Combination with portosystemic shunt occlusion and antiviral therapy improves prognosis of decompensated cirrhosis

Abstract

Background and aim: Portosystemic shunt occlusion using endovascular treatment can transiently improve liver function in patients with decompensated cirrhosis. In recent years, viral hepatitis can be easily controlled. The present study aimed to clarify the safety and efficacy of endovascular treatment in decompensated cirrhotic patients, and to elucidate whether viral treatment improves the prognosis after shunt occlusion.

Methods: Among 98 cirrhotic patients who received portosystemic shunt occlusion from January 2007 to June 2016, we retrospectively analyzed 61 decompensated cirrhotic patients.

Results: Forty-five patients had viral hepatitis. Recovery rates of liver function to Child A within 6 months in viral hepatitis, non-viral hepatitis, and overall were 78% (35/45), 81% (13/16), and 79% (48/61), respectively. Recovery rates according to baseline Child-Pugh score were as follows: score 7, 88% (15/17); score 8, 89% (24/27); score 9, 69% (9/13); and score ≥ 10, 0% (0/4). Three-year reprogression rates to decompensated cirrhosis for non-virus, non-sustained viral negativity (SVN), and SVN groups were 23 100, and 0%, respectively (P < 0.01). Three-year survival rates for those were 63, 62, and 91%, respectively (P < 0.01). Eight-year survival rate for SVN group was also 91%. Multivariate analysis revealed age, baseline ammonia level, baseline Child class, and SVN as independent contributors to survival.

Conclusions: SVN in patients with viral hepatitis appears prerequisite to maintaining recovered liver function by shunt occlusion and to improving prognosis. Combination therapy with shunt occlusion and antiviral treatment should be considered as a first-line treatment for decompensated cirrhotic patients with viral hepatitis and large portosystemic shunt growth.

Keywords: decompensated cirrhosis; portosystemic shunt; viral hepatitis.

Figure 1

Changes of albumin‐bilirubin (ALBI) score after endovascular treatment according to patient's groups. Note: Albumin‐bilirubin (ALBI) score was significantly lower in non‐virus and sustained viral negativity (SVN) groups than in non‐SVN patients at 3 and 6 months after endovascular treatment (at 3 months; P = 0.048, at 6 months; P = 0.002). Values were expressed as median. , Non‐SVN (n=18); , SVN (n=27); , Non‐virus (n=16).

Figure 2

Cumulative re‐progression rates to decompensated cirrhosis after shunt occlusion according to patient group. Three‐year reprogression rates to decompensated cirrhosis in non‐virus, non‐SVN (sustained viral negativity), and SVN groups were 23, 100, and 0%, respectively (non‐virus vs. non‐SVN; P = 0.002, SVN vs. non‐virus; P = 0.016, SVN vs. non‐SVN; P < 0.001). , SVN (n = 23); , Non‐SVN (n = 12); , Non‐virus (n = 13)

Figure 3

Cumulative aggravation rates of esophageal varices after shunt occlusion according to patient group. Three‐year aggravation rates for esophageal varices in non‐virus, non‐sustained viral negativity (SVN), and SVN groups are 37, 44, and 46%, respectively. No significant differences among groups are evident. , SVN (n = 27); Non‐SVN (n = 18); , Non‐virus (n = 16)

Figure 4

Cumulative survival rates after shunt occlusion according to patient group. Three‐year survival rates of non‐virus, non‐sustained viral negativity (SVN), and SVN groups are 63, 62, and 91%, respectively. The survival rate was significantly higher in SVN group than in non‐virus or non‐SVN group (SVN vs. non‐virus, P = 0.003; SVN vs. non‐SVN, P < 0.001). No significant difference was seen between non‐virus and non‐SVN group (P = 0.576). The 8‐year survival rate of the SVN group was also maintained at 91%. , SVN (n = 27); , Non‐SVN (n = 18); , Non‐virus (n = 16)