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| 1 | 在肝的感染移植接受者显示文摘 Liver transplantation is a standard life-saving procedure for the treatment of many end-stage liver diseases. The success of this procedure may be limited by infectious complications.In this article,we review the contemporary state of infectious complications during the post-operative period,with particular emphasis on those that occur most commonly during the first 6 mo after liver transplantation.Bacteria,and less commonly Candida infections,remain the predominant pathogens during the immediate post-operative period,especially during the first month,and infections caused by drugresistant strains are emerging.Infections caused by cytomegalovirus and Aspergillus sp.present clinically during the'opportunistic'period characterized by intense immunosuppression.As newer potent immunosuppressive therapies with the major aim of reducing allograft rejection are developed,one potential adverse effect is an increase in certain infections.Hence,it is essential for liver transplant centers to have an effective approach to prevention that is based on predicted infection risk,local antimicrobial resistance patterns,and surveillance.A better understanding of the common and most important infectious complications is anticipated to lead to improvements in quality of life and survival of liver transplant recipients. | Fabian A Romero Raymund R Razonable | 2011 | World Journal of Hepatology2011，3，4： | 28 |
| 2 | Cytomegalovirus infection after liver transplantation: Current concepts and challenges显示文摘Cytomegalovirus (CMV) is a common viral pathogen that influences the outcome of liver transplantation. In addition to the direct effects of CMV syndrome and tissue-invasive diseases, CMV is associated with an increased predisposition to acute and chronic allograft rejection, accelerated hepatitis C recurrence, and other opportunistic infections, as well as reduced overall patient and allograft survival. Risk factors for CMV disease are often interrelated, and include CMV D+/R-serostatus, acute rejection, female gender, age, use of high-dose mycophenolate mofetil and prednisone, and the overall state of immunity. In addition to the role of CMV-specif ic CD4+ and CD8+ T lymphocytes, there are data to suggest that functionality of the innate immune system contributes to CMV disease pathogenesis. In one study, liver transplant recipients with a specific polymorphism in innate immune molecules known as Toll-like receptors were more likely to develop higher levels of CMV replication and clinical disease. Because of the direct and indirect adverse effects of CMV disease, its prevention, whether through antiviral prophylaxis or preemptive therapy, is an essential component in improving the outcome of liver transplantation. In the majority of transplant centers, antiviral prophylaxis is the preferred strategy over preemptive therapy for the prevention of CMV disease in CMV-seronegative recipients of liver allografts from CMV-seropositive donors (D+/R-). However, the major drawback of antiviral prophylaxis is the occurrence of delayed-onset primary CMV disease. In several prospective and retrospective studies, the incidence of delayed-onset primary CMV disease ranged from 16% to 47% of CMV D+/R-liver transplant recipients.Current data suggests that delayed-onset CMV disease is associated with increased mortality after liver transplantation. Therefore, optimized strategies for prevention and novel drugs with unique modes of action are needed. Currently, a randomized controlled clinical trial is being performed comparing the effi cacy and safety of maribavir, a novel benzimidazole riboside, and oral ganciclovir as prophylaxis against primary CMV disease in liver transplant recipients. The treatment of CMV disease consists mainly of intravenous (IV) ganciclovir, and if feasible, a reduction in the degree of immunosuppression. A recent controlled clinical trial demonstrated that valganciclovir is as effective and safe as IV ganciclovir for the treatment of CMV disease in solid organ (including liver) transplant recipients. In this article, the author reviews the current state and the future perspectives of prevention and treatment of CMV disease after liver transplantation. | Raymund Rabe Razonable | 2008 | World Journal of Gastroenterology2008，14，31： | 19 |
| 3 | Management of cytomegalovirus infection and disease in liver transplant recipients显示文摘Cytomegalovirus(CMV) is one of the most common viral pathogens causing clinical disease in liver transplant recipients, and contributing to substantial morbidity and occasional mortality. CMV causes febrile illness often accompanied by bone marrow suppression, and in some cases, invades tissues including the transplanted liver allograft. In addition, CMV has been significantly associated with an increased predisposition to acute and chronic allograft rejection, accelerated hepatitis C recurrence, and other opportunistic infections, as well as reduced overall patient and allograft survival. To negate the adverse effects of CMV infection on transplant outcome, its prevention, whether through antiviral prophylaxis or preemptive therapy, is an essential component to the management of liver transplant recipients. Two recently updated guidelines have suggested that antiviral prophylaxis or preemptive therapy are similarly effective in preventing CMV disease in modest-risk CMV-seropositive liver transplant recipients, while antiviral prophylaxis is the preferredstrategy over preemptive therapy for the prevention of CMV disease in high-risk recipients [CMV-seronegative recipients of liver allografts from CMV-seropositive donors(D+/R-)]. However, antiviral prophylaxis has only delayed the onset of CMV disease in many CMV D+/Rliver transplant recipients, and such occurrence of lateonset CMV disease was significantly associated with increased all-cause and infection-related mortality after liver transplantation. Therefore, a search for better strategies for prevention, such as prolonged duration of antiviral prophylaxis, a hybrid approach(antiviral prophylaxis followed by preemptive therapy), or the use of immunologic measures to guide antiviral prophylaxis has been suggested to prevent late-onset CMV disease. The standard treatment of CMV disease consists of intravenous ganciclovir or oral valganciclovir, and if feasible, reduction in pharmacologic immunosuppression. In one clinical trial, oral valganciclovir was as effective as intravenous ganciclovir for the treatment of mild to moderate CMV disease in solid organ(including liver) transplant recipients. The aim of this article is to provide a state-of-the art review of the epidemiology, diagnosis, prevention, and treatment of CMV infection and disease after liver transplantation. | Jackrapong Bruminhent Raymund R Razonable | 2014 | World Journal of Hepatology2014，6，6： | 10 |
| 4 | Current concepts on cytomegalovirus infection after liver transplantation显示文摘Cytomegalovirus (CMV) is the most common viral pa- thogen that negatively impacts on the outcome of liver transplantation. CMV cause febrile illness often ac com panied by bone marrow suppression, and in some cases, invades tissues including the transplanted allog raft. In addition, CMV has been signif icantly asso- ciated with an increased predisposition to allograft re- jection, accelerated hepatitis C recurrence, and other opportunistic infections, as well as reduced overall pa tient and allograft survival. To negate the adverse effects of CMV on outcome, its prevention, whether through antiviral prophylaxis or preemptive therapy, is regarded as an essential component to the medical management of liver transplant patients. Two recent guidelines have suggested that antiviral prophylaxis or preemptive therapy are similarly effective in preventing CMV disease in modest-risk CMV-seropositive liver trans plant recipients, while antiviral prophylaxis is the preferred strategy over preemptive therapy for the preven tion of CMV disease in high-risk recipients [CMV-ser o-negative recipients of liver allografts from CMV-seropositive donors (D+/R-)]. However, antiviral prophylax is has only delayed the onset of CMV disease in many CMV D+/R- liver transplant recipients, and at least in one study, such occurrence of late-onset primary CMV disease was significantly associated with increased mortality after liver transplantation. Therefore, optimized strategies for prevention are needed, and aggressive treatment of CMV infection and disease should be pursued. The standard treatment of CMV disease consists of intravenous ganciclovir or oral valganciclovir, and if fea sible, one should also reduce the degree of immuno-suppression. In one recent controlled clinical trial, val ganc iclovir was found to be as effective and safe as intravenous ganciclovir for the treatment of mild to mo d erate CMV disease in solid organ (including liver) tran splant recipients. In this article, the authors review the current state and the future perspectives of prev ention and treatment of CMV disease after liver trans plantation. | Sang-Oh Lee Raymund R Razonable | 2010 | World Journal of Hepatology2010，2，9： | 6 |
| 5 | Human herpesvirus 6 infections after liver transplantation显示文摘Human herpesvirus 6(HHV-6) infections occur in > 95% of humans.Primary infection,which occurs in early childhood as an asymptomatic illness or manifested clinically as roseola infantum,leads to a state of subclinical viral persistence and latency.Reactivation of latent HHV-6 is common after liver transplantation,possibly induced and facilitated by allograft rejection and immunosuppressive therapy.Since the vast majority of humans harbor the virus in a latent state,HHV-6 infections after liver transplantation are believed to be mostly due to endogenous reactivation or superinfection(reactivation in the transplanted organ).In a minority of cases,however,primary HHV-6 infection may occur when an HHV-6 negative individual receives a liver allograft from an HHV-6 positive donor.The vast majority of documented HHV-6 infections after liver transplantation are asymptomatic.In a minority of cases,HHV-6 has been implicated as a cause of febrile illness with rash and myelosuppression,hepatitis,pneumonitis,and encephalitis after liver transplantation.In addition,HHV-6 has been associated with a variety of indirect effects such as allograft rejection,and increased predisposition and severity of other infections including cytomegalovirus(CMV),hepatitis C virus,and opportunistic fungi.Because of the uncommon nature of the clinical illnesses directly attributed to HHV-6,there is currently no recommended HHV-6-specific approach to prevention.However,ganciclovir and valganciclovir,which are primarily intended for the prevention of CMV disease,are also active against HHV-6 and may prevent its reactivation after transplantation.The treatment of established HHV-6 disease is usually with intravenous ganciclovir,cidofovir,or foscarnet,complemented by reduction in the degree of immunosuppression.This article reviews the current advances in the pathogenesis,clinical diagnosis,and therapeutic modalities against HHV6 in the setting of liver transplantation. | Rima Camille Abdel Massih Raymund R Razonable | 2009 | World Journal of Gastroenterology2009，15，21： | 5 |
| 6 | Cytomegalovirus infection in liver transplant recipients: Updates on clinical management显示文摘Cytomegalovirus(CMV) infection is a common complication after liver transplantation, and it is associated with multiple direct and indirect effects. Management of CMV infection and disease has evolved over the years,and clinical guidelines have been recently updated.Universal antiviral prophylaxis and a pre-emptive treatment strategy are options for prevention. A currentlyrecruiting randomized clinical trial is comparing the efficacy and safety of the two prevention strategies in the highest risk D+R- liver recipients. Drug-resistant CMV infection remains uncommon but is now increasing in incidence. This highlights the currently limited therapeutic options, and the need for novel drug discoveries.Immunotherapy and antiviral drugs with novel mechanisms of action are being investigated, including letermovir(AIC246) and brincidofovir(CMX001). This article reviews the current state of CMV management after liver transplantation, including the updated practice guidelines, and summarizes the data on investigational drugs and vaccines in clinical development. | Jasmine Riviere Marcelin Elena Beam Raymund R Razonable | 2014 | World Journal of Gastroenterology2014，20，31： | 4 |
| 7 | Impact of human herpes virus 6 in liver transplantation显示文摘Human herpes virus 6 (HHV-6) infects > 95% of humans.Primary infection which occurs mostly during the f irst 2 years of life in the form of roseola infantum,non-spe cif ic febrile illness,or an asymptomatic illness,results in latency.Reactivation of latent HHV-6 is common after liver transplantation.Since the majority of human beings harbor the latent virus,HHV-6 infections after liver transplantation are most probably caused by end ogenous reactivation or superinfection.In a minority of cases,primary HHV-6 infection may occur when an HHV-6-seronegative individual receives a liver allograft from an HHV-6-seropositive donor.The vast major ity of HHV-6 infections after liver transplantation are asy-mptomatic.Only in a minority of cases,when HHV-6 causes a febrile illness associated with rash and mye- losuppression,hepatitis,gastroenteritis,pneumonitis,and encephalitis after liver transplantation.In addition,HHV-6 has been implicated in a variety of indirect effects,such as allograft rejection and increased predis- pos ition to and severity of other infections,includingcytomegalovirus,hepatitis C virus,and opportunistic fungi.Because of the uncommon nature of the clinical illnesses directly attributed to HHV-6,there is currently no recommended HHV-6-specific approach prevention after liver transplantation.Asymptomatic HHV-6 infection does not require antiviral treatment,while treatment of established HHV-6 disease is treated with intravenous ganciclovir,foscarnet,or cidofovir and this should be com plemented by a reduction in immunosuppression. | Raymund R Razonable Irmeli Lautenschlager | 2010 | World Journal of Hepatology2010，2，9： | 2 |
| 8 | Secretion of proin- flammatory cytokines and chemokines during amphotericin B ex- posure is mediated by coactivation of toll-like receptors 1 and 2 显示文摘 | Razonable RR Henauh M Lee LN | 2005 | Antimicrob Agents Chemother2005，49，4： | 1 |
| 9 | Effect of educational intervention on antibiotic prescription practices for upper respiratory infections in children:a multi- centre study 显示文摘 | Razon Y Ashkenazi S Cohen A | 2005 | J Antimicrob Chemother2005，56，5： | 1 |
| 10 | Increased apoptosis coincides with onset of involution in hemangioma显示文摘 | Razon MJ Kraling BM Mulliken JB | 1998 | Mircocir Culation1998，5，23： | 1 |
| 11 | Linezolid therapy for orthopedic infections显示文摘 | Razonable RR Osmon DR Steckelberg JM | | 0，，9： | 1 |
| 12 | Herpesvirus infections in transplant recipients: current challenges in the clinical management of cytomegalovirus and epstein-barr virus infections显示文摘 | Razonable RR Paya CV | 2003 | Herpes2003，10，3： | 1 |
| 13 | Delayed epidural hematoma:a review 显示文摘 | Milo R Razon N Schiffer J | 1987 | Acta Neurochir Wien1987，84，12： | 1 |
| 14 | Linezolid therapy for orthopedic infections 显示文摘 | Razonable RR Osmon DR Steckelberg JM | 2004 | Mayo Clin Proc2004，79，9： | 1 |
| 15 | Expression of epidermal growth factor receptors in human brain tumor 显示文摘 | Libermann TA Razon N Bartal AD | 1984 | Cancer Res1984，44，： | 1 |
| 16 | Secretion of proinflammatory cytokines and chemokines during amphotericin B exposure is mediated by coactivation of Toll-like receptors 1 and 2显示文摘 | Razonable RR Henault M Lee LN | 2005 | Antimicrob Agents Chemother2005，49，4： | 1 |
| 17 | Increased apoptosis coincides with onset of involution in infantile hemangioma显示文摘 | Razon MJ Kraling BM Mulliken JB | 1998 | Microcirculation1998，5，23： | 1 |
| 18 | Dynamics of cytomegalovirus replication during preemptive therapy with oral ganciclovir显示文摘 | Razonable RR van Cruijsen H Brown RA | 2003 | J Infect Dis2003，187，11： | 1 |
| 19 | Increased apoptosis coincides with onset of involution in infantile hemangioma 显示文摘 | Razon MJ Kraling BM Mulliken JB | 1998 | Mircocirculation1998，5，23： | 1 |
| 20 | Amplification,cnhartced expression and possible rearrangement of EGF receptor gene in primary human brain tumours of glial orgigin显示文摘 | Libermann TA Nusbaum HR Razon N | 1985 | Nature1985，313，： | 1 |
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