous portal vein recanalization in cirrhosis has been evaluated by at least three previous case series. [5],[6],[7] The incidence of spontaneous recanalization varies from 30% to 50% in cirrhotic patients with PVT.

In this issue of The Saudi Journal of Gastroenterology, the concept of spontaneous portal vein recanalization has been further reinforced. [8] The investigators found that partial PVT could be spontaneously recanalized or unchanged in 72.7% (16/22) of patients, and worsened in only 27.3% (6/22) of patients. [8] More importantly, in spite of a small sample size (n = 22), the study showed a significantly higher incidence of hepatic decompensation and mortality in the cirrhotic patients with worsened PVT than in those with recanalized or unchanged PVT. [8] In line with the previous studies, [5] these impressive findings suggested that anticoagulation therapy should be selectively performed in patients who would develop the thrombus extension, thereby improving survival; by contrast, it is unnecessary in those who would develop the spontaneous thrombus resolution. However, the accurate predictors of spontaneous recanalization remain poorly recognized in this study. Therefore, the behavior to stop any interventions for partial PVT in all cirrhotic patients might be radical.

In accordance with previous studies, [5] the investigators also found that the severity of liver function (i.e. MELD score) was the only independent predictor for the survival and hepatic decompensation in the multivariate Cox regression analysis. In the absence of any detailed information, we fail to clearly understand whether or not the progression of PVT had been incorporated as a variable into the multivariate analysis. But it appeared to be rational that the worsened PVT and deteriorated liver function jointly increased the mortality. This consideration could be potentially supported by the accumulated evidence regarding a vicious cycle between the development of PVT and deterioration of liver function [Figure 1]. First, the portal vein flow velocity decreases with worsening liver fibrosis and liver function. [9],[10] Subsequently, a decreased portal vein flow velocity predicts a higher risk of developing PVT. [11] portal vein flow velocity decreases with worsening liver fibrosis and liver function. [9],[10] Subsequently, a decreased portal vein flow velocity predicts a higher risk improved liver function, thereby producing the scouring effect and spontaneously resolving the thrombus within the portal vein.[12]
Figure 1: A scheme regarding the association between the severity of liver function and development of portal vein thrombosis

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Collectively, spontaneous portal vein recanalization can be frequently observed in patients with partial PVT. This phenomenon may be attributed to the improvement of liver function. In addition, further work should focus on identifying the candidates who will develop the thrombus extension or is suitable for anticoagulation therapy. [12]

 
   References Top

1.D'Amico G, de Franchis R; Cooperative Study Group. Upper digestive bleeding in cirrhosis. Post-therapeutic outcome and prognostic indicators. Hepatology 2003;38:599-612.  Back to cited text no. 1
    
2.Qi X, Bai M, Yang Z, Yuan S, Zhang C, Han G, et al. Occlusive portal vein thrombosis as a new marker of decompensated cirrhosis. Med Hypotheses 2011;76:522-6.  Back to cited text no. 2
    
3.Qi X, Han G, Fan D. Management of portal vein thrombosis in cirrhosis. Nat Rev Gastroenterol Hepatol 2014;11:435-46.  Back to cited text no. 3
    
4.Qi X, Han G, Wu K, Fan D. Anticoagulation for portal vein thrombosis in cirrhosis. Am J Med 2010;123:E19-20.  Back to cited text no. 4
    
5.Luca A, Caruso S, Milazzo M, Marrone G, Mamone G, Crino F, et al. Natural course of extrahepatic nonmalignant partial portal vein thrombosis in patients with cirrhosis. Radiology 2012;265:124-32.  Back to cited text no. 5
    
6.Maruyama H, Okugawa H, Takahashi M, Yokosuka O. De novo portal vein thrombosis in virus-related cirrhosis: Predictive factors and long-term outcomes. Am J Gastroenterol 2013;108:568-74.  Back to cited text no. 6
    
7.John BV, Konjeti R, Aggarwal A, Lopez R, Atreja A, Miller C, et al. Impact of untreated portal vein thrombosis on pre and post liver transplant outcomes in cirrhosis. Ann Hepatol 2013;12:952-8.  Back to cited text no. 7
    
8.Girleanu I, Stanciu C, Cojocariu C, Boiculese L, Singeap A, Trifan A. Natural course of non malignant partial portal vein thrombosis in cirrhotic patients. Saudi J Gastroenterol 2014;20:In this issue.  Back to cited text no. 8
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9.Lutz HH, Gassler N, Tischendorf FW, Trautwein C, Tischendorf JJ. Doppler ultrasound of hepatic blood flow for noninvasive evaluation of liver fibrosis compared with liver biopsy and transient elastography. Dig Dis Sci 2012;57:2222-30.  Back to cited text no. 9
    
10.Zironi G, Gaiani S, Fenyves D, Rigamonti A, Bolondi L, Barbara L. Value of measurement of mean portal flow velocity by Doppler flowmetry in the diagnosis of portal hypertension. J Hepatol 1992;16:298-303.  Back to cited text no. 10
    
11.Zocco MA, Di Stasio E, De Cristofaro R, Novi M, Ainora ME, Ponziani F, et al. Thrombotic risk factors in patients with liver cirrhosis: Correlation with MELD scoring system and portal vein thrombosis development. J Hepatol 2009;51:682-9.  Back to cited text no. 11
    
12.Wanless IR, Wong F, Blendis LM, Greig P, Heathcote EJ, Levy G. Hepatic and portal vein thrombosis in cirrhosis: Possible role in development of parenchymal extinction and portal hypertension. Hepatology 1995;21:1238-47.  Back to cited text no. 12
    

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Correspondence Address:
Daiming Fan
Xijing Hospital of Digestive Diseases, Fourth Military Medical University, No. 127 Changle West Road, Xi'an, 710032
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1319-3767.141680

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