Custom Liver Transplant Rejection essay paper sample
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Allograft rejection is and still remains a challenge in renal transplantation. The main barrier today is rejection of transplanted organs which occurs as a result of cellmediated and humoral responses by the recipient to antigens called Human Leukocyte Antigen (HLA). Rejection can still occur in absence of lymphocytotoxic antibodies. This suggests that non-HLA antigen systems may have a role to play in allograft rejection. The aim of this paper is to identify development of posttransplant anti-HLA and MICA bodies in response to life related donor.
Patients and Methods
Panigrahi et al. reports that between 199-2004, 185 patients were transplanted with live related kidney at an Indian hospital and patients were followed after two years after the sample date. A pretransplant PRA analysis was performed on the patients by the cytotoxicity method. Patients who were experiencing reversible rejections during this time were considered to have undergone acute rejection and were treated with methylprednisolone for three days. It was found that chances of liver transplant were 72 percent.
Of the 185 patients, 22.7 percent showed acute rejection within one year, 9 showed presence of IgG HLA class I antibodies with a 2 year graft survival rate of 44 percent as compared to 84 percent in ELISA negative patients which had a high number of acute rejection rates.
Immunosuppressive consisted of a standard triple-drug therapy with methylprednisolone, cyclosporine A (5-10 mg/kg/day) and azathioprine. The initial concentration of cyclosporine was 300-400 for induction. The acute rejection diagnosis was based on clinical biochemical and histological criteria. Doppler echography was carried out to exclude hepatic ischemia when serum liver enzyme levels increased.
Simultaneous Presence of Anti-HLA and MICA Antibodies and Their Influence on Graft Survival and Acute Rejection
All the patients’ serum samples were analyzed for detection of antibodies against MICA. It was found that 16 percent of the patients developed MICA antibodies against at least one of the alleles. Further analysis was done the simultaneous anti-HLA and anti-MICA antibodies (Moya-Quiles, et al.).
The results of the report indicate that for the first time, there is an existence of a correlation between the presence of HLA allele in liver recipients and protection against the risk of suffering acute rejection. The protective effect was associated with presence an Asn80 epitope. But it was found to disappear after excluding HLA-Cw*07 patients that indicated that this allele was the one responsible for the observed protective effect. The protective effect was at first associated with the presence of the Asn80 epitope. But it semed to disappear after HLA-Cw*07 was exluded patients from the analysis. This indicated that only this allele was responsible for the observed protective effect. The HLA-Cw*07 effect seems not to be influenced by linking disequilibrium, because in this series no positive or negative associations between any of the most frequent HLA-A-B-Cw*07 haplotypes and protection against rejection was found. It was found that this effect appears independent of HLA-A_B_C class I mismatching, also for most frequent liver diseases, as well as age and gender (Moya-Quiles, et al.).
Studies have shown the importance of anti-HLA and non-HLA antibodies in humoral rejection of the renal allograft. Results of the study indicate that development of anti-HLA class I IgG antibodies associated with graft loss. The reasons behind nondonor directed HLA antibodies correlation with rejection is still not clear. Donor specific antibodies are usually observed in situ in the liver and when saturated they spill out into the periphery. Many patients however show that antibodies fix onto the antigenic sites of the donor (Panigrahi et al.).
Suppressing the Hosts Immune Responses
To prevent liver transplant rejection, that the role of immunosuppression in the liver can greatly be used for this purposes. This can be achieved by vascularization and immunosuppressive therapy. Vascularization however can be minimized by irridation, keratoplasty (tectonic), stem cell transplantation and topical corticosteroids. Liver graft rejection with preoperative and postoperative has also been studied. This is by understanding that liver graft rejection is just but a cell-mediated response that is controlled by CD4+ T cells and therefore occurs when the antiCD4 molecules are blocked (Panda et al., 2007).
During transplantation of the liver, the recipient may reject the organ from the donor. The major cause of human allograft failure can be due to irreversible immune rejection of the transplanted liver and the immunological process can cause reversible or irreversible damage and therefore it is prudent that prevention of transplant rejection is first observed. Liver graft rejection encompasses complex series of responses involving recognition of histocompatibility. Thus the needs for systematic interventions are required. Prevention of liver graft rejection hence is crucial and lies with reduction of donor antigenic tissue load. This in turn reduces host and donor incompatibility by suppressing the host immune response and by tissue matching. Early detection and use of therapy for prevention and management for of liver graft rejection is also very crucial.