According to the classification and diagnosis criteria of hyperuricemia, drugs that promote uric acid excretion, such as benzbromarone, fenofibrate, losartan, and those drugs that can inhibit uric acid production such as allopurinol, febuxostat and topiroxostat, can be selected[56]

According to the classification and diagnosis criteria of hyperuricemia, drugs that promote uric acid excretion, such as benzbromarone, fenofibrate, losartan, and those drugs that can inhibit uric acid production such as allopurinol, febuxostat and topiroxostat, can be selected[56]. lifestyle modification, individualization of immunosuppressive regimen, and drug therapy. In addition to the contents related to diabetes mellitus, hypertension, and dyslipidemia, this edition of consensus also includes the related contents of hyperuricemia and obesity, aiming at guiding the standardized management of metabolic disease in a more comprehensive way. FOREWORD Thanks to mature surgical techniques and standardized perioperative and long-term management, the survival rate of Chinese liver transplant recipients has gradually improved. According to the Report on the Medical Quality of Liver Transplantation GnRH Associated Peptide (GAP) (1-13), human in China in 2018[1], mortality within 1 wk after liver transplantation decreased COL4A1 from 3.7% in 2015 to 2.2% in 2018; the 3-year cumulative survival rate was 78.51% in liver transplant recipients with benign end-stage liver diseases and 75.87% in those with hepatocellular carcinoma who met Hangzhou Criteria. This means that the survival in Chinese liver transplant recipients has reached the international leading level as described in the annual data report 2018 of Organ Procurement and Transplant Network/Scientific Registry of Transplant Recipients[2]. However, chronic diseases after liver transplantation, including GnRH Associated Peptide (GAP) (1-13), human metabolic disease, chronic kidney disease, and cardiovascular diseases, GnRH Associated Peptide (GAP) (1-13), human are increasing year by year. Metabolic complications, including diabetes mellitus, hypertension, dyslipidemia, obesity, and hyperuricemia, are common after liver transplantation. Relevant reports show that the incidence rates of diabetes mellitus, hypertension, dyslipidemia, hyperuricemia, and obesity are 30%-40%[3], over 50%[4], 40%-66%[5], 14%-53%[6-9], and 18%-30%[10,11], respectively, and tend to increase with time after liver transplantation[12]. Metabolic disease is closely associated with the development of chronic kidney disease, infections, and cardiovascular diseases and greatly affects the quality of life and long-term survival of recipients[13,14]. However, metabolic disease can be prevented and treated through early intervention. This consensus is aimed at providing recommendations for the prophylaxis and treatment of metabolic disease in Chinese liver transplant recipients to improve the long-term survival of the recipients. RECOMMENDATIONS FOR THE PROPHYLAXIS AND TREATMENT OF METABOLIC DISEASE IN LIVER TRANSPLANT RECIPIENTS Effective immunosuppressive therapy is essential for ensuring the long-term survival of liver grafts after liver transplantation[14], but long-term use of immunosuppressive agents can lead to or aggravate post-transplant metabolic disease. Different immunosuppressive agents have different effects on metabolic disease. Calcineurin inhibitors (CNIs), including tacrolimus (TAC) and cyclosporine A (CsA), are GnRH Associated Peptide (GAP) (1-13), human often associated with hypertension, diabetes mellitus, dyslipidemia, and hyperuricemia; glucocorticoids are associated with hypertension, diabetes mellitus, GnRH Associated Peptide (GAP) (1-13), human obesity; mammalian target of rapamycin (mTORi) inhibitors are associated with dyslipidemia. However, mycophenolic acids (MPA), represented by mycophenolate mofetil (MMF), and antibody drugs such as rabbit antithymocyte globulin and basiliximab have no effect on metabolic disease (Table ?(Table1).1). Studies have found that basiliximab induction, combined with MMF and the glucocorticoid-free or early withdrawal regimen, or MMF combined with the dose-reduced CNI can decrease the occurrence of immunosuppressive agent-caused metabolic disease and adverse effects by ensuring immunosuppressive efficacy in liver transplant recipients[15-21]. Therefore, based on the improvement of dietary structure and lifestyle, metabolic disease should be well managed through individualized selection of appropriate immunosuppressive agents at a minimum dose according to clinical characteristics of recipients and the use of additional drugs when necessary. It requires involvement of the follow-up doctors of liver transplant recipients when the immunosuppressive regimens need adjustment. Table 1 Adverse effects of immunosuppressive agents on post-liver transplant metabolic disease thead align=”center” Metabolic diseaseGlucocorticoidsCNIs (TAC)CNIs (CsA)mTORiMPAAntibody drugs (ATG/basiliximab) /thead Diabetes mellitus+++++++–Hypertension++++++—Dyslipidemia++++++++–Obesity+++—Hyperuricemia-++++— Open in a separate window CNI: Calcineurin inhibitor; TAC: Tacrolimus; CsA: Cyclosporine A; mTORi: Mammalian target of rapamycin; MPA: Mycophenolic acids. Recommendation 1: The prophylaxis and treatment of post-liver transplantation metabolic disease should be based on changes in dietary habits and lifestyle, paying attention to the adverse effects of immunosuppressive providers, advocating personalized medication. The routine with basiliximab induction and glucocorticoid-free or CNI minimization comprising MPA is definitely feasible. Prophylaxis and treatment of diabetes mellitus Post-transplant diabetes mellitus (PTDM) includes pre-existing diabetes mellitus and new-onset diabetes after transplantation (NODAT) in liver transplant recipients. PTDM is definitely a common complication that occurs after solid organ transplantation[15]. In recent years, a considerable number of recipients are diagnosed as diabetes after transplantation because preoperative analysis of diabetes has not been standardized. In this case, it cannot be determined whether the individuals develop NODAT. As a result, PTDM has been widely used. The.