The cumulative survival rates were significantly different Rapamycin supplier between the SRS (+) and SRS (−) groups and between the SRS (+) and B-RTO groups. The vital prognosis worsened for the SRS (+) group. Conclusions:  The presence of a large splenorenal shunt (portosystemic shunt) was indicated to lower liver function and vital prognosis. B-RTO, which completely obliterates large splenorenal

shunts, inhibited the lowering of hepatic functional reserve and the worsening of vital prognosis, indicating a protective role. Liver pathology and the presence of a large portosystemic shunt each separately result in progressive liver dysfunction and worsen the survival rate. We found that such a pathological condition had occurred due to a large portosystemic shunt, and it should be called ‘portosystemic shunt syndrome. It is well known that portal hypertensive patients develop various collateral pathways (shunts). A splenorenal shunt

(SRS) is a major shunt that is a representative collateral pathway. Gastric fundal varices (GFV) are formed in the course of this collateral pathway. The GFV diagnosed by endoscopy have large SRS at high rates of ≥90%.1 Balloon-occluded retrograde transvenous obliteration (B-RTO)2 is known as an effective treatment mainly for large GFV.3–8 In addition, B-RTO totally obliterates large splenorenal INCB024360 nmr shunts. It is possible to totally eradicate GFV due to this anatomical characteristic as well as to treat hepatic encephalopathy.9–11 There have been reports of short-term improvement of liver function due to increased portal venous blood flow.6,10,12 However, there has not been any report examining the long-term effects of SRS on liver function and survival. In this study, we compared the long-term effects of SRS, a major portosystemic shunt, on

liver selleck kinase inhibitor function and survival in three groups of patients: cirrhotic portal hypertensive patients with SRS and those without SRS, and patients with completely obliterated SRS by B-RTO. The subjects were patients with liver cirrhosis (LC) who were followed up between January 1998 and December 2002 at the Kurume University Hospital. The diagnosis of LC was made comprehensively by physical findings (such as spider angioma, gynecomastia, and palmar erythema), imaging (ultrasonography [US] and computed tomography [CT]), markers for fibrosis (hyaluronic acid and Type IV collagen), and liver biopsy tissue. To examine the long-term liver function changes due to SRS alone, we carefully, strictly, and retrospectively extracted patients with no hepatocellular carcinoma (HCC) in the first 3 years of the follow-up period, patients without antiviral treatment such as interferon or lamivudine, and patients with a Child–Pugh classification13 of A or B. The patient enrollment was done by four experts in this field. Gastric varices were classified according to the Japanese endoscopic classification14 for esophagogastric varices.