Number Of Mucosal Breaks Research Articles

Xerostomia and prevention of dryness with a Pycnogenol® mouth spray: a pilot study.

The aim of this pilot, supplement study was the evaluation of primary, idiopathic mucosal mouth dryness (xerostomia or dry mouth) in subjects without systemic diseases. Subjects with xerostomia were managed either with standard management (SM) or with SM and a Pycnogenol® mouth spray (Hankintatukku Oy, Karkkila, Finland), at the dosage of 60 mg/day in 30 spurts, for 2 weeks. A total of 50 subjects were included in the study: 25 controls using only standard management (SM) and 25 subjects using the Pycnogenol® mouth spray. No side effects and no tolerability problems were observed with the Pycnogenol® mouth spray. The groups were comparable for characteristics and symptoms at baseline. These otherwise healthy subjects had a BMI<26. After 2 weeks, salivary flow and salivary oxidative stress (in Carr Units) were improved significantly with Pycnogenol® mouth spray as compared to controls (P<0.05), whereas minimal improvements in salivary flow were seen with SM. The subjective symptomatic dry mouth score and the number of mucosal breaks and ulcerations (all minimal, <1 mm in length or diameter) were significantly decreased with the Pycnogenol® mouth spray supplement compared to SM controls (P<0.05). The Pycnogenol® mouth spray led to significant improvement in salivary lysozyme levels, compared to controls (P<0.05). Based on these preliminary results, Pycnogenol® mouth spray could be a new supplementary option for the management of primary xerostomia.

Xerostomia: prevention with Pycnogenol® supplementation: a pilot study.

The aim of this pilot study was the evaluation of primary, idiopathic mucosal dryness (xerostomia or dry mouth) in subjects without cancer. A group of non-diabetic subjects and a group of diabetics were managed with standard management (SM) or with SM+Pycnogenol® (150 mg/day) for 2 weeks. In total, 48 subjects were included in the study; 24 diabetics and 24 non-diabetics. 12 diabetics and 12 non-diabetics took Pycnogenol® and 12 diabetics and 12 non-diabetics were followed up with standard management only and served as controls. No side effects and no tolerability problems were observed with Pycnogenol®. The registry groups were comparable for characteristics and symptoms at baseline. All otherwise healthy subjects had a BMI<26 kg/m2. In 2 weeks, salivary flow and oxidative stress improved significantly in both groups of subjects (non-diabetics and diabetics) with 150 mg/day Pycnogenol® (P<0.05), while minimal improvements in salivary flow were seen with SM. The subjective score and the number of mucosal breaks and ulcerations, all minimal (<1 mm in length or diameter), were significantly decreased with Pycnogenol® supplementation (P<0.05) with minimal variations in the SM controls. Finally, the mean lysozyme level in parotid saliva samples was significantly increased in the Pycnogenol® group (P<0.05) both in diabetics and non-diabetics. Based on these preliminary results, Pycnogenol® could be a new, valid option for the treatment of xerostomia.

Amelioration of Small Bowel Injury by Switching from Nonselective Nonsteroidal Anti-Inflammatory Drugs to Celecoxib in Rheumatoid Arthritis Patients: A Pilot Study

Background/Aims: Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used in patients with rheumatoid arthritis (RA) but have several side effects including mucosal damage in the small intestine. We aimed to evaluate whether the small bowel injury is ameliorated by switching from nonselective NSAIDs to celecoxib in patients with RA. Methods: Sixteen patients with RA who were treated with nonselective NSAIDs were enrolled in this study. Nonselective NSAIDs were converted to celecoxib for 12 weeks. Capsule endoscopy was performed before and after treatment with celecoxib. Videos were screened by gastroenterologists blinded to the patients' treatment. Results: Before the administration of celecoxib, reddened folds, denuded areas, petechiae/red spots and mucosal breaks were observed in 63, 63, 88 and 69% of the patients, respectively. In the 14 patients who completed this study, conversion to celecoxib significantly reduced the number of petechiae/red spots, the number of mucosal breaks, and Lewis scores. RA activity and cytokine levels in the peripheral blood were not significantly different before and after treatment with celecoxib. Conclusions: The incidence of small bowel injury by nonselective NSAIDs is high in patients with RA. Conversion from nonselective NSAIDs to celecoxib can be useful for protecting patients with RA from small bowel injury.

Sa1625 The Evaluation of Portal Hypertensive Enteropathy Using Capsule Endoscopy in Cirrhotic Patients: a Multicenter Study

significantly reduced the number of such lesions at week 10. In NSAID irsogladine group, the number of mucosal breaks was significantly smaller than that at week 2 and 6 compared to NSAID PPI group. Conclusions: In concludion, long-term PPI administration did not show any preventive efficacy for small intestinal lesions induced by NSAIDs although it is a standard medication for NSAIDs induced gastrointestinal lesions. Small intestinal lesions at week 6 are less severe as compared to those at week 2 by small intestinal mucosal adaptation. On the other hand, irsogladine prevented small intestinal lesions by NSAIDs and showed therapeutic benefit for such lesions achieved with NSAIDs and PPIs.

884 Regulation of NKCC1 Surface Expression By PKC Involves Dynamin II and Clathrin-Dependent Endocytic Machinery

G A A b st ra ct s before and after medication were analyzed for small intestinal injuries. NSAID treatment significantly increased the mean number of mucosal breaks and reddened lesions per subject in the Control-group, from 0.1±0.3 to 15.8±71.5 and from 4.0±3.9 to 10.0±10.3 respectively; but only up from 0.1±0.3 to 4.2±7.8 and from 5.4±6.3 to 9.2±6.6 in the Rebamipide-group. The percentage of subjects with at least one mucosal break at post-treatment was also higher in the Control-group (63%) than in the Rebamipide-group (47%); (NS). The percentage of subjects with post-treatment increases in reddened lesions ≥ 10 was significantly higher in the Control-group (46%) than in the Rebamipide-group (14%); (P=0.04). Conclusion: Rebamipide administration reduced the incidence of small intestinal lesions induced by twoweek administration of diclofenac sodium. Further studies are warranted to determine whether a higher rebamipide dosage can further protect against NSAID-induced small intestinal mucosal breaks.

885 Preserved Abundance But Functional Dysregulation of Na+/H+ Exchanger Isoform NHE3 in the Small and Large Intestine in CD45RBhigh Transfer Colitis Mice with Diarrhea

G A A b st ra ct s before and after medication were analyzed for small intestinal injuries. NSAID treatment significantly increased the mean number of mucosal breaks and reddened lesions per subject in the Control-group, from 0.1±0.3 to 15.8±71.5 and from 4.0±3.9 to 10.0±10.3 respectively; but only up from 0.1±0.3 to 4.2±7.8 and from 5.4±6.3 to 9.2±6.6 in the Rebamipide-group. The percentage of subjects with at least one mucosal break at post-treatment was also higher in the Control-group (63%) than in the Rebamipide-group (47%); (NS). The percentage of subjects with post-treatment increases in reddened lesions ≥ 10 was significantly higher in the Control-group (46%) than in the Rebamipide-group (14%); (P=0.04). Conclusion: Rebamipide administration reduced the incidence of small intestinal lesions induced by twoweek administration of diclofenac sodium. Further studies are warranted to determine whether a higher rebamipide dosage can further protect against NSAID-induced small intestinal mucosal breaks.

Prevention of nonsteroidal anti-inflammatory drug–induced small-intestinal injury by prostaglandin: a pilot randomized controlled trial evaluated by capsule endoscopy

There is no known preventive agent against nonsteroidal anti-inflammatory drug (NSAID) induced small-intestinal injury. To evaluate by capsule endoscopy whether coadministration of prostaglandin (PG) can prevent small-intestinal damage induced by short-term NSAID treatment. Single-blind, randomized, controlled trial. All procedures were performed at Nippon Medical School. Thirty-four healthy male volunteers. All subjects were randomly assigned to 2 groups: an NSAID-control group, who underwent NSAID (diclofenac sodium, 25 mg 3 times daily) and omeprazole (20 mg once daily) treatment, and an NSAID-PG group, who received PG (misoprostol, 200 microg 3 times daily) in addition to the same NSAID-omeprazole treatment. Eligible subjects, 15 per group, underwent capsule endoscopy before and 14 days after treatment. The number of mucosal breaks at capsule endoscopy. NSAID treatment significantly increased the mean (SD) number of mucosal breaks per subject, from a basal level of 0.1 +/- 0.3 up to 2.9 +/- 6.3 lesions in the NSAID-control group (P = .012). In contrast, there was no significant change in the mean number of mucosal breaks before and after PG cotreatment (P = 0.42). Thus, the mean number of posttreatment mucosal breaks per subject was significantly higher in the NSAID-control group than in the NSAID-PG group (P = .028). There was a significant increase in the percentage of subjects in the NSAID-control group, with at least 1 mucosal break after treatment (from 6.7% to 53.3%), whereas there was no change in the incidence of mucosal breaks in the NSAID-PG group, which remained at 13.3%. (P = .002). Single-center, open-label study. PG cotherapy reduced the incidence of small-intestinal lesions induced by a 2-week administration of diclofenac sodium.