Increased systemic Th17 cytokines are associated with diastolic dysfunction in children and adolescents with diabetic ketoacidosis

PLoS One. 2013 Aug 27;8(8):e71905. doi: 10.1371/journal.pone.0071905. eCollection 2013.

Abstract

Diastolic dysfunction suggestive of diabetic cardiomyopathy is established in children with T1DM, but its pathogenesis is not well understood. We studied the relationships of systemic inflammatory cytokines/chemokines and cardiac function in 17 children with T1DM during and after correction of diabetic ketoacidosis (DKA). Twenty seven of the 39 measured cytokines/chemokines were elevated at 6-12 hours into treatment of DKA compared to values after DKA resolution. Eight patients displayed at least one parameter of diastolic abnormality (DA) during acute DKA. Significant associations were present between nine of the cytokine/chemokine levels and the DA over time. Interestingly, four of these nine interactive cytokines (GM-CSF, G-CSF, IL-12p40, IL-17) are associated with a Th17 mediated cell response. Both the DA and CCL7 and IL-12p40, had independent associations with African American patients. Thus, we report occurrence of a systemic inflammatory response and the presence of cardiac diastolic dysfunction in a subset of young T1DM patients during acute DKA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Child
  • Cytokines / blood*
  • Diabetes Mellitus, Type 1 / blood*
  • Diabetes Mellitus, Type 1 / immunology
  • Diabetes Mellitus, Type 1 / physiopathology
  • Diabetic Ketoacidosis / blood*
  • Diabetic Ketoacidosis / immunology
  • Diabetic Ketoacidosis / physiopathology
  • Diastole
  • Female
  • Humans
  • Hypertension / blood
  • Hypertension / etiology
  • Hypertension / immunology
  • Inflammation Mediators / blood
  • Male
  • Th17 Cells / immunology
  • Th17 Cells / metabolism
  • Ventricular Dysfunction, Left / blood*
  • Ventricular Dysfunction, Left / etiology
  • Ventricular Dysfunction, Left / immunology

Substances

  • Cytokines
  • Inflammation Mediators

Grants and funding

The study was funded by Johns Hopkins Center for Autoimmune Disease Research. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.