FECAL ALPHA-1-ANTITRYPSIN - A MARKER OF INTESTINAL VERSUS SYSTEMIC INFLAMMATION IN PEDIATRIC CROHNS-DISEASE

Citation
D. Herzog et al., FECAL ALPHA-1-ANTITRYPSIN - A MARKER OF INTESTINAL VERSUS SYSTEMIC INFLAMMATION IN PEDIATRIC CROHNS-DISEASE, Inflammatory bowel diseases, 2(4), 1996, pp. 236-243
Citations number
30
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
10780998
Volume
2
Issue
4
Year of publication
1996
Pages
236 - 243
Database
ISI
SICI code
1078-0998(1996)2:4<236:FA-AMO>2.0.ZU;2-Z
Abstract
Growth failure and malnutrition are major concerns in pediatric patien ts with frequent relapses of Crohn's disease (CD). In search of an ear ly, noninvasive marker of relapse, we prospectively examined the relat ionship between levels of fecal alpha 1-antitrypsin (alpha 1-AT) in co mparison with other known inflammatory parameters and disease activity using a pediatric CD Activity Index (P-CDAI), as well as in relation to growth. Forth-two pediatric patients (29 M, 13 F, 7-16 years old, m ean 12.8 years) with ileal or ileocolonic CD were prospectively examin ed at 4 monthly intervals over a 1 year period. Median (interquartile range) fecal alpha 1-AT values did not differ between children in clin ical relapse (P-CDAI > 150, n = 10) compared with CD patients (n = 42) with quiescent disease [1.84 (3.67) mg/g, respectively, p = ns]. Howe ver, children with growth failure (n = 14) had a significantly higher fecal alpha 1-AT [3.63 (5.65) mg/g] despite clinical remission [median P-CDAI 22 (72.5)] compared with those with normal growth [1.41 (1.66) mg/g, p = 0.02]. Very high fecal alpha 1-AT levels (>4 mg/g) were not associated with clinically active disease [median P-CDAI 23 (71.5)]. Overall however, levels in CD were significantly higher than that of 1 7 pediatric control patients with diarrheal disorders unrelated to IBD [0.98 (1.21), p < 0.05]. Fecal alpha 1-AT seems therefore not to be a reliable marker of clinically evident disease activity, but was best related with chronic malnutrition and subclinical disease activity.