Matthew P. Klein

Data on the cost implications of continuous glucose monitoring (CGM) use in type 1 diabetes (T1D) pregnancies in the United States are sparse. Drawing on associations identified in real-world evidence from a retrospective chart review at the Barbara Davis Center for Diabetes, we conducted a cost-consequences analysis of CGM use versus self-monitoring of blood glucose (SMBG), inclusive of neonatal intensive care unit (NICU) spending. In the base-case analysis assuming per-label CGM use and per-guideline finger-stick frequency, the per-person cost was $16,254 for CGM versus $15,182 for SMBG. In a real-world scenario analysis, the per-person cost was $13,708 for CGM versus $14,524 for SMBG. In both analyses, there was a cost savings for NICU admissions of $2,903 with CGM use. In the probabilistic sensitivity analysis, CGM was cost saving in 25% of base-case model iterations and 46% of real-world model iterations. This study adds to the growing evidence base that the increased costs of CGM use versus SMBG to manage T1D pregnancies are likely offset by better neonatal health outcomes.

The effectiveness of Hybrid Closed-Loop (HCL) therapy is rarely studied in type 1 diabetes (T1D) pregnancies. T1D pregnancies (n = 15) managed off-label during gestation using a commercially available HCL system, Tandem Control IQ, were retrospectively reviewed for baseline characteristics, continuous glucose monitoring (CGM), insulin pump use, insulin doses, and gestational health outcomes. Analyses for unadjusted descriptive statistics of baseline characteristics, glycemic parameters, and gestational health outcomes were performed (mean ± standard deviation (SD) or median with interquartile range (IQR) for continuous variables). Control IQ was used prior to pregnancy by 12 of the 15 cases, with 3 initiating use during gestation. On average, targets were met for pregnancy-specific Time-In-Range (psTIR, 63-140 mg/dL for > 70%) during most of gestation, pregnancy-specific Time-Below-Range (psTBR, < 63 mg/dL for < 4%) throughout gestation, and pregnancy-specific Time-Above-Range (psTAR, > 140 mg/dL for < 25%) from 10- to 17-week gestation. Targets for non-pregnancy TIR (70-180 mg/dL), TAR (> 140 mg/dL), and TBR (< 70 mg/dL) were met preconception and post-partum. Glycemic metrics improved after the first pregnancy visit wherein assistive techniques were applied for off-label use of this HCL system. Gestational health outcomes were as anticipated for T1D pregnancies. Tandem Control IQ HCL therapy used with assistive techniques in 15 T1D pregnancies was associated with improved glycemic levels from the first clinic visit onward.

Background: Once weekly Glucagon-Like Peptide-1 Receptor Agonists (GLP-1 RA) have been shown to improve glycemic outcomes and cause significant weight loss. However, 9% to 27% of individuals have little or no response to these drugs. In this article, we investigated the efficacy of GLP-1 RA therapy among adults with type 1 diabetes and obesity likely related to genetic mutations compared with obesity likely unrelated to genetic mutations. Methods: In this retrospective study, we compared body weight and glycated hemoglobin (HbA1c) change with the use of GLP-1 RA therapy (including a dual agonist, Tirzepatide) over six months among adults with type 1 diabetes and obesity likely (n = 11, median age 39.5 years with a median BMI of 43.0 kg/m ² ) versus unlikely related to genetic mutation(s) (n = 15, median age 45.8 years with a median BMI of 38.7 kg/m ² ). Results: Six months of GLP-1 RA treatment resulted in a numerically lower reduction of weight (−5.75 ± 9.46 kg vs −8.65 ± 9.36 kg, P = .44) and HbA1c (−0.28 ± 0.96% vs −0.43 ± 0.57%, P = .64) among individuals with obesity likely versus unlikely related to a genetic mutation(s), respectively. Fewer individuals with genetic obesity met goal weight loss ≥5% or HbA1c decrease ≥0.4% than did individuals with obesity unlikely related to a genetic cause (36.4% vs 80.0%, P = .04). Conclusions: The weight loss and glycemic lowering effects of GLP-1 RA therapy may be decreased in people with type 1 diabetes and obesity likely related to genetic causes. Further research is needed to understand GLP-1 RA mechanisms via energy regulating genes.