Abstract

Adipokine Resistin Levels at Time of Pediatric Crohn Disease Diagnosis Predict Escalation to Biologic Therapy

Inflamm Bowel Dis. 2020 Sep 26;izaa250. doi: 10.1093/ibd/izaa250. Online ahead of print.

Jacob A Kurowski 1, Jean-Paul Achkar 2, Rishi Gupta 3, Iulia Barbur 4, Tracey L Bonfield 5, Sarah Worley 6, Erick M Remer 7, Claudio Fiocchi 8, Satish E Viswanath 4, Marsha H Kay 1

 
     

Author information

  • 1Pediatric Gastroenterology, Hepatology, and Nutrition, Cleveland Clinic, Cleveland, Ohio, United States.
  • 2Gastroenterology, Hepatology, and Nutrition, Cleveland Clinic, Cleveland, Ohio, United States.
  • 3Pediatric Gastroenterology, University of Rochester, Rochester, New York, United States.
  • 4Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio, United States.
  • 5Pediatrics, Case Western Reserve University, Cleveland, Ohio, United States.
  • 6Quantitative Health Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, United States.
  • 7Imaging Institute, Cleveland Clinic, Cleveland, Ohio, United States.
  • 8Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, United States.

Abstract

Background: Hypertrophy of visceral adipose tissue (VAT) is a hallmark of Crohn disease (CD). The VAT produces a wide range of adipokines, biologically active factors that contribute to metabolic disorders in addition to CD pathogenesis. The study aim was to concomitantly evaluate serum adipokine profiles and VAT volumes as predictors of disease outcomes and treatment course in newly diagnosed pediatric patients with CD.

Methods: Pediatric patients ages 6 to 20 years were enrolled, and their clinical data and anthropometric measurements were obtained. Adipokine levels were measured at 0, 6, and 12 months after CD diagnosis and baseline in control patients (CP). The VAT volumes were measured by magnetic resonance imaging or computed tomography imaging within 3 months of diagnosis.

Results: One hundred four patients undergoing colonoscopy were prospectively enrolled: 36 diagnosed with CD and 68 CP. The serum adipokine resistin and plasminogen activator inhibitor (PAI)-1 levels were significantly higher in patients with CD at diagnosis than in CP. The VAT volume was similar between CD and CP. Baseline resistin levels at the time of diagnosis in patients with CD who were escalated to biologics was significantly higher than in those not treated using biologic therapy by 12 months (29.8 ng/mL vs 13.8 ng/mL; P = 0.004). A resistin level of ≥29.8 ng/mL at the time of diagnosis predicted escalation to biologic therapy in the first year after diagnosis with a specificity of 95% (sensitivity = 53%; area under the curve = 0.82; P = 0.015 for model with log-scale). There was a significantly greater reduction in resistin (P = 0.002) and PAI-1 (P = 0.010) at the 12-month follow-up in patients on biologics compared with patients who were not treated using biologics.

Conclusions: Serum resistin levels at diagnosis of pediatric CD predict the escalation to biologic therapy at 12 months, independent of VAT volumes. Resistin and PAI-1 levels significantly improved in patients with CD after treatment using biologics compared with those not on biologics. These results suggest the utility of resistin as a predictive biomarker in pediatric CD.

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