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1.
Digestion ; 92(1): 32-8, 2015.
Article in English | MEDLINE | ID: mdl-26138365

ABSTRACT

BACKGROUND/AIMS: While lactose malabsorption is a well-investigated condition, few epidemiologic data are available for fructose and sorbitol malabsorption. The aim of this study was to assess the prevalence rates for primary lactose malabsorption, fructose and sorbitol malabsorption, and carbohydrate-specific small intestinal bacterial overgrowth (cs-SIBO) in an Austrian outpatient center. METHODS: In total, 306 adult patients, who were primarily referred with suspected carbohydrate malabsorption by general practitioners to our outpatient clinic, underwent genetic testing (C/T-13910 polymorphism) for primary lactose malabsorption, and a combined hydrogen (H2)/methane (CH4) breath test for fructose (25 g) and sorbitol (12.5 g) malabsorption. Cohen's kappa (κ) was calculated for agreement between positive breath test results and self-reported symptoms during the test. RESULTS: Seventy-eight (25.49%) patients were C/C-13910 homozygotes, indicating primary lactose malabsorption. Thirty-four (11.11%) and 57 (18.63%) patients were classified as fructose and sorbitol malabsorbers. Cohen's κ measuring agreements between positive fructose and sorbitol breath test results and self-reported symptoms during the test were 0.33 and 0.49, respectively. Twenty-nine (9.50%) patients with an early H2/CH4 peak (i.e. within 60 minutes after fructose and/or sorbitol ingestion) were diagnosed with cs-SIBO. CONCLUSION: In Austria, carbohydrate malabsorption is a frequent condition in patients referred by general practitioners to carbohydrate malabsorption testing.


Subject(s)
Fructose/metabolism , Malabsorption Syndromes/epidemiology , Sorbitol/metabolism , Adolescent , Adult , Aged , Aged, 80 and over , Ambulatory Care Facilities/statistics & numerical data , Austria/epidemiology , Blind Loop Syndrome/epidemiology , Blind Loop Syndrome/genetics , Blind Loop Syndrome/metabolism , Breath Tests/methods , Female , Fructose Intolerance/epidemiology , Fructose Intolerance/genetics , Homozygote , Humans , Hydrogen , Lactose Intolerance/epidemiology , Lactose Intolerance/genetics , Malabsorption Syndromes/genetics , Malabsorption Syndromes/metabolism , Male , Methane , Middle Aged , Prevalence , Young Adult
2.
Inflamm Bowel Dis ; 15(3): 359-64, 2009 Mar.
Article in English | MEDLINE | ID: mdl-18844217

ABSTRACT

BACKGROUND: Detergents and emulsifiers added to food may destroy the mucus barrier, which normally isolates bacteria from the intestinal wall, and lead to chronic bowel inflammation in susceptible persons. We investigated the influence of 2% carboxymethylcellulose (CMC) on the biostructure of the intestinal microbiota in IL-10 gene-deficient mice. METHODS: Twenty to 27-week-old IL-10 gene-deficient mice received either 2% CMC solution (n = 7) or water (n = 6) orally for 3 weeks. Intestinal bacteria were investigated using fluorescence in situ hybridization in paraffin-fixed sections of the intestine. RESULTS: CMC-treated IL-10 gene-deficient mice demonstrated a massive bacterial overgrowth, distention of spaces between villi, with bacteria filling these spaces, adherence of bacteria to the mucosa, and migration of bacteria to the bottom of the crypts of Lieberkuehn. Leukocytes migrated into the intestinal lumen in 4 of the 7 CMC mice. The changes were similar to those observed in Crohn's disease in humans and were absent in control animals. CONCLUSIONS: CMC induces bacterial overgrowth and small bowel inflammation in susceptible animals. Because of its ubiquity in products and its unrestricted use in food of the industrial world, CMC is an ideal suspect to account for the rise of IBD in the 20th century.


Subject(s)
Bacteria/growth & development , Blind Loop Syndrome/genetics , Carboxymethylcellulose Sodium/toxicity , Genetic Predisposition to Disease , Interleukin-10/deficiency , Intestine, Small/microbiology , Animals , Bacteria/isolation & purification , Bacteria/pathogenicity , Blind Loop Syndrome/metabolism , Blind Loop Syndrome/microbiology , Disease Models, Animal , In Situ Hybridization, Fluorescence , Inflammation/genetics , Inflammation/metabolism , Inflammation/pathology , Interleukin-10/genetics , Intestinal Mucosa/drug effects , Intestinal Mucosa/metabolism , Intestinal Mucosa/pathology , Intestine, Small/drug effects , Intestine, Small/pathology , Mice
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