Stratification of type 2 diabetes based on routine clinical markers

Narges Safai*, Ashfaq Ali, Peter Rossing, Martin Ridderstråle

*Corresponding author for this work
12 Citations (Scopus)

Abstract

Aims: We hypothesized that patients with dysregulated type 2 diabetes may be stratified based on routine clinical markers. Methods: In this retrospective cohort study, diabetes related clinical measures including age at onset, diabetes duration, HbA1c, BMI, HOMA2-β, HOMA2-IR and GAD65 autoantibodies, were used for sub-grouping patients by K-means clustering and for adjusting. Probability of diabetes complications (95% confidence interval), were calculated using logistic regression. Results: Based on baseline data from patients with type 2 diabetes (n = 2290), the cluster analysis suggested up to five sub-groups. These were primarily characterized by autoimmune β-cell failure (3%), insulin resistance with short disease duration (21%), non-autoimmune β-cell failure (22%), insulin resistance with long disease duration (32%), and presence of metabolic syndrome (22%), respectively. Retinopathy was more common in the sub-group characterized by non-autoimmune β-cell failure (52% (47.7–56.8)) compared to other sub-groups (22% (20.1–24.1)), adj. p < 0.001. The prevalence of cardiovascular disease, nephropathy and neuropathy also differed between sub-groups, but significance was lost after adjustment. Conclusions: Patients with type 2 diabetes cluster into clinically relevant sub-groups based on routine clinical markers. The prevalence of diabetes complications seems to be sub-group specific. Our data suggests the need for a tailored strategy for the treatment of type 2 diabetes.

Original languageEnglish
JournalDiabetes Research and Clinical Practice
Volume141
Pages (from-to)275-283
ISSN0168-8227
DOIs
Publication statusPublished - 2018

Keywords

  • Clusters
  • Heterogeneity
  • Personalized medicine
  • Sub-group
  • Type 2 diabetes

Fingerprint

Dive into the research topics of 'Stratification of type 2 diabetes based on routine clinical markers'. Together they form a unique fingerprint.

Cite this