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. 2023 Apr 1;207(7):945-949.
doi: 10.1164/rccm.202210-1988LE.

Tight Glycemic Control, Inflammation, and the ICU: Evidence for Heterogeneous Treatment Effects in Two Randomized Controlled Trials

Collaborators, Affiliations

Tight Glycemic Control, Inflammation, and the ICU: Evidence for Heterogeneous Treatment Effects in Two Randomized Controlled Trials

Matt S Zinter et al. Am J Respir Crit Care Med. .
No abstract available

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Figures

Figure 1.
Figure 1.
Differential response to tight glycemic control according to prerandomization inflammatory class. Data are depicted for patients in the CAF-PINT (Coagulation and Fibrinolysis in Pediatric Insulin Titration) trial. (A) Logistic regression models were fit for the outcome of mortality as predicted by pretreatment log10-transformed biomarker and treatment group, allowing for an interaction term. Estimated mortality was then plotted for each biomarker stratified by treatment group (top row), and the difference in estimated mortality between the treatment groups (i.e., conditional average treatment effect) was plotted with 95% confidence interval (bottom row). (B) Unsupervised latent class analysis detected two groups of patients with contrasting levels of pretreatment inflammatory biomarkers. Kaplan-Meier in-hospital survival estimates were plotted over 90 days. (Right) Hyperinflamed patients who were treated with a target glucose of 80–110 mg/dl (TG80–110) had lower mortality (6% mortality with TG80–110 vs. 48% mortality for patients with TG150–180; log-rank P = 0.004), whereas (Left) hypoinflamed patients who were treated with TG80–110 showed a trend toward higher mortality (14% mortality with TG80–110 vs. 7% mortality with TG150–180; log-rank P = 0.055). TNFR-1 = tumor necrosis factor receptor 1.

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