Publication
Pancreas-Kidney Transplantation and the Evolution of
| dc.contributor.author | Martins, L. | |
| dc.contributor.author | Malheiro, J. | |
| dc.contributor.author | Henriques, A.C. | |
| dc.contributor.author | Dias, L. | |
| dc.contributor.author | Dores, J. | |
| dc.contributor.author | Oliveira, F. | |
| dc.contributor.author | Seca, R. | |
| dc.contributor.author | Almeida, R. | |
| dc.contributor.author | Sarmento, A.M. | |
| dc.contributor.author | Cabrita, A. | |
| dc.contributor.author | Teixeira, M. | |
| dc.date.accessioned | 2010-06-09T11:15:27Z | |
| dc.date.available | 2010-06-09T11:15:27Z | |
| dc.date.issued | 2009 | |
| dc.description.abstract | ABSTRACT The recurrence or persistence of pancreatic autoantibodies after pancreas-kidney trans- plantation (PKT) is an intriguing finding. We prospectively analyzed 77 PKTs, searching for risk factors for the expression of these autoimmune markers and their impact on pancreas graft function. Among the 77 PKTs, 24.7% had HLA matches, 20.8% displayed delayed graft function, and 14.3% had acute rejection episodes. Immunosuppression included antithymocyte globulin (ATG)tacrolimus, mycophenolate mofetil (MMF)and steroids. Sixty-five patients had both grafts functioning as follow-up of more than months. In 11 patients anti–glutamic acid decarboxylase (GAD) positivity persists (8) or has recurred (3)of whom show increasing titers. Two patients maintain positive islet cell antibodies (ICA) and anti-GAD antibodies. The patients positive for ICA included who were negative before PKT and who remain positive. The “positive” group (22 patients with positive ICA and/or anti-GAD) did not differ from the global group of 65 functioning PKT in terms of acute rejection episodes, HLA match, and steroid withdrawal. Among the positive patients, there were with borderline glucose levels; however, among the entire “positive” group, the mean fasting glucose, HbA1c, and C-peptide measurements were not significantly different, when compared with the other 65 PKTs. In conclusion, pancreatic autoantibodies may be persistently positive or recur after PKT, despite appropriate immunosuppression. Its impact on long-term pancreas graft survival is unknown. We could not identify risk factors for their expression. An extended follow-up with monitoring and search for other risk factors may be necessary to increase our knowledge in this field. | pt |
| dc.identifier.uri | http://hdl.handle.net/10400.16/274 | |
| dc.language.iso | eng | pt |
| dc.publisher | Transplantation Proceedings | pt |
| dc.title | Pancreas-Kidney Transplantation and the Evolution of | pt |
| dc.type | journal article | |
| dspace.entity.type | Publication | |
| rcaap.rights | openAccess | pt_PT |
| rcaap.type | article | pt |