Peter R Farrell1, Elaina K Jones2, Lindsey Hornung3, Tyler Thompson4, Jyoti Patel4, Tom K Lin5, Jaimie D Nathan6, David S Vitale5, Aida Habtezion2, Maisam Abu-El-Haija5. 1. Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio; Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. Electronic address: peter.farrell@cchmc.org. 2. Division of Gastroenterology, Stanford University College of Medicine, Palo Alto, California. 3. Division of Biostatistics and Epidemiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. 4. Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. 5. Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio; Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. 6. Division of Pediatric General and Thoracic Surgery, Cincinnati Children's Hospital Medical Center; Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Abstract
OBJECTIVES: To utilize a Luminex platform to examine multiple cytokines simultaneously as well as clinical laboratory testing in order to identify markers that predict acute pancreatitis (AP) severity in the pediatric population on admission. STUDY DESIGN: Patients (<19 years) prospectively enrolled over a 4-year period in a single institution AP database were included in separate derivation and validation cohorts. Plasma samples were obtained within 48 hours of admission and stored for analysis. Samples from mild AP and SAP (moderately severe and severe combined) were analyzed using Luminex panels and C-Reactive Protein (CRP) testing. RESULTS: The derivation cohort examined 62 cytokines in 66 subject samples (20 control, 36 mild AP, 10 SAP) and identified interleukin 6 (IL-6) [P = .02] and monocyte chemotactic protein-1 (MCP-1) [p=0.02] as cytokines that were differentially expressed between mild and SAP. Our validation cohort analyzed 76 cytokines between 10 controls, 19 mild AP and 6 SAP subjects. IL-6 (p=0.02) and MCP-1 (p=0.007) were again found to differentiate mild AP from SAP. CRP values were obtained from 53 of the subjects, revealing a strong association between elevated CRP values and progression to severe disease (P<0.0001). CONCLUSION: This study identified and validated IL-6 and MCP-1 as predictors of SAP using 2 distinct cohorts, and showed that CRP elevation is a marker of progression to SAP. These biomarkers have not been extensively studied in the pediatric AP population. Our data allows for risk-stratification of AP patients, and represent novel insight into the immunologic response in SAP.
OBJECTIVES: To utilize a Luminex platform to examine multiple cytokines simultaneously as well as clinical laboratory testing in order to identify markers that predict acute pancreatitis (AP) severity in the pediatric population on admission. STUDY DESIGN:Patients (<19 years) prospectively enrolled over a 4-year period in a single institution AP database were included in separate derivation and validation cohorts. Plasma samples were obtained within 48 hours of admission and stored for analysis. Samples from mild AP and SAP (moderately severe and severe combined) were analyzed using Luminex panels and C-Reactive Protein (CRP) testing. RESULTS: The derivation cohort examined 62 cytokines in 66 subject samples (20 control, 36 mild AP, 10 SAP) and identified interleukin 6 (IL-6) [P = .02] and monocyte chemotactic protein-1 (MCP-1) [p=0.02] as cytokines that were differentially expressed between mild and SAP. Our validation cohort analyzed 76 cytokines between 10 controls, 19 mild AP and 6 SAP subjects. IL-6 (p=0.02) and MCP-1 (p=0.007) were again found to differentiate mild AP from SAP. CRP values were obtained from 53 of the subjects, revealing a strong association between elevated CRP values and progression to severe disease (P<0.0001). CONCLUSION: This study identified and validated IL-6 and MCP-1 as predictors of SAP using 2 distinct cohorts, and showed that CRP elevation is a marker of progression to SAP. These biomarkers have not been extensively studied in the pediatric AP population. Our data allows for risk-stratification of AP patients, and represent novel insight into the immunologic response in SAP.