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Plasma C-reactive protein levels in severe diabetic ketoacidosis
Rory R Dalton1, William H Hoffman, Gregory G Passmore
1Department of Pathology, Medical College of Georgia, Augusta, Georgia 30912, USA.
Insights
C-reactive protein (CRP) can increase in young patients with severe diabetic ketoacidosis (DKA), even without infection. This suggests DKA itself may trigger a non-infectious inflammatory response.
Area of Science:
- Biochemistry
- Immunology
- Pediatrics
Background:
- Elevated C-reactive protein (CRP) and Interleukin-6 (IL-6) are infection markers in adults with diabetic ketoacidosis (DKA).
- CRP and pro-inflammatory cytokines can rise without infection, complicating diagnosis.
- The role of CRP in pediatric DKA without infection is not well-defined.
Purpose of the Study:
- To investigate if CRP levels increase in young patients with severe DKA, independent of infection.
- To determine if CRP elevation in DKA is associated with systemic inflammatory response syndrome (SIRS).
- To explore the relationship between CRP and key inflammatory cytokines in DKA.
Main Methods:
- Measured plasma CRP, IL-6, IL-1beta, and TNF-alpha in 7 young patients with severe DKA without infection.
- Collected samples before, during, and after DKA correction (baseline at 96 hours).
- Analyzed CRP levels and their correlation with cytokine levels.
Main Results:
- CRP was transiently elevated in 4 out of 7 patients during or before DKA treatment compared to baseline.
- Significant positive correlations were found between CRP and IL-6/IL-1beta pre-treatment.
- CRP also correlated with IL-6, IL-1beta, and TNF-alpha at 6 hours post-treatment, and IL-1beta at 24 hours.
Conclusions:
- Severe DKA and its treatment can increase CRP levels in young patients, even without infection.
- DKA may be associated with a non-infectious form of SIRS.
- CRP may serve as a marker for the systemic inflammatory response in DKA.
Abstract:
Elevated plasma levels of C-reactive protein (CRP) and IL-6 have been reported to be sensitive indicators of infection in adults with diabetic ketoacidosis (DKA). However, both CRP and the pro-inflammatory cytokines, which regulate CRP, can be elevated without infection. Our hypothesis was that CRP is increased in young patients with severe DKA, even in the absence of an infection, and may serve as a marker for systemic inflammatory response syndrome (SIRS). In 7 patients with severe DKA without infection, we measured plasma CRP, IL-6, IL-1beta and TNF-alpha levels prior to, during, and following correction of DKA. CRP was significantly but transiently elevated in 4 of the patients prior to or during treatment of DKA, compared to their baseline values (96 hr after correction of DKA). There were significant positive relationships between CRP and both IL-6 and IL-1beta prior to treatment (p <0.05); between CRP and IL-6, IL-1beta, and TNF-alpha at 6 hr (p <0.05); and between CRP and IL-1beta at 24 hr (p <0.05). The results support the hypothesis that CRP is increased in some patients by severe DKA and its treatment, and that DKA can be associated with a non-infectious form of SIRS.
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