Background: Significance of pancreatic autoantibodies determined by using exocrine pancreas (PAB) and antibodies against recombinant pancreas antigen (rPAB), as well as the importance of autoantibodies against goblet cells (GAB), is not known in pediatric patients with inflammatory bowel disease (IBD). Our aim was to determine the complex analysis of PAB, rPAB, GAB, antibodies against Saccharomyces cerevisiae, and perinuclear components of neutrophils in pediatric patients with IBD. Moreover, association with NOD2/CARD15 and disease phenotype was determined.
Methods: A total of 152 pediatric patients (median age 13.9 years) with IBD (103 patients with Crohn disease [CD] and 49 patients with ulcerative colitis [UC]) and 104 controls were included. Serum autoantibodies were determined by indirect immunofluorescence assay. NOD2/CARD15 variants were tested by polymerase chain reaction/restriction fragment length polymorphism.
Results: The presence of PAB and rPAB was significantly higher in CD (34% and 35.9%) and in UC (20.4% and 24.5%) compared with pediatric control cohort (0% and 0%, P < 0.0001). In addition, GAB positivity was significantly increased in patients with UC in comparison with CD and controls, respectively (UC, 12.2%; CD, 1.9%; controls, 1.9%; P = 0.02). Specificity of PAB and rPAB was 100%; however, sensitivity was low. The combination of PAB and/or antibodies against Saccharomyces cerevisiae/perinuclear components of neutrophils improved the sensitivity of serological markers in CD (87.4%) and in UC (79.6%); specificities were 89.3% and 93.2%, respectively. Pancreatic autoantibodies (PAB, rPAB) and GAB were not related to clinical presentation, medical therapy, or need for surgery in CD or in UC.
Conclusions: Pancreatic autoantibodies and GAB were specific for IBD, but the sensitivity was limited as well because there was lack of correlation with clinical phenotype. Combinations of these antibodies have shown increased sensitivity; therefore, it may be recommended in the diagnostic procedure of IBD.
*Department of Pediatrics, Petz Aladár County and Teaching Hospital, Győr
†1st Department of Medicine, Semmelweis University, Budapest
‡2nd Department of Medicine, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
§Euroimmun Medizinische Labordiagnostika AG, Luebeck, Germany
||Department of Pediatrics, Medical and Health Science Center, University of Debrecen, Debrecen
¶Madarász Children's Hospital, Budapest
#Pediatric Health Centre, Borsod-A-Z County and University Teaching Hospital, Miskolc
**Department of Pediatrics, Pándy Kálmán Hospital, Gyula
††Department of Pediatrics, Cholnoky Ferenc County Hospital, Veszprém
‡‡1st Department of Pediatrics, Semmelweis University, Budapest, Hungary.
Address correspondence and reprint requests to Gabor Veres, MD, PhD, 1st Department of Pediatrics, Semmelweis University, 53 Bókay St, 1083 Budapest, Hungary (e-mail: firstname.lastname@example.org).
Received 1 March, 2012
Accepted 20 March, 2012
G.V. holds the János Bolyai Research Grant; this article was supported by the János Bolyai Research Scholarship of the Hungarian Academy of Sciences.
The authors report no conflicts of interest.