APPROXIMATELY HALF OF cirrhotic patients have esophageal varices at the time of diagnosis, and incidence of varices may increase to 90% in the long-term follow up.[23] Among endoscopic grades of esophageal varices, grades 2 and 3 are of particular importance because they can cause life-threatening upper gastrointestinal

hemorrhage. Therefore, it is crucial to grade the varices for prevention and treatment of the hemorrhage.[24] The LGV, which is the inflowing vein of the varices and originates from the SV or PV as shown on ultrasonography, plays an important role in the formation and development of the varices.[17, 25] Recent studies find more showed a correlation between the variceal bleeding and hepatofugal flow in the LGV on ultrasonography, and the LGV velocity and diameter were found to correlate with the occurrence

of variceal bleeding.[17, 26] However, others found that dilatation of the LGV could not be present at the time of the occurrence of variceal hemorrhage.[27] These published articles suggest that there is an inconsistency regarding the association of this variceal hemorrhage with LGV velocity or diameter. In this study, we initially used MR portography to visualize the LGV and its originating vein, and to determine whether their diameters could be associated with the presence and endoscopic grades of the varices. Our study initially suggested that the diameters of LGV and its main originating vein – the SV – measured on MR imaging could be used to identify the presence and endoscopic grades of the

varices. Compared to other researches which SCH727965 price have been performed to identify predictive non-invasive factors for the varices such as platelet count of 82 000/uL or less, PV diameter of 11.5 mm or more, and anteroposterior splenic measurement selleckchem of 103 mm or more,[8-11] we used MR portography to display the varices, the inflowing vein of the varices and its originating vein, which was visualized and effective to investigate the previous associations. As shown in our study, esophageal varices could be found in most of the cirrhotic patients, the LGV could be the inflowing vein of the varices, and the diameter of the LGV and of the predominant originating veins (SV) of this inflowing vein would increase with the progress of the varices from grade 0 to 3. The possible mechanism of these findings may be explained as follows. Because of portal outflow obstruction (elevated intrahepatic portal vascular resistance) in cirrhotic patients, increased blood flow in the PV and SV cannot enter the liver via the PV, and a considerable percentage of the PV and SV flow is forced to bypass the liver.[1, 28, 29] One of the most important shunting routes is LGV originating from PV or SV, and our findings suggested that SV was the predominant originating vein.

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