Enteric-drained pancreas transplants monitored by fine-needle aspiration biopsy.

As we previously reported1•2 documentation of pancreas rejection remains problematic because of the lack of specific and sensitive markers. Since most pancreas transplants are performed simultaneous with a kidney, clinical dysfunction from rejection, documented by an increase in serum creatinine and renal-core biopsy, automatically leads to the treatment of both grafts. Rejections of pancreatic grafts are in some way preemptively treated by the initiation of kidney-transplant treatment. Nevertheless, in combined kidney-pancreas transplantation, an incidence of isolated pancreas rejection has been documented.3 .4 We report herein our experience in documenting rejection episodes with fine-needle aspiration biopsy (FNAB) in pancreas transplant patients. The FNAB rationale resides in the fact that the immunoactivation phenomenon begins in the graft. where infiltrating mononuclear cells endure a transformation process into "blasts." Acute cellular rejection is defined by an accumulation of immature cells (lymphoblasts. plasmablasts. monoblasts) that can be quantified according to established cytologic criteria. Vascular rejection is generally assigned to humoral immunity with the proliferation of mononuclcar phagocytcs and tissue macrophages. However, on several occasions the cellular and humoral component of rejcction can be simultaneously detected.