Endocrine Abstracts

Background: Among chronic hypoparathyroidism (HypoPT) patients, the baseline prevalence of type 2 diabetes (T2D) appeared to be higher than the general population in previous studies. Since little is known about the potential assocation between HypoPT and T2D, this study evaluated whether HypoPT is associated with increased risk of T2D.

Methods: A retrospective cohort study, based on a US commercial claims database (Q1 2007 – Q2 2017), was conducted to investigate the risk of T2D associated with chronic HypoPT (both identified using diagnosis codes). The study cohort included chronic HypoPT patients (excluding those receiving parathyroid hormone) and randomly selected non-HypoPT patients during 5 years of follow-up. For HypoPT patients, the first date of follow-up (i.e., index date) was the earliest HypoPT diagnosis date ≥6 months after the initial HypoPT diagnosis (to establish chronic HypoPT); for non-HypoPT patients, it was the date of a randomly selected medical claim. Patient characteristics at baseline (the 6 months prior to index date) were compared between cohorts. The risk of development of incident T2D was compared between HypoPT and non-HypoPT cohorts among those free of T2D during the baseline period using Kaplan-Meier analysis and multivariable Cox proportional hazards models adjusting for baseline demographic characteristics (age, sex, race, region, and index year). A sensitivity analysis was conducted among the subset of patients with glucose monitoring (defined as having at least one procedure code for a glucose test) during the study period to address potential detection bias.

Results: The study included 8,097 chronic HypoPT patients and 40,485 non-HypoPT patients. At baseline, HypoPT patients were older than non-HypoPT patients (58.6 years vs 47.3 years) and higher proportions were female (76.2% vs 54.4%) and had T2D (20.6% vs 10.8%) (all P<0.001). HypoPT patients had an increased risk of developing incident T2D compared with non-HypoPT patients in both the main and the sensitivity analyses (both P<0.001 based on Kaplan-Meier analyses). The adjusted hazard ratios (95% confidence intervals) associated with HypoPT versus non-HypoPT were 1.80 (1.64, 1.96) in the overall analysis and 1.48 (1.35, 1.63) in the sensitivity analysis (both P<0.001).

Conclusions: Chronic HypoPT was associated with increased risk of developing type 2 diabetes. Further research is warranted to understand the potential mechanisms for the relationship of chronic HypoPT and/or its management with the observed risk of type 2 diabetes.