Two main categories of patients are thought to be suitable candidates for islet transplantation today:
- In the Nordic Network, to date we have only transplanted patients already on immunosuppressive medication due to previous kidney transplantation. Islet transplantation adds no risk concerning immunosuppression to them, but gives them the chance to obtain better metabolic control.
- The other category of patients include them who have severe problems with metabolic control rendering frequent hypoglycemias. Iatrogenic hypoglycemia is a major unresolved problem for some patients with T1D. It is one limiting factor in the management of T1D, causing some deaths as well as recurrent physical, and recurrent (or even persistent) psychosocial, morbidity.
Neuroglycopenia can cause social embarrassment, and even lead to ostracism or be mistaken for disorderly or unlawful behavior. The more distressing the severe hypoglycemic episode, the greater the psychological fear of hypoglycemia. The threat and fear of severe hypoglycemia can significantly discourage patients and health care providers from pursuing intensive insulin therapy and can therefore be a major but unrecognized impediment to achieving euglycemia. Pramming et al. found that their patients were as concerned about the development of severe hypoglycemia as they were about the development of blindness or renal failure.
Ryan et al. documented the absence of episodes of severe hypoglycemia in 12 successful islet transplant recipients (median follow-up, 10.2 months) 8 whose diabetes was complicated by recurrent episodes of severe hypoglycemia pretransplant. This would suggest that hypoglycemia associated autonomic failure associated with defective counterregulation and impaired sympathodrenal responses is not just due to recurrent hypoglycemia. After a sustained period without any hypoglycemia most patients post islet transplant still had defective responses to hypoglycemia. The absence of clinically significant hypoglycemia post islet transplant despite the persistent defect in counterregulation in most subjects demonstrates the dominance of the absence of glucose regulated insulin secretion in the pathogenesis of severe hypoglycemia. Correction of this can only currently be attained with transplantation of beta cell tissue.