The beta score, a composite measure of beta cell function after islet transplantation, has limited sensitivity because of its categorical nature and requires a mixed‐meal tolerance test (MMTT). We developed a novel score based on a single fasting blood sample. The BETA‐2 score used stepwise forward linear regression incorporating glucose (in millimoles per liter), C‐peptide (in nanomoles per liter), hemoglobin A1c (as a percentage) and insulin dose (U/kg per day) as continuous variables from the original beta score data set (n = 183 MMTTs). Primary and secondary analyses assessed the score's ability to detect glucose intolerance (90‐min MMTT glucose ≥8 mmol/L) and insulin independence, respectively. A validation cohort of islet transplant recipients (n = 114 MMTTs) examined 12 mo after transplantation was used to compare the score's ability to detect these outcomes. The BETA‐2 score was expressed as follows (range 0–42): normalBETA−20.166667emnormalscore=)(normalfasting0.166667emnormalC−normalpeptide0.166667emfalse(normalnmolfalse/normalLfalse)×(1−normalinsulin0.166667emnormaldose0.166667emfalse[normalunitsfalse/normalkgfalse])normalFasting0.166667emnormalplasma0.166667emnormalglucose0.166667emfalse(normalmmolfalse/normalLfalse)×normalHbA1normalc(%)×1000 A score <20 and ≥15 detected glucose intolerance and insulin independence, respectively, with >82% sensitivity and specificity. The BETA‐2 score demonstrated greater discrimination than the beta score for these outcomes (p < 0.05). Using a fasting blood sample, the BETA‐2 score estimates graft function as a continuous variable and shows greater discrimination of glucose intolerance and insulin independence after transplantation versus the beta score, allowing frequent assessments of graft function. Studies examining its utility to track long‐term graft function are required.

Overall, at simulated altitude, no differences were observed between the performance of GDH and GOX meters. Overestimation of blood glucose concentration was seen among individual meters evaluated, but none of the results obtained would have resulted in dangerous failure to detect and treat blood glucose errors or in giving treatment that was actually contradictory to that required.

Little is known about how early islet graft function evolves in the clinical setting. The BETA-2 score is a validated index of islet function that can be calculated from a single blood sample and lends itself to frequent monitoring of graft function. In this study, we characterized early graft function by calculating weekly BETA-2 score in recipients who achieved insulin independence after single transplant (group 1, n = 8) compared to recipients who required a second transplant before achieving insulin independence (group 2, n = 7). We also determined whether graft function 1-week post-transplant was associated with insulin independence in individuals who received initial transplant between 2000–2017 (n = 125). Our results show that graft function increased rapidly reaching a plateau 4–6 weeks post-transplant. The BETA-2 score was higher in group 1 compared to group 2 as early as 1-week post-transplant (15 + 3 vs. 9 + 2, p = 0.001). In an unselected cohort, BETA-2 at 1-week post-transplant was associated with graft survival as defined by insulin independence during median follow up of 12 months (range 2–119 months) with greater survival among those with BETA-2 score &gt;10 (p &lt; 0.001, log-rank test). These findings suggest that primary graft function is established within 4–6 weeks post-transplant and graft function at 1-week post-transplant predicts long-term transplant outcomes.

The impact of clinical islet transplant (CIT) on glycemic variability compared with type 1 diabetes (T1D) subjects and nondiabetic controls has not been explored. Aim: To evaluate the relationship between glycemic variability (by CGM) and islet graft function in CIT vs. T1D subjects on Continuous Subcutaneous Insulin Infusions (CSII), using healthy, nondiabetic subjects as reference. Methods: CIT recipients n=39, (insulin independent vs. dependent: n=15 vs. n=24) and subjects on CSII therapy (n=10) all with T1D were assessed at 1 year post-intervention with CGM. Published data from nondiabetic controls were used for comparison. Fasting glucose, C-peptide and HbA1c concentrations and insulin dose were recorded (including in a control cohort, n=28) where applicable; BETA-2 scores were calculated in those with endogenous C-peptide. Results: CIT recipients had decreased coefficient variation of glucose and lower time in hypoglycemia vs. those on CSII therapy; BETA-2 scores were ∼20% lower in CIT recipients vs. controls (p&lt;0.05). Conclusion: Islet transplant recipients have diminished glycemic variability with abrogation of hypoglycemia vs. CSII at 1 year. Normalisation of time in range and glycemic variability was observed in insulin independent CIT recipients despite beta cell function ∼20% lower than in nondiabetic subjects. Disclosure S. Forbes: None. T. Olateju: None. A. Lam: None. J. Casey: None. J. Campbell: None. L. Reid: None. R.A. Oram: Other Relationship; Self; Randox. A.J. Malcolm: None. A. Shapiro: Consultant; Self; Viacyte, Inc., Protokinetix. P.A. Senior: Consultant; Self; Abbott, AstraZeneca. Research Support; Self; AstraZeneca, Prometic Life Sciences Inc., Novo Nordisk Inc., Sanofi. Consultant; Self; Eli Lilly and Company. Speaker's Bureau; Self; Eli Lilly and Company, Novo Nordisk Inc.. Consultant; Self; Novo Nordisk Inc., Janssen Pharmaceuticals, Inc.. Speaker's Bureau; Self; Janssen Pharmaceuticals, Inc.. Consultant; Self; Boehringer Ingelheim Pharmaceuticals, Inc.. Speaker's Bureau; Self; AstraZeneca, Merck & Co., Inc., Abbott. Research Support; Self; Viacyte, Inc..