Liver Cirrhosis Contributed to the Immunocompromised Status by Shedding the Membranous TNFRII T.N. Lin 1 , C.H. Chao 1 , I.S. Sheen 1 , Y.P. Ho 1 , W.T. Chen 1 , C.J. Lin 1 , C.T. Yeh 1 , C.Y. Lin 1 1 Liver Research Unit, Linkou Medical Center, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan, Taiwan Background & Aim: Patients with decompensated liver cirrhosis (DLC) were regarded as immunocompromised, reflected by high incidence of bacterial infection. Paradoxically, the proinflammatory cytokine like TNFincreased significantly in patients with DLC even in the face of this immunocompromised status. On the other hand, regulatory T cell (Treg cell) is believed to play an important role in inhibiting immune responses, including innate immune responses like blockade of TNF-effect through soluble TNFRII. Here, we studied the role of Treg cells and TNFRII in patients with decompensated liver cirrhosis. Patients and Methods: 33 healthy volunteers and 78 cirrhotic patients were enrolled. The percentage of Treg cells were enumerated by flow and serum levels of IL-10, TGF-and TNF-by ELISA. Results: The percentage of Treg cells increased significantly in patients with DLC associated with increased serum levels of IL-10 and TGF-. In addition, these Treg cells were mainly memory type reflected as high CD45RO. Furthermore, the TNFRII expression increased significantly on these Treg cells of DLC. Interestingly, these membranous TNFRII on Treg cells could be shed-off. Lastly, we found the serum soluble TNFRII concentration increased significantly in patients with DLC when compared with normal volunteers. Conclusion: Our results demonstrated memory Treg cells with high TNFRII expression increased significantly in patients with decompensated liver cirrhosis that could possibly blocked the biological effect of TNF-by shedding membranous TNFRII and contributed to the immunocompromized status of DLC. Background: Portal pressure measured as hepatic venous pressure gradient (HVPG) correlates with severity of portal hypertension and the development of complications. HVPG measurement is invasive. Recently, liver stiffness measurement has been shown to correlate with liver biopsy and helps predict outcome in chronic liver disease patients. This study was conducted with the aim to study the correlation between portal pressure as measured by HVPG and liver stiffness as measured by fibroscan among patients with portal hypertension due to various causes. Methods: Between August and September 2008, consecutive patients with portal hypertension were included and were subjected to HVPG measurement and fibroscan (Echosens, France). Results: Of the 18 patients with portal hypertension, both HVPG and liver stiffness were measurable in 12[9 (75%) males; mean age 37.5(10.6) years]. The etiological distribution was HBV related cirrhosis in 3 patients, HCV cirrhosis in 3, cryptogenic cirrhosis in 2, alcoholic cirrhosis in 2, HBV and alcoholic cirrhosis in 1and primary extra-hepatic portal vein obstruction in1. The mean HVPG and liver stiffness of this group were 13.9 (5.1) mm hg and 26.6 (16.5) kPa respectively. There was a strong positive correlation between HVPG and liver stiffness [r = 0.708; p = 0.01]. Conclusions: Non-invasive measurement of liver stiffness correlates well with invasive measurement of portal pressure. Liver stiffness measurement could be used as a prognostic indicator to predict the severity of portal hypertension.