Vasculitis & polymyalgia rheumatica

Glycolipid metabolic changes during remission induction in ANCA-associated vasculitis: a retrospective study of the lipid paradox

Clin Exp RheumatolPublished retrospective cohort study

Authors' conclusion

Patients with AAV show a high burden of baseline dyslipidaemia and dynamic glycolipid metabolic changes during remission induction. The observed increase in lipid concentrations together with decreases in fasting glucose and the TC/HDL-C ratio suggests a lipid-paradox pattern and a close relationship between inflammation and metabolic status. Further prospective studies with standardised treatment exposure and cardiovascular outcome assessment are needed to clarify the clinical significance of these metabolic trajectories.

Study context

Population
Patients with antineutrophil cytoplasmic antibody-associated vasculitis (AAV) during remission inductionpatients with AAV
Participants
973 patients
Exposure
Paired baseline vs post-remission induction glycolipid parameters in the longitudinal cohort
Outcome
Dyslipidaemia at baseline
Follow-up
Baseline
Methodological detailsmultivariable models
  • Multivariable models

Main finding

As reported in the abstract

  • Dyslipidaemia was highly prevalent at baseline

Observational data: associations, not effects.

Further findings

Factors associated with dyslipidaemia · baseline

Inflammatory markers, including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), were associated with dyslipidaemia

Glycolipid parameters during remission induction

Triglyceride, total cholesterol and LDL-C levels increased
Fasting glucose and the TC/HDL-C ratio decreased
  • Consistent with a lipid-paradox pattern

Comparison of patients with and without longitudinal data

Additional analyses suggested potential selection bias in the longitudinal cohort

Original publication

Glycolipid metabolic changes during remission induction in ANCA-associated vasculitis: a retrospective study of the lipid paradox. Clin Exp Rheumatol. Published 24 February 2026. doi:10.55563/clinexprheumatol/4bjsym

Composed by AI from the published abstract and checked against it. How Briefs are made →

Get them every week

New studies on this topic in My Week and in your Monday e-mail.

We e-mail you a sign-in link and a code. No password, no spam.