# Glucocorticoid-induced diabetes mellitus: mechanisms, risk factors, and clinical pathways with insights from autoimmune rheumatic diseases

## TL;DR

This paper reviews how glucocorticoid use in autoimmune rheumatic diseases can lead to diabetes, focusing on mechanisms, risk factors, and management strategies.

## Contribution

The paper provides a comprehensive review of glucocorticoid-induced diabetes in autoimmune rheumatic diseases, highlighting disease-specific risk factors and gaps in current knowledge.

## Key findings

- Glucocorticoids increase gluconeogenesis and reduce insulin sensitivity, contributing to hyperglycemia.
- Risk factors include higher GC doses, disease activity, and metabolic conditions like obesity and hypertriglyceridemia.
- GIDM incidence varies by autoimmune rheumatic disease, with notable rates in systemic lupus erythematosus and polymyalgia rheumatica.

## Abstract

Diabetes mellitus (DM) is characterized by persistent hyperglycemia due to impaired insulin secretion, action, or both. Glucocorticoid-induced DM (GIDM) is a clinically significant subtype, especially in rheumatology, where glucocorticoids (GCs) are widely used for the management of autoimmune rheumatic diseases (ARDs). GCs increase gluconeogenesis, reduce insulin sensitivity, impair β-cell function, and alter adipokines and hypothalamic signaling, promoting hyperglycemia. Oral GCs carry the greatest risk, though intra-articular and intramuscular injections can also cause dysglycemia. Risk factors include older age, higher body mass index (BMI) and central adiposity, hypertriglyceridemia, family history of DM, higher GC dose and treatment duration, and disease activity. In non-ARD populations, GIDM occurs in 15–52% of GC-treated individuals, while in ARDs, rates vary by disease. In Systemic lupus erythematosus, occurrence ranges from 10–26% and, beyond classic metabolic risk factors, higher disease activity and damage scores, higher GC doses, and mycophenolate mofetil are associated with increased risk, whereas hydroxychloroquine seems to be protective. In Rheumatoid arthritis, true incidence remains uncertain, though GC dose, especially > 10 mg/day, and prolonged duration correlate with increased risk. In Polymyalgia rheumatica and Giant cell arteritis, GIDM increases dose-dependently, with an occurrence of 6% and 13%, respectively. Evidence for other ARDs is limited. Management of GIDM should be guided by a multidisciplinary approach, aiming for a personalized therapeutic strategy. This review summarizes current knowledge on the mechanisms, epidemiology, and risk factors of GIDM in ARDs, aiming to raise awareness within the rheumatology community, highlight key gaps in the literature, and outline implications for future research.

The online version contains supplementary material available at 10.1007/s00296-026-06099-z.