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Abstract

To date, tests of small intestinal passive permeability have involved the ingestion of test molecules whose permeation is assessed indirectly by measuring their urinary recovery. Excretion ratios of marker molecules (eg, lactulose-to-mannitol excretion ratio, LMER) are useful clinically. Measurement of permeability markers in serum would improve the convenience of the tests. Our aim was to assess small intestinal permeability in celiac patients using serum lactulose and mannitol levels with calculation of lactulose to mannitol serum ratios (LMSR) and to compare the results with the standard methods using urinary recoveries. Twenty-four newly diagnosed celiacs and 10 control subjects were studied; 10 celiacs were restudied while established on a gluten-free diet. Test subjects and patients ingested 10 g lactulose and 2.5 g mannitol in 50 ml water. In 10 untreated celiacs and the controls, blood was taken from 0 to 120 min and all urine was collected for 6 hr. The remaining 14 untreated and the 10 treated celiacs had a single serum sample taken 60 min after ingestion of the test solution. At 1 hr after ingestion, the mean mannitol level in normals (0.156 mmol/liter) was significantly higher than in untreated celiacs (0.06 mmol/liter). The 1-hr mean serum lactulose level in normals (0.125 micromol/liter) was significantly lower than in untreated celiacs (0.56 micromol/liter). The median 1-hr LMSR in untreated celiacs was 0.42 compared with 0.039 in normals and 0.08 in treated celiacs. There was a significant correlation between LMSR and LMER. Permeability testing using serum measurements of lactulose and mannitol gave comparable results in celiac patients to the tests using urinary recovery of the permeability markers and may prove to be more convenient, especially in pediatric patients.

Intermittent Suckling in Combination with an Older Weaning Age Improves Growth, Feed Intake and Aspects of Gastrointestinal Tract Carbohydrate Absorption in Pigs after Weaning

“…The observed pattern of mannitol absorption in the CW28 piglets corresponded to previously reported values [19]. Although some mannitol passes through the epithelial layer via the paracellular route, it is mostly absorbed via the transcellular route via water-filled pores in the enterocyte membrane, making mannitol a surrogate marker of functional mucosal mass in the SI [18]. In the pre-weaning period, the trend for the IS groups (when combined) to have lower mannitol concentrations than the CW28 group suggests that IS reduces intestinal surface area before weaning.…”

“…A subsample of piglets from sows in three of the batches (a total of nine piglets per treatment) were subjected to sugar absorption tests (SAT) as markers of intestinal absorption based on methodologies described by Thymann et al [17], Cox et al [18] and Berkeveld et al [19]. Briefly, two piglets were selected per litter and sugar absorption across the GIT using either 10% mannitol (≥98%; Sigma Aldrich, St Louis, MO, USA) (5 mL/kg body weight (BW)) or 10% galactose (≥99%; Sigma Aldrich, St Louis, MO, USA) (5 mL/kg BW) was assessed.…”

The Effect of Intestinal Permeability and Endotoxemia on the Prognosis of Acute Pancreatitis

“…IP is usually expressed as a percentage of the excreted amount in urine to the administered amount of a certain test drug, and the normal value is <2% 19. In clinical practice, clinicians most commonly use polysaccharides, such as lactulose, which are relatively large molecules and pass through the intercellular space of the intestinal mucosa and monosaccharides, such as lamnose or mannitol, which are relatively small molecules and move into the cell interior 20. We used this test in the study.…”

Increased Bacterial Translocation in Gluten-Sensitive Mice Is Independent of Small Intestinal Paracellular Permeability Defect

“…1a). A defect in the paracellular pathway is relevant not only to this animal model but also to celiac disease [16, 17]. We have previously shown that in HCD4/HLA-DQ8 mice, gliadin causes an increased flux of the transcellular macromolecular probe HRP as well as an augmented short circuit current, which is not observed at this magnitude in haplotype controls (HLA-DQ6) and wild-type (C57BL/6) mice treated with gliadin [12, 14].…”