Disaccharidase activity in children with inflammatory bowel disease.

BACKGROUND/AIMS: The etiopathogenesis of inflammatory bowel disease (IBD) is multifactorial and not well explained. Environmental, genetic, and dietary factors play an important role. The aim of the study was the evaluation of lactase, saccharase, and maltase activity in patients with IBD. MATERIALS AND METHODS: The study comprised 65 children, aged 3-18 years. During a routine endoscopy, we took biopsies from the descending part of the duodenum. In these biopsies, we determined disaccharidase activity using Dahlquist's method. RESULTS: Decreased lactase activity in the biopsies taken from the small intestine mucosa was most frequently observed in patients with Crohn's disease (5/15-33%) and least frequently seen in children with lymphocytic colitis (in 1/10-10%). The lowest mean values of lactase activity were found in the children with Crohn's disease and ulcerative colitis (1.7-2.5 U/1 g). Decreased saccharase activity in the biopsies obtained from the small intestine mucosa was most frequently observed in patients with lymphocytic colitis (in 5/10-50%) and ulcerative colitis (9/20-45%) and least frequently seen in children with non-specific undetermined colitis (in 7/20-35%). Decreased maltase activity in the small bowel mucosa was the most frequently observed in patients with Crohn's disease (in 5/15-33%) and least frequently seen in children with ulcerative colitis (in 3/20-15%). The lowest mean values of maltase activity were found in the children with Crohn's disease (5.4 U/1 g). CONCLUSION: Therefore, it seems reasonable to perform diagnostic examinations aimed at lactose, saccharose, and maltose intolerance and to initiate a dietary regimen in children with IBD.

The behavior of matrix metalloproteinase-9 in lymphocytic colitis, collagenous colitis and ulcerative colitis.

Matrix metalloproteinases play an important role in extracellular matrix remodelling. It has been proposed that matrix metalloproteinase-9 (MMP-9) is involved in epithelial damage in ulcerative colitis (UC). However, to our knowledge, no data are available in terms of MMP-9 expression in microscopic colitis. Determination of mucosal protein expression levels of MMP-9 in lymphocytic colitis (LC), collagenous colitis (CC) and UC. MMP-9 immunohistochemical expressions were analyzed in paraffin-embedded tissue samples by immunohistochemistry including patients with LC, CC, UC, active diverticulitis, inactive diverticular disease and healthy control subjects. UC was also subgrouped according to the severity of inflammation. Immunostaining was determined semiquantitatively. Independent colonic biopsies from healthy and severe UC cases were used for gene expression analyses. For further comparison MMP-9 serum antigen levels were also determined in patients with UC and control patients without macroscopic or microscopic changes during colonoscopy. MMP-9 mucosal expression was significantly higher in UC (26.7 ± 19.5%) compared to LC (6.6 ± 9.3%), CC (6.4 ± 7.6%), active diverticulitis (5.33 ± 2.4%), inactive diverticular disease (5.0 ± 2.2%) and controls (6.3 ± 2.6%) (P < 0.001). The immunohistochemical expression of MMP-9 in LC and CC was similar as compared to controls. MMP-9 expression was significantly higher in each inflammatory group of UC compared to controls (mild: 11.0 ± 2.8%, moderate: 23.9 ± 3.7%, severe UC: 52.6 ± 3.9% and 6.3 ± 2.6%, respectively, P < 0.005). The gene expression microarray data and RT-PCR results demonstrated a significantly higher expression of MMP-9 in severely active UC compared to healthy controls (P < 0.001). Significantly higher MMP-9 serum antigen concentrations were observed in UC patients compared with the control group (P < 0.05). MMP-9 seems to play no role in the inflammatory process of LC and CC. In contrast, the mucosal up-regulation of MMP-9 correlated with the severity of inflammation in UC. The increased MMP-9 expression could contribute to the severity of mucosal damage in active UC.