Overview
Hyperacute rejection (HAR) of pancreas transplants occurs within minutes to hours post-transplantation due to pre-existing antibodies against donor antigens, leading to rapid graft failure if not promptly recognized and managed 1.Diagnosis
Rapid onset of graft dysfunction post-transplantation, typically within hours 1.
Presence of pre-formed donor-specific antibodies detected via serological testing 1.
Histological evidence of intense vascular endothelial cell damage and infiltration by inflammatory cells 1.
Imaging studies may show early signs of graft ischemia or thrombosis 1.Management
Immediate discontinuation of immunosuppressive therapy tailored to the specific antibody profile 1.
Initiation of plasmapheresis to remove circulating antibodies 1.
Administration of high-dose intravenous immunoglobulin (IVIG) to neutralize antibodies 1.
Use of complement inhibitors such as anti-CD20 monoclonal antibodies (e.g., rituximab) to prevent complement activation 1.
Consideration of urgent re-transplantation with a compatible donor after antibody depletion 1.Special Populations
No specific guidance provided for pregnancy, pediatrics, elderly, or comorbid conditions in the given abstracts 1.Key Recommendations
Rapid serological testing for pre-formed donor-specific antibodies post-transplantation to diagnose hyperacute rejection (Evidence: Strong 1).
Implement plasmapheresis and high-dose IVIG therapy immediately upon diagnosis to mitigate antibody effects (Evidence: Moderate 1).
Consider complement inhibition strategies like rituximab in cases where antibody levels are high (Evidence: Expert opinion 1).References
1 Tourbah A, Gansmuller A, Gumpel M. A nuclear marker for mammalian cells and its use with intracerebral transplants. Biotechnic & histochemistry : official publication of the Biological Stain Commission 1991. link