P031 Role of donor specific antibody (DSA) in hand transplantation

Abstract

Aim Hand transplantation (HT) is now a recognized therapy, with UNOS regulation and oversight, which provides functional, sensory, and cosmetic reconstruction of upper extremity loss. A challenge in solid organ transplant recipients is de novo DSA, which portend a significant risk of acute or chronic antibody-mediated rejection (AMR). Whether, and to what extent, DSA confer risk for HT recipients is unknown and few reports of AMR in HT exist. We examined the incidence, specificity, and levels of DSA in a series of 9 HT recipients and related these findings to the clinical course. Methods Nine HT recipients (8 male, 1 female; mean age of 47 ± 11 years at the time of transplant) were evaluated. DSA were evaluated by single antigen beads quarterly and when clinically indicated; any positive results were reflexed to C1q testing. The clinical course, including changes in function and episodes of rejection, were evaluated in relation to changes in DSA. Results Two of 9 subjects developed de novo DSA. One patient developed a de novo DQ8 antibody at ∼10,000MFI that was also positive by C1q at 3 yr 9mo post-transplant. However, a biopsy revealed no signs of AMR and clinical presentation and function were stable. No treatment was initiated and the DSA has persisted while graft function remains stable. The second patient developed de novo DSA to DR53 and DQ2, both at ∼20,000MFI, that were also positive by C1q at 7 years post-transplant. This patient did experience steroid resistant rejection, but biopsies were more consistent with acute cellular rejection than AMR. This patient was treated with ATG, but the antibodies persist. Additionally, one patient with chronic rejection does not have any evidence of DSA. Conclusions Our findings suggest monitoring DSA may have limited utility in managing HT recipients. The presence, specificity, and level of DSA generally did not parallel or anticipate rejection or other immune complications. DSA in circulation may be a late sign of donor specific immunity, which may explain the poor correlation observed between DSA and clinical course in HT. In order to minimize risk and increase benefit and accessibility of HT, we need to understand when DSA should be aggressively treated or only monitored. T.K. Roberts: 2. Consultant; Company/Organization; Immucor Inc., Clinical Lab Consulting LLC.