Ultrasound echo-intensity predicts severe pancreatic affection in cystic fibrosis patients

PLoS One. 2015 Mar 24;10(3):e0121121. doi: 10.1371/journal.pone.0121121. eCollection 2015.

Abstract

Background: Pancreatic destruction affects the majority of patients with cystic fibrosis. We aimed to relate ultrasound findings to exocrine pancreatic function and cystic fibrosis genotype.

Methods: Patients with cystic fibrosis and a matched group of healthy controls were included. We performed transabdominal ultrasound, and recorded echo intensities of the pancreas and parenchymal characteristics according to endoscopic ultrasound based Rosemont criteria.

Results: We included 39 patients and 29 healthy controls. The cystic fibrosis patients were grouped according to exocrine pancreatic function; Cystic fibrosis, insufficient (n = 20) and sufficient (n = 19). Echo intensity measures and visual score demonstrated hyper-echogenicity in the pancreas insufficient group compared to the pancreas sufficient groups (p<0.001). Ductal and parenchymal changes were not prevalent in any of the groups.

Conclusion: The hyper-echoic pancreas was the most frequent ultrasonographic finding in exocrine pancreas insufficient cystic fibrosis patients. Pancreatic echo levels correlated to pancreatic phenotype.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Case-Control Studies
  • Cystic Fibrosis / diagnostic imaging*
  • Cystic Fibrosis / genetics
  • Cystic Fibrosis / physiopathology
  • Cystic Fibrosis Transmembrane Conductance Regulator / genetics
  • Exocrine Pancreatic Insufficiency / diagnostic imaging*
  • Exocrine Pancreatic Insufficiency / physiopathology
  • Female
  • Forecasting
  • Genetic Association Studies
  • Humans
  • Male
  • Middle Aged
  • Pancreas / diagnostic imaging*
  • Pancreas / physiopathology
  • Ultrasonography / methods

Substances

  • CFTR protein, human
  • Cystic Fibrosis Transmembrane Conductance Regulator

Grants and funding

This work was supported by the Norwegian gastroenterology assosciation (http://legeforeningen.no/Fagmed/Norsk-gastroenterologisk-forening/) through limited grants for TE, FE, and GD, and the Norwegian cystic fibrosis Foundation (http://www.cfnorge.no/) through a grant for TE. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.