L'ACTIVITE BETA-GALACTOSIDASIQUE FECALE EST DIMINUEE AU COURS DE LA MALADIE DE CROHN

An increased degradation of colonic mucus by bacterial enzymes might participate in the development of mucosal lesions in inflammatory bowel disease. The biodisponibility of drugs used in the treatment of such disease relies upon the metabolic activity of colonic bacterial flora. This activity can be indirectly assessed by measuring fecal enzymatic activities. The aim of this study was to compare fecal β-galactosidase (β-gal) activity in controls, in patients suffering from extradigestive inflammatory disease and in patients with Crohn's disease (CD). Three groups were studied including 11 healthy volunteers (6 F, 5 M) mean age 29 years (21-37), 20 patients with rheumatoid arthritis (RA) (17 F, 3 M), mean age 61.5 years, and 34 patients with non operated CD (21 F, 13 M) mean age: 27 years (13-50). The Crohn disease activity index (CDAI) was > 150 in 24 and < 150 in 10. β-gal activity was measured in fecal extracts by its ability to hydrolyze paranitrophenyl β-D-galactopyranoside and expressed as units of enzymatic activity/gram of fecal proteins. β-gal activity was significantly decreased in patients with CD (16 ± 4.5 U/g) (m ± sem) as compared with patients with RA (353 ± 64 U/g) (P < 0.0001) and to controls (263 ± 40 U/g) (P = 0.002). β-gal activity was not significantly different in controls and in patients with RA. Patients with active CD had a significantly lower β-gal activity than patients with quiescent CD (9.5 ± 3.7 U/g vs 31.4 ± 11.5 U/g) (P = 0.006). Decreased fecal β-gal activity in patients with CD appeared to be related to intestinal inflammation since it was not found in patients with RA and was more pronounced during flare-ups of CD. This could reflect deep impairment of metabolic activity of colonic flora bringing into question the use of drug presentations aiming whose goal is to deliver specifically active products into the colon after liberation by colonic bacterial activity.