Showing papers by "Didier Samuel published in 2013"
University of Paris1, Pierre-and-Marie-Curie University2, French Institute of Health and Medical Research3, University of Lyon4, Université Bordeaux Segalen5, University of Paris-Sud6, Metz7, Paris Diderot University8, University of Limoges9, University of Auvergne10, University of Rennes11, University of Burgundy12, University of Lorraine13
TL;DR: The safety profile was poor and patients with platelet count ≤ 100,000/mm(3) and serum albumin <35 g/L should not be treated with the triple therapy, and the on-treatment virological response was high.
431 citations
TL;DR: Enhanced retrotransposon capture sequencing is applied to hepatocellular carcinoma genomes and substantiate L1-mediated retrotransposition as an important etiological factor in HCC, substantiating its significance in cancer.
350 citations
TL;DR: This randomized trial of MARS in patients with ALF was unable to provide definitive efficacy or safety conclusions because many patients had transplantation before administration of the intervention.
Abstract: Background: Albumin dialysis with the Molecular Adsorbent Recirculating System (MARS) (Gambro, Lund, Sweden), a noncell artificial liver support device, may be beneficial in acute liver failure (ALF). Objective: To determine whether MARS improves survival in ALF. Design: Randomized, controlled trial. (ClinicalTrials.gov: NCT00224705) Setting: 16 French liver transplantation centers. Patients: 102 patients with ALF. Intervention: Conventional treatment (n = 49) or MARS with conventional treatment (n = 53), stratified according to whether paracetamol caused ALF. Measurements: 6-month survival and secondary end points, including adverse events. Results: 102 patients (mean age, 40.4 years [SD, 13]) were in the modified intention-to-treat (mITT) population. The per-protocol analysis (49 conventional, 39 MARS) included patients with at least 1 session of MARS of 5 hours or more. Six-month survival was 75.5% (95% CI, 60.8% to 86.2%) with conventional treatment and 84.9% (CI, 71.9% to 92.8%) with MARS (P = 0.28) in the mITT population and 75.5% (CI, 60.8% to 86.2%) with conventional treatment and 82.9% (CI, 65.9% to 91.9%) with MARS (P = 0.50) in the per-protocol population. In patients with paracetamol-related ALF, the 6-month survival rate was 68.4% (CI, 43.5% to 86.4%) with conventional treatment and 85.0% (CI, 61.1% to 96.0%) with MARS (P = 0.46) in the mITT population. Sixty-six of 102 patients had transplantation (41.0% among paracetamol-induced ALF; 79.4% among non―paracetamol-induced ALF) (P < 0.001). Adverse events did not significantly differ between groups. Limitation: The short delay from randomization to liver transplantation (median, 16.2 hours) precludes definitive efficacy or safety evaluations. Conclusion: This randomized trial of MARS in patients with ALF was unable to provide definitive efficacy or safety conclusions because many patients had transplantation before administration of the intervention. Acute liver failure not caused by paracetamol was associated with greater 6-month patient survival. Primary Funding Source: Assistance Publique―Hopitaux de Paris.
194 citations
TL;DR: The GTPase HRas, activated downstream of EGFR signaling, is identified as a key host signal transducer for EGFR-mediated HCV entry and shown to be relevant for entry of other viruses, including influenza.
169 citations
TL;DR: Patients with a MELD score ≥20, and particularly patients with a score ≥30, are candidates for antifungal prophylaxis, according to a retrospective, single‐center analysis of 667 liver transplants.
Abstract: Antifungal prophylaxis is recommended in high-risk patients, but risk criteria remain unclear and the predictive value of Model of End-Stage Liver Disease (MELD) score is unknown. In a retrospective, single-center analysis of 667 liver transplants, potential risk factors for fungal infection were assessed, including MELD score. Antifungal prophylaxis was administered in 198 patients (29.4%). During follow-up (mean 43.6 ± 29.6 months), 263 patients (39.4%) developed ≥ 1 episode of fungal infection, and 187 (28.0%) patients developed a probable or proven invasive fungal infection requiring systemic antifungal treatment. Patients receiving antifungal prophylaxis had a lower incidence of fungal infection (29.8% vs. 43.5% without prophylaxis, p < 0.001) and invasive fungal infection (17.7% vs. 32.4%, p < 0.001). One-yr patient survival was 91%, 85% and 69%, respectively, in patients with no fungal infection, fungal colonization and treated invasive fungal infection (p < 0.001); graft survival was 88%, 85% and 66% (p < 0.001). Multivariate analysis indicated that MELD score of 20-30 or ≥ 30 was associated with a 2.0-fold or 4.3-fold increase in relative risk of fungal infection, respectively, and a 2.1-fold or 3.1-fold increase in relative risk of invasive fungal infection. In conclusion, liver transplant patients with a MELD score ≥ 20, and particularly patients with a score ≥ 30, are candidates for antifungal prophylaxis.
79 citations
TL;DR: Early referral of cirrhotic patients to ICU before the development of multiple extrahepatic organ failure is essential to improve outcome.
Abstract: Purpose of reviewGive an update on the importance of prognostic scores at admission to the ICU for defining short-term outcome in critically ill cirrhotic patients. Highlight the correlation between the development of sepsis and/or organ failure and outcome.Recent findingsICU mortality rate of cirrh
73 citations
TL;DR: The preliminary results of triple therapy with boceprevir or telaprevir in terms of efficacy and safety in liver transplant recipients are described, indicating a new era in HCV‐associated liver disease.
Abstract: Hepatitis C virus (HCV) infection is one of the leading causes of end-stage liver disease and the main indication for liver transplantation (LT) in most countries. All patients who undergo LT with detectable serum HCV RNA experience graft reinfection. Between 20 and 30% of patients develop cirrhosis within 5 years post-LT. The outcome of transplant patients with cirrhosis on the graft is severe, with a rate of decompensation at 1 year of around 40%. To date, retransplantation is the only option for patients who develop decompensation. Until 2011, standard antiviral therapy, using pegylated interferon (PEG-IFN) and ribavirin (RBV), was the only effective therapy. Obtaining a sustained virological response (SVR) in the setting of LT greatly improves overall and graft survival, but this only concerns 30% of transplanted patients. Direct-acting antivirals (DAA) such as protease inhibitors, polymerase or other non-structural proteins inhibitors represent a new era in HCV-associated liver disease. Although their use in the field of liver transplantation seems to be essential, there are some limitations due to safety and tolerance. One limitation is the potential interaction with calcineurin inhibitors. We describe the preliminary results of triple therapy with boceprevir or telaprevir in terms of efficacy and safety in liver transplant recipients.
56 citations
TL;DR: A novel paradigm is delineated where HCV may be related to liver pathogenesis through its ability to induce a local, intrahepatic TGF-β activation, which argues for a dual impact of HCV core on liver fibrosis and liver carcinogenesis.
51 citations
TL;DR: Although HHV8 transmission is a frequent event after organ transplantation,HHV8‐related morbidity is rather rare but can be life threatening, anddonor screening is advisable for monitoring HHV 8 seronegative liver transplant recipients.
42 citations
TL;DR: In developed countries, acute hepatitis E virus infections are increasingly reported mostly due to zoonotic genotypes 3 and 4 strains, and risk factors for these sporadic cases include consumption of raw or undercooked infected meat or direct contact with infected animals.
Abstract: In developed countries, acute hepatitis E virus (HEV) infections are increasingly reported mostly due to zoonotic genotypes 3 and 4 strains (1). Risk factors for these sporadic cases include consumption of raw or undercooked infected meat or direct contact with infected animals (1). In immunocomprom
42 citations
TL;DR: SHIP2 siRNA and its catalytically inactive mutant disrupt epithelial polarity, and SHIP2 rescues core-induced loss of polarity through RhoA activation.
Abstract: The main targets of hepatitis C virus (HCV) are hepatocytes, the highly polarized cells of the liver, and all the steps of its life cycle are tightly dependent on host lipid metabolism. The interplay between polarity and lipid metabolism in HCV infection has been poorly investigated. Signaling lipids, such as phosphoinositides (PIs), play a vital role in polarity, which depends on the distribution and expression of PI kinases and PI phosphatases. In this study, we report that HCV core protein, expressed in Huh7 and Madin-Darby canine kidney (MDCK) cells, disrupts apicobasal polarity. This is associated with decreased expression of the polarity protein Dlg1 and the PI phosphatase SHIP2, which converts phosphatidylinositol 3,4,5-trisphosphate into phosphatidylinositol 4,5-bisphosphate (PtdIns(3,4)P2). SHIP2 is mainly localized at the basolateral membrane of polarized MDCK cells. In addition, PtdIns(3,4)P2 is able to bind to Dlg1. SHIP2 small interfering RNA or its catalytically dead mutant disrupts apicobasal polarity, similar to HCV core. In core-expressing cells, RhoA activity is inhibited, whereas Rac1 is activated. Of interest, SHIP2 expression rescues polarity, RhoA activation, and restricted core level in MDCK cells. We conclude that SHIP2 is an important regulator of polarity, which is subverted by HCV in epithelial cells. It is suggested that SHIP2 could be a promising target for anti-HCV treatment.
TL;DR: There is long‐term persistence of antibodies to yellow fever in SOT recipients who have been vaccinated prior to transplantation, and this data suggest that transplant candidates planning to travel in countries where yellow fever is endemic should be vaccinated priorto transplantation.
TL;DR: A histologic pattern of centrilobular injury including increased NIA and increased PC infiltration correlates with measurements of autoimmunity in liver recipients and could be used to segregate cases for further study and introduced into the AIH scoring systems.
Abstract: BACKGROUND: Autoimmune hepatitis (AIH) after liver transplantation has been defined histologically as a "hepatitic" pattern of injury, characterized by lymphoplasmacytic inflammation with necroinflammatory activity (NIA), comparable with findings seen in native livers. This definition, however, is difficult to apply in practice because specific histologic criteria are not clearly delineated. This study aimed to determine which histologic features correlated best with clinical and serologic features of dAIH. METHODS: Index liver biopsies from patients with autoimmune-like hepatitis transplanted for non-AIH in two centers (n=35 and 20) were reviewed. Histologic features were correlated with the clinical diagnosis of AIH based on a retrospective review of clinical and serologic data, including therapeutic response. RESULTS: A clinical diagnosis of AIH was retrospectively assigned to 24 of 35 (68%) and 18 of 20 (90%) patients, respectively (P=0.10). In multivariate analysis, centrilobular NIA and centrilobular plasma cell (PC) ratio of 30% to 50% were independently discriminating for a clinical diagnosis of AIH (P=0.04 and 0.05, respectively). The best level of predictability (99.6%) was mathematically achieved when severe centrilobular NIA and centrilobular PC ratio of 30% to 50% were both present. CONCLUSION: A histologic pattern of centrilobular injury including increased NIA and increased PC infiltration correlates with measurements of autoimmunity in liver recipients. It could be used to segregate cases for further study and introduced into the AIH scoring systems when applied in the context of liver transplantation.
TL;DR: The group highlighted that the distinctions according to the delay between onset of jaundice and HE, such as hyperacute or fulminant, acute or subfulminant and subacute, do not have prognostic significance distinct from the cause of illness.
TL;DR: This study provides data supporting the pathogenic role of HHV-6 for liver allografts and suggests the presence of confluent periportal necrosis could be a clue for prompt diagnosis of HHv-6-induced graft hepatitis.
Abstract: Objectives: To correlate human herpesvirus 6 (HHV-6) viral load with pathologic features in graft acute hepatitis of unknown origin. Methods: Liver frozen samples from 26 patients with graft hepatitis of unknown origin were available for HHV-6 DNA quantification. Results: In 10 (38.5%) of 26 liver samples, HHV-6 DNA was detectable, with a median viral load of 3.84 log 10 copies/10 6 cells. Confluent periportal necrosis was observed in 4 of 10 patients and associated with high viral load. These 4 patients responded to antiviral therapy. Mild unspecific hepatitis was observed in 4 patients with low intragraft viral load and in 2 patients with high viral load in a context of deep immunosuppression. Patients with HHV-6–negative graft hepatitis disclosed lobular necrotico-inflammatory activity without periportal necrosis. Conclusions: Our study provides data supporting the pathogenic role of HHV-6 for liver allografts. The presence of confluent periportal necrosis could be a clue for prompt diagnosis of HHV-6–induced graft hepatitis.
TL;DR: SVR, which was achieved by approximately one‐third of the retreated patients, can be predicted with the same variables used for naive LT recipients (age, disease severity, adherence, and viral kinetics) and is associated with enhanced survival.
TL;DR: Results indicate that the NIS gene is a direct target of the p53 family and suggests that the modulation of NIS by DNA-damaging agents is potentially exploitable to boost NIS upregulation in vivo.
Abstract: Thyroid iodide accumulation via the sodium/iodide symporter (NIS; SLC5A5) has been the basis for the longtime use of radio-iodide in the diagnosis and treatment of thyroid cancers. NIS is also expressed, but poorly functional, in some non-thyroid human cancers. In particular, it is much more strongly expressed in cholangiocarcinoma (CCA) and hepatocellular carcinoma (HCC) cell lines than in primary human hepatocytes (PHH). The transcription factors and signaling pathways that control NIS overexpression in these cancers is largely unknown. We identified two putative regulatory clusters of p53-responsive elements (p53REs) in the NIS core promoter, and investigated the regulation of NIS transcription by p53-family members in liver cancer cells. NIS promoter activity and endogenous NIS mRNA expression are stimulated by exogenously expressed p53-family members and significantly reduced by member-specific siRNAs. Chromatin immunoprecipitation analysis shows that the p53-REs clusters in the NIS promoter are differentially occupied by the p53-family members to regulate basal and DNA damage-induced NIS transcription. Doxorubicin strongly induces p53 and p73 binding to the NIS promoter, leading to an increased expression of endogenous NIS mRNA and protein in HCC and CCA cells, but not in PHH. Silencing NIS expression reduced doxorubicin-induced apoptosis in HCC cells, pointing to a possible role of a p53-family-dependent expression of NIS in apoptotic cell death. Altogether, these results indicate that the NIS gene is a direct target of the p53 family and suggests that the modulation of NIS by DNA-damaging agents is potentially exploitable to boost NIS upregulation in vivo.
TL;DR: The case of a 72‐year‐old patient with partial recovery from acquired amyloid neuropathy following retransplantation with a deceased donor 7 years after DLT performed for end‐stage liver disease is described.
TL;DR: Evidence of a distinct regulation of Bcl-2 family proteins in EBV-positive versus negative PTLD is provided and the low-expression pattern of the proapoptotic proteins Bim and cleaved PARP together with the high-expression patterns of the antiapoptosis protein B cl-2 by trend suggests disruption of the apoptotic pathway by EBV in PTLD, promoting survival signals in the host cells.
Abstract: Posttransplant lymphoproliferative disorders (PTLD) represent a spectrum of lymphoid diseases complicating the clinical course of transplant recipients. Most PTLD are Epstein-Barr virus (EBV) associated with viral latency type III. Several in vitro studies have revealed an interaction between EBV latency proteins and molecules of the apoptosis pathway. Data on human PTLD regarding an association between Bcl-2 family proteins and EBV are scarce. We analyzed 60 primary PTLD for expression of 8 anti- (Bcl-2, Bcl-XL, and Mcl-1) and proapoptotic proteins (Bak and Bax), the so-called BH3-only proteins (Bad, Bid, Bim, and Puma), as well as the apoptosis effector cleaved PARP by immunohistochemistry. Bim and cleaved PARP were both significantly (p = 0.001 and p = 5.251e-6) downregulated in EBV-positive compared to EBV-negative PTLD [Bim: 6/40 (15%), cleaved PARP: 10/43 (23%), vs. Bim: 13/16 (81%), cleaved PARP: 12/17 (71%)]. Additionally, we observed a tendency toward increased Bcl-2 protein expression (p = 0.24) in EBV-positive PTLD. Hence, we provide evidence of a distinct regulation of Bcl-2 family proteins in EBV-positive versus negative PTLD. The low-expression pattern of the proapoptotic proteins Bim and cleaved PARP together with the high-expression pattern of the antiapoptotic protein Bcl-2 by trend in EBV-positive tumor cells suggests disruption of the apoptotic pathway by EBV in PTLD, promoting survival signals in the host cells.
TL;DR: The results indicate that P55-70 of hnRNP B1 is a potential biomarker for AIH in immunological tests and suggest the role of circulating nucleic acids, (eg miRNA), present or absent according to the autoimmune disorders and involved in antigen-antibody stability.
Abstract: Background : Heterogeneous nuclear ribonucleoprotein (hnRNP) A2/B1 is a target for antinuclear autoantibodies in systemic Lupus erythematosus (SLE), rheumatoid arthritis (RA), and autoimmune hepatitis (AIH).
Aim : To monitor molecular interactions between peptides spanning the entire sequence of hnRNP A2/B1 and serafrom patients and healthy controls.
Methods : Sera from 8 patients from each pathology and controls were passed across a surface plasmon resonanceImagery (SPRi) surface containing 39 overlapping peptides of 17 mers covering the human hnRNP B1. Interactionsinvolving the immobilised peptides were followed in real time and dissociation rate constants koff for each interactionwere calculated.
Results : Several significant interactions were observed: i) high stability (lower koff values) between P55-70 and the AIHsera compared to controls (p= 0.003); ii) lower stability (higher koff values) between P118-133 and P262-277 and SLE sera,P145-160 and RA sera compared to controls (p=0.006, p=0.002, p=0.007). The binding curves and koff values observedafter the formation of complexes with anti-IgM and anti-IgG antibodies and after nuclease treatment of the serumindicate that i) IgM isotypes are prevalent and ii) nucleic acids participate in the interaction between anti-hnRNAP B1and P55-70 and also between controls and the peptides studied.
Conclusions : These results indicate that P55-70 of hnRNP B1 is a potential biomarker for AIH in immunological testsand suggest the role of circulating nucleic acids, (eg miRNA), present or absent according to the autoimmunedisorders and involved in antigen-antibody stability.
TL;DR: Treatment of posttransplantation hepatitis B is a less important clinical problem than it was historically because effective antiviral therapies exist to rescue patients who failed initial prophylaxis.
TL;DR: Noncovered metallic stents are placed extending from the portal trunk to the contralateral tumor free portal pedicle to prevent the malignant progression from a portal branch to the main portal trunk.
Abstract: Background and Aims
Macroscopic portal vein invasion complicating hepatocellular carcinoma in the setting of cirrhosis is associated with a very low survival. To prevent the malignant progression from a portal branch to the main portal trunk, we have placed noncovered metallic stents extending from the portal trunk to the contralateral tumor free portal pedicle.
Methods
Fifty-Four patients (age: 60 ± 11 years) were treated. Thirty-four (60%) patients were Child A and 20 (40%) were Child B–C. Tumoral thrombosis involved 1st or 2nd order branches in 41 (82%) patients and partially the main trunk in 13 (24%). Open surgical insertion (via ileal vein) as an alternative to a percutaneous approach was used in 14 (24%) patients.
Results
Early mortality ( 30 µmol/L and open surgical insertion were predictive of short-term mortality. In the good group, overall survival at 6, 12, and 24 months were 69%, 61%, and 46%, respectively.
Conclusions
The transhepatic deployment of metallic stent seems to improve survival of patients with hepatocellular carcinoma complicated by portal vein tumoral thrombosis and could allow subsequent treatments. J. Surg. Oncol. 2013;107:696–701. © 2012 Wiley Periodicals, Inc.
TL;DR: The marked and significant differences in infection rates and requirement for systemic treatment in this large population suggest that targeted use of low-dose ABLC therapy to high-risk patients is a valid prophylactic strategy following liver transplantation.
Abstract: Antifungal prophylaxis with liposomal amphotericin B in high-risk liver transplant recipients is recommended, but experience with amphotericin B lipid complex (ABLC, Abelcet®) in this setting is limited. Data from 615 liver transplants performed during 1999–2005 were analyzed retrospectively. High-risk patients (n = 146) received a mean cumulative ABLC dose of 955 ± 609 mg (mean duration of 23.3 ± 11.9 days). Low-risk patients (n = 469) received no prophylaxis. During a mean follow-up of 43.8 ± 29.2 months, fungal infections occurred in 32.2% of ABLC patients versus 43.5% of non-prophylaxis patients (P = 0.015). The overall rate of invasive fungal infection was 12.3% in the ABLC group versus 15.6% in the non-prophylaxis patients (P = 0.34). Any Candida infection (ABLC 29.5%, non-prophylaxis 41.2%, P = 0.011), probable or proven invasive Candida infection requiring systemic antifungal treatment (ABLC 18.5%, non-prophylaxis 32.4%, P = 0.001) and invasive abdominal candidiasis during the first 3 months (ABLC...
TL;DR: It is reported, for the first time, the outcome of anti-hepatitis C virus (HCV) triple therapy with telaprevir in an HIV/HCV co-infected transplanted patient with a sustained virological response.
Abstract: We report, for the first time, the outcome of anti-hepatitis C virus (HCV) triple therapy with telaprevir in an HIV/HCV co-infected transplanted patient. After liver transplantation, the patient experienced a severe HCV recurrence with fibrosing cholestatic hepatitis, and anti-HCV therapy with pegylated interferon alpha 2a, ribavirin and telaprevir was initiated. A sustained virological response was achieved after 48 weeks of anti-HCV therapy. Drug-drug interactions between antiretroviral therapy, immunosuppressive agents and anti-HCV therapy could be managed.
TL;DR: Using specific computer programs improves the intensive process of manual coding by shortening the time required as well as reducing errors, which in turn positively impacts the ICU budget allocation.
TL;DR: This is the first immunological description of potentially severe non‐GVHD hepatitis occurring after BMT, determined using a proteomic approach and enabling a discussion of the mechanisms that transform an alloimmune reaction into an autoimmune response.
Journal Article•
TL;DR: Extracorporeal liver support (or liver dialysis) might serve as a bridge to transplantation for patients with acute liver failure as mentioned in this paper, and uncontrolled studies of an albumin dialysis system suggest possibl...
Abstract: Extracorporeal liver support (or liver dialysis) might serve as a bridge to transplantation for patients with acute liver failure. Uncontrolled studies of an albumin dialysis system suggest possibl...
TL;DR: The outcomes of four HIVinfected patients transplanted for NRH are reported on, answering the question regarding the potential recurrence of NRH on the graft.
Abstract: Regenerative Hyperplasia in Human Immunodeficiency VirusYInfected Patients: Does the Disease Recur? Noncirrhotic portal hypertension (NCPH) in human immunodeficiency virus (HIV)Yinfected patients is mainly due to nodular regenerative hyperplasia (NRH). The pathophysiology of NRH in these patients may be linked to their prothrombotic status and/or to anti-HIV drug toxicity, with an intrahepatic blood flow disorder leading to severe complications. We previously reported our experience of liver transplantation (LT) in three HIVinfected patients (1). To answer the question regarding the potential recurrence of NRH on the graft, we report here on the outcomes of four HIVinfected patients transplanted for NRH.
TL;DR: These studies suggest that increases in Th2 cytokines correlate with HCC progression, and this Th2 response may counteract the Th1 effect when Th1 functions are upregulated and inversely.
Abstract: The immune system is composed of a variety of cells and mediators interacting in a complex dynamic network to protect the host. One component of the immune system that molds the host response to foreign pathogens is the cytokine, a secreted or membrane-bound protein that regulates growth, differentiation and activation of immune cells and plays an important role in angiogenesis, inflammation and cell growth. Cytokines are released in response to diverse cellular stresses, including infection, inflammation and carcinogen-induced injury (Table 1). These proteins are generally grouped into two categories, proand antiinflammatory, although some cytokines do not specifically fit into either category. In fact, many cytokines have pleiotropic functions, and some may act in a synergistic manner. Several cytokines, particularly those produced by CD4 Th cells, are defined as Th1 or Th2 and are comprised mainly of interleukins (ILs). Th1 cytokines (e.g., IL-1, IL-2, IL-12, IL-15 and non-ILs, e.g., TNFa and IFN c) are generally referred to as proinflammatory, while Th2 cytokines (e.g., IL-4, IL-8, IL-10 and IL-5) induce antiinflammatory responses [1]. The expression levels of proand antiinflammatory cytokines have been quantified in hepatocellular carcinoma (HCC) tumors and comparative normal samples (Table 1). Many studies have shown associations between the expression of several Th1 cytokines and HCC. Differing results have been obtained for TNFa expression, with some studies showing higher levels in HCC patients than healthy individuals [2, 3] and others showing lower levels [4, 5]. However, the production of TNFa is stimulated by other Th1 cytokines, IL-1, IL-2, IL-12 and IL-15, which are mainly upregulated in HCC [6–8]. This leads to a proinflammatory state that probably induces a protumorigenic role (Fig. 1). The expression of IFN c was measured in HCC and shown to be slightly higher than in normal, surrounding tissue [9]. Conversely, Jang et al. [10] have reported lower levels in HCC than healthy patients. So, further studies are warranted to examine the expression of IFN c in HCC. Among Th2 cytokines, IL-10 is the most studied with regard to HCC expression. The authors have shown that IL10 is highly expressed in HCC tumors and individuals with HCC versus non-tumorous-surrounding tissue controls or healthy cohorts, respectively [6, 7, 9]. IL-4 and IL-8 were also overexpressed in HCC compared to healthy patients [5, 10]. These studies suggest that increases in Th2 cytokines correlate with HCC progression. However, this Th2 response may counteract the Th1 effect when Th1 functions are upregulated and inversely. There are few data concerning the role of IL-5 in HCC, and it needs to be substantiated in future studies. Indeed, Budhu et al. [1] suggested that IL-5 is associated with the metastatic phenotype of tumors, impairing Th1-mediated anti-tumor immunity. Other studies have demonstrated changes in cytokine expression resulting from various treatment regimens for Editorial to Chung-Pin Li et al, Cytokines are associated with postembolization fever and survival in hepatocellular carcinoma patients receiving transcatheter arterial chemoembolization
TL;DR: It is indicated that HCV per se is not a contraindication to LT in HIV patients, but recipient and donor selection and the management of acute rejection strongly influence outcomes.