Diabetic ketoacidosis (DKA) in children with type 1 diabetes mellitus (T1DM) is accompanied by systemic inflammatory activation, but the specific mediator profile is not fully defined. A study published in BMJ Open Diabetes Research & Care characterized inflammatory mediators during and after DKA using multiplex immunoassay analysis.

Inflammatory biomarkers were measured in several pediatric groups: children hospitalized with acute DKA 6–8 hours after treatment initiation (n = 15), children evaluated 2-5 days following DKA (n = 14), children with new-onset T1DM without DKA within 24 hours of insulin therapy (n = 9), and children with new-onset T1DM without DKA assessed 2-5 days after starting insulin (n = 14). A reference cohort included children with chronic T1DM and glycated hemoglobin (HbA1c) <8.0% undergoing routine blood sampling (n = 59).

Compared with the reference group, acute DKA was associated with significant changes in multiple inflammatory mediators. These included IL-1RA, interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10), interleukin-18 (IL-18), chemokine C-X-C motif ligand-5 (CXCL5), CXCL10, chemokine C-C motif ligand-27 (CCL27), tumor necrosis factor-related apoptosis-inducing ligand, granulocyte colony-stimulating factor, TIMP-2, TIMP-4, and several MMPs, including MMP-2, MMP-3, MMP-7, MMP-9, and MMP-10.

Several mediators remained elevated after recovery from acute DKA. MMP-3, MMP-10, TIMP-1, and IL-1RA were increased 2-5 days after the episode. In contrast, children with new-onset T1DM without DKA showed early alterations in MMP-2 and MMP-9 within 24 hours of insulin initiation, while no significant inflammatory changes were observed 2-5 days later.

Overall, the findings indicate that DKA is associated with a distinct inflammatory signature compared with inflammatory responses related to acute hyperglycemia or autoimmune processes in T1DM, with MMPs and their tissue inhibitors contributing prominently to this profile.