assessment revealed persistently positive anti-IA2 antibodies and a strong decrease in anti-antibodies. After six months, less severe hyperglycaemia recurred. Anti-ZnT8 antibody level raised again. Antiislet and anti-GAD 65 antibodies were positive. A new rescue treatment was employed: 5 plasmaphereses, ATG, and IvIg. The patient did not require exogenous insulin for the first two weeks, preceding a definitive return to low exogeneous insulin therapy. Fasting C peptide level remained positive ranging from 1 to 1.4 ng/ml. Renal function remained normal all over follow-up.

Vendrame et al reported T1DM recurrence in 7% of SPK recipients. 2 Cardinal features of T1DM recurrence include selective loss of insulin secretion, insulitis, and/or β-cell loss on pancreatic biopsy, presence of autoantibodies (mostly seroconversion), and circulating autoreactive T cells. 2,3 Circulating autoreactive memory T cells but not autoantibodies have a pathogenic role. 4 Three patients with T1DM recurrence after SPK treated with strong immunosuppressive treatments have been described, without remission. 4 Unfortunately, we did not have the ability to test autoreactivity of T cells. However, the absence of insulin staining on the islet and seroconversion of T1DM autoantibodies were evidences in favor of T1DM recurrence. Anti-ZnT8 antibodies correlated with clinical events, preceding the onset of hyperglycaemia and declined after immunosuppressive treatment. Of interest, we observe positivity of anti-ZnT8 antibodies in approximately 30% of our patients (personal data). T1DM recurrence may be an underestimated cause of pancreas allograft failure. Temporary remission and persistent insulin secretion after T1DM recurrence in a pancreatic transplant patient could be obtained. More studies are needed to determine the reliability of anti-ZnT8 seroconversion and the timing and choice of the immunosuppressive regimen to be applied.