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A large proportion of clinical islet transplant recipients fail to initially achieve or sustain meaningful independence from exogenous insulin use. We hypothesized that immediate allograft injury is a key constraint on independence from exogenous insulin use.

The ability of supplemental islet infusions (SII) to restore insulin independence in islet transplant recipients with graft dysfunction has been attributed to the coadministration of exenatide. However, improving islet transplant outcomes could explain the success of SII. We aimed to determine the effect on islet graft function and insulin independence of SII using these new protocols, without the use of exenatide.

Successful islet transplantation can result in insulin independence in many patients with type 1 diabetes mellitus, but it often requires more than one islet infusion. The ability to achieve insulin independence with a single donor is an important goal in clinical islet transplantation due to the limited organ supply.

An accurate monitoring would help understanding the fate of islet grafts after transplantation.

The health-related quality of life (HRQL; Health Utilities Index Mark 2) and the fear of hypoglycemia (Hypoglycemia Fear Survey) were assessed after islet transplant; the impact of a single islet infusion and of the metabolic outcome were determined. A control group included 166 patients with type 1 diabetes. Islet transplant had no impact on overall HRQL. Prior to transplant, islet recipients had more fear of hypoglycemia than controls (P<0.000001), but this improved up to 36 months after transplant (P<0.00001, pretransplant vs. each time point). With a single islet infusion, this fear improved substantially (P<0.00001), but improved further with subsequent islet infusions (P≤0.01). Fear of hypoglycemia correlated with the occurrence of hypoglycemia (r0.47, P0.01), and even more so with blood glucose stability (r0.56, P0.0007) and insulin requirement (r0.69, P0.000002).

Impairment of the fibrinolytic system is one of the most sensitive markers of endothelial dysfunction, and a major risk factor for future cardiovascular disease in adults. Persistent endothelial dysfunction, which is an early pathophysiological event in atherogenesis, occurs in some patients following Kawasaki disease (KD). The aim of this study was to assess whether impaired fibrinolysis is present in long-term survivors of KD. The study included 42 children with a documented history of KD presenting without coronary lesions (n = 22), with resolved coronary aneurysms (n = 13), or with persistent giant aneurysms (n = 7), and 26 healthy age-matched teenagers as controls. Blood samples were collected from all patients and controls prior to and following venous occlusion (VO) stress testing, and assayed for tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI)-1, plasminogen, alpha2-antiplasmin (a2-AP), alpha2-macroglobulin (a2-M), D-Dimer, fibrinogen, and von Willebrand factor (vWF). Significantly decreased fibrinolytic activity following VO was detected in patients compared to controls due to decreased tPA antigen, and increased PAI-1 activity. In addition, patients had significantly increased plasma concentrations of plasminogen and fibrinogen, which were related to similar increases of a2-M compared to controls. Decreased fibrinolytic activity was found in patients with coronary aneurysms but also in those without coronary lesions. In summary, a decreased fibrinolytic activity reflects persistent endothelial damage following acute KD, potentially predisposing these patients to accelerated atherosclerosis and cardiovascular disease in early adult life.