Treating diabetes with islet transplantation: lessons from the past decade in Lille.

Type 1 diabetes (T1D) is due to the loss of both beta-cell insulin secretion and glucose sensing, leading to glucose variability and a lack of predictability, a daily issue for patients. Guidelines for the treatment of T1D have become stricter as results from the Diabetes Control and Complications Trial (DCCT) demonstrated the close relationship between microangiopathy and HbA1c levels. In this regard, glucometers, ambulatory continuous glucose monitoring, and subcutaneous and intraperitoneal pumps have been major developments in the management of glucose imbalance. Besides this technological approach, islet transplantation (IT) has emerged as an acceptable safe procedure with results that continue to improve. Research in the last decade of the 20th century focused on the feasibility of islet isolation and transplantation and, since 2000, the success and reproducibility of the Edmonton protocol have been proven, and the mid-term (5-year) benefit-risk ratio evaluated. Currently, a 5-year 50% rate of insulin independence can be expected, with stabilization of microangiopathy and macroangiopathy, but the possible side-effects of immunosuppressants, limited availability of islets and still limited duration of insulin independence restrict the procedure to cases of brittle diabetes in patients who are not overweight or have no associated insulin resistance. However, various prognostic factors have been identified that may extend islet graft survival and reduce the number of islet injections required; these include graft quality, autoimmunity, immunosuppressant regimen and non-specific inflammatory reactions. Finally, alternative injection sites and unlimited sources of islets are likely to make IT a routine procedure in the future.

[Blood amylase and lipase in diabetic ketoacidosis]. / Amylasémie et lipasémie au cours de la céto-acidose diabétique.

The relation between increase of amylasaemia and increase of lipasaemia was studied during ketoacidosis in 31 insulin-dependent diabetics. The effects of metabolic disturbances on amylase production during the acute phase of ketoacidosis were also evaluated. The greatest increase of amylasaemia was observed after 24 hours in 17 cases (55%), with return to normal values after 3 to 7 days. Amylasuria was closely correlated with amylasaemia (r = 0.7; P less than 0.01). No correlation was found between hyperamylasaemia and the degree of ketoacidosis, but there was a correlation between plasma osmolality and hyperamylasaemia (r = 0.44; P less than 0.02). The increase of lipasaemia, considered more specific of pancreatic damage, was closely correlated with that of amylasaemia (r = 0.63: P less than 0.01). The electrolyte disturbances associated with ketoacidosis are responsible for cellular damage with release of enzymes in many tissues. The hyperamylasaemia consecutive to pancreatic damage might be of similar origin and aggravated by splanchnic hypoperfusion.