The presence of spontaneous portosystemic shunts increases the risk of ă complications after transjugular intrahepatic portosystemic shunt (TIPS) ă placement

International audiencePurpose: The goal of this study was to identify clinical and imaging ă variables that are associated with an unfavorable outcome during the 30 ă days following transjugular intrahepatic portosystemic shunt (TIPS) ă placement. ă Material and methods: Fifty-four consecutive patients with liver ă cirrhosis (Child-Pugh 6-13, Model for End-stage Liver Disease 7-26) ă underwent TIPS placement for refractory ascites (n = 25), recurrent or ă uncontrolled variceal bleeding (n = 23) or both (n = 6). Clinical, ă biological and imaging variables including type of stent (covered n = ă 40; bare-stent n = 14), presence of spontaneous portosystemic shunt (n = ă 31), and variations in portosystemic pressure gradient were recorded. ă Early severe complication was defined as the occurrence of overt hepatic ă encephalopathy or death within the 30 days following TIPS placement. ă Results: Sixteen patients (30%) presented with early severe ă complication after TIPS placement. Child-Pugh score was independently ă associated with complication (HR = 1.52, P < 0.001). Among the imaging ă variables, opacification of spontaneous portosystemic shunt during TIPS ă placement but before its creation was associated with an increased risk ă of early complication (P = 0.04). The other imaging variables were not ă associated with occurrence of complication. ă Conclusion: Identification of spontaneous portosystemic shunt during ă TIPS placement reflects the presence of varices and is associated with ă an increased risk of early severe complication

Transfusion-associated TT virus co-infection in patients with hepatitis C virus is associated with type II mixed cryoglobulinemia but not with B-cell non-Hodgkin lymphoma

International audienceOBJECTIVE:To assess the prevalence of TT virus (TMV) infection in a series of patients with chronic hepatitis C virus (HCV) infection, with or without benign (mixed cryoglobulinemia) or malignant (B-cell non-Hodgkin lymphoma (B-NHL)) lymphoproliferative disease.METHODS:Sixty-six HCV patients were studied, including patients with mixed cryoglobulinemia (n=30), B-NHL (n=15), and no mixed cryoglobulinemia or B-NHL (n=21). All HCV patients had increased transaminase levels and were HCV RNA positive. Patients were considered to have mixed cryoglobulinemia if two successive determinations of their serum cryoglobulin level were above 0.05 g/L. Mixed cryoglobulinemia-negative patients never had mixed cryoglobulins in their serum on multiple determinations. Subjects without HCV infection included 79 patients with histologically proven B-NHL, and 50 healthy blood donors. Serum samples were analyzed for TTV DNA by nested polymerase chain reaction, with two couples of primers in different regions of the genome, in two independent laboratories.RESULTS:In the group of HCV-positive patients, TTV DNA was found in one of 15 (6.7%) patients with B-NHL, and in nine of 51 (17.6%, P = 0.43) of those without B-NHL. Among HCV-positive patients without B-NHL, TTV DNA was more frequently found in those with type II mixed cryoglobulinemia vasculitis than in those without it (six of 16 (37.5%) versus two of 21 (9.5%), P = 0.05). In subjects without HCV infection, TTV DNA was present in 10 of 79 (12.7%) patients with B-NHL and in seven of 50 (14.0%, P = 0.82) blood donors.CONCLUSION:In patients chronically infected with HCV, TTV co-infection: (1) is not associated with the presence of B-NHL; and (2) is more frequently found in patients presenting a type II mixed cryoglobulinemia vasculitis