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INTRODUCTION: The Baveno VI consensus guidelines and an expanded algorithm suggest that transient elastography (TE) and platelet (PLT) count can be used to identify patients with cirrhosis who can avoid esophagogastroduodenoscopy (EGD). The primary aims of this study were to assess the ability of a simple algorithm, which uses only laboratory parameters, to predict medium/large esophageal varices (EV) in patients with hepatitis C virus (HCV) and cirrhosis from the Rete Sicilia Selezione Terapia–HCV (RESIST-HCV) cohort and to compare the performance of the algorithm with Baveno VI and Expanded Baveno VI criteria. The secondary aim was to assess the role of TE in ruling out large EV. METHODS: In total, 1,381 patients with HCV-associated cirrhosis who had EGD and TE within 1 year of starting treatment with direct-acting antivirals were evaluated. Using multivariate logistic analysis, laboratory variables were selected to determine which were independently associated with medium/large EV to create the RESIST-HCV criteria. These criteria were tested in a training cohort with patients from a single center (Palermo) and validated with patients from the 21 other centers of the RESIST-HCV program (validation cohort). RESULTS: In the entire cohort, medium/large EV were identified in 5 of 216 patients (2.3%) using the Baveno VI criteria and 13 of 497 patients (2.6%) using the Expanded Baveno VI criteria. PLT count and albumin level were independently associated with medium/large EV. The best cut-off values were a PLT count greater than 120 × 109 cells/μL and serum albumin level greater than 3.6 g/dL; negative predictive values (NPVs) were 97.2% and 94.7%, respectively. In the training cohort of 326 patients, 119 (36.5%) met the RESIST-HCV criteria and the NPV was 99.2%. Among 1,055 patients in the validation cohort, 315 (30%) met the RESIST-HCV criteria and the NPV was 98.1%. Adding TE to the RESIST-HCV criteria reduced the avoided EGDs for approximately 25% of patients and the NPV was 98.2%. DISCUSSION: The “easy-to-use” RESIST-HCV algorithm avoids EGD for high-risk EV screening for more than 30% of patients and has the same performance criteria as TE. Using these criteria simplifies the diagnosis of portal hypertension.

Real-world evidence on the course of Hepatitis C Virus (HCV) chronic liver disease after Sustained Virologic Response (SVR) obtained with direct-acting antiviral drugs (DAAs) are still limited, and the effects on mortality remain unclear. We evaluated the post-treatment survival of 4307 patients in the RESIST-HCV cohort (mean age 66.3 ± 11.6 years, 56.9% males, 24.7% chronic hepatitis, 66.9% Child-PughThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

A central problem in tumor immunology has been to explain how immunogenic tumors escape destruction by the immune defenses of their immunocompetent hosts. The results of studies performed during the past few years in this laboratory (reviewed in 1) support the hypothesis that certain tumors with tumorspecific, transplantation antigens avoid destruction by the immune response of their hosts by evoking the production of a population of suppressor T cells that functions to downregulate the immune response before enough effector T cells are generated to cause tumor regression . These published studies (2, 3) show that growth of the immunogenic tumors under investigation evokes the generation of an underlying state of concomitant immunity, which develops progressively between days 6 and 9 of tumor growth, and which is mediated by Ly-2 + effector T cells. After day 9, however, there is progressive loss of effector T cells, and this is temporarily associated with the progressive acquisition of Ly-1 +,2-suppressor T cells that are functionally defined by their ability to inhibit, on passive transfer, the expression of adoptive immunity against an established tumor in immunodepressed test recipients. It was postulated, on the basis of these and other results (1), that the loss of effector T cells results from negative regulation by tumor-induced suppressor T cells.However, other investigators have described the generation of a different type of suppressor T cell in mice bearing progressive immunogenic tumors (reviewed in 4). This second type of suppressor T cell displays the Ly1 -,2+, I-J' membrane phenotype, is generated at a very early stage of tumor growth, and is defined by its ability to suppress, on passive transfer, a delayed-type hypersensitivity (DTH)' reaction to tumor antigens in tumor-immune recipients. Because these suppressors of DTH are generated progressively during the first 6-7 d of tumor growth (5, 6), but are then progressively lost (6), it seems unlikely that they would exert a meaningful suppressor function in those situations where a tumor evokes the generation of a state of concomitant antitumor immunity that does not peak until day 9 of tumor growth, and does not undergo decay until after days 9-12.

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