Physiologic replacement of insulin in patients with type 1 (insulin-depende
nt) diabetes following pancreas allograft transplantation results in normog
lycaemia during fasting and postprandial states. However, this is achieved
at the expense of peripheral hyperinsulinaemia in the heterotopic pancreas
allograft recipients with systemic insulin drainage. In addition, the pancr
eas allograft is denervated and thus devoid of autonomic nervous regulation
of pancreatic beta-cell secretion. Recent reports of hypoglycaemia (sympto
matic and asymptomatic), which can be fatal, have raised serious concerns r
egarding the aetiology of the hypoglycaemic epiphenomon in type 1 diabetic
pancreas allograft recipients. Although the prevalence of significant hypog
lycaemia following pancreas transplantation remains unknown, it is importan
t to conduct studies to determine the mechanisms, the natural history, pred
ictors and treatment as well as the long-term prognosis (graft and patient
survival rates) of type 1 diabetic patients who develop pancreas allograft-
associated hypoglycaemia hypoglycaemia. Indeed, predictors of hypoglycaemia
following pancreas allograft could significantly impact on the selection o
f appropriate therapeutic options for pancreas allograft transplantation, F
inally, whether postpancreas allograft transplantation-associated hypoglyca
emia in type 1 diabetic patients carries greater morbidity and mortality wh
en compared to those without hypoglycaemia deserves to be investigated.