Deployment of carboxymethyl cellulose sheets to prevent esophageal stricture after full circumferential endoscopic submucosal dissection: A porcine model.

BACKGROUND AND AIM: Esophageal stricture is a serious adverse event secondary to extensive endoscopic submucosal dissection (ESD). The present study aimed to investigate the efficacy of carboxymethyl cellulose (CMC) sheets for the prevention of esophageal stricture after full circumferential ESD in an animal model. METHODS: Fourteen porcine models were randomized into a control group (n = 7) and a CMC group (n = 7). Five-centimeter-long circumferential esophageal ESD was carried out at a distance of 40 to 45 cm from the incisors in all models. In the CMC group, CMC sheets were placed over the mucosal defect completely after ESD, whereas the control group underwent routine ESD only. Endoscopic examination was conducted after the first and second week post-ESD. Esophageal specimens were harvested during post-mortem and were evaluated for macroscopic and histological appearance. Blood serum levels of four pro-inflammatory or profibrotic cytokines were measured quantitatively. RESULTS: The CMC group had better food tolerability during the second week post-ESD. The CMC group showed a significantly lower esophageal mucosal stricture rate compared to the control group. Histological assessments showed less fibrosis in the submucosal layer, milder damage to the muscularis propria, and enhanced re-epithelization in the CMC group. Serum transforming growth factor beta 1 levels were significantly lower in the CMC group post-ESD. CONCLUSION: Deployment of CMC sheets on the mucosal defect appears to be a promising method for preventing esophageal strictures after extensive ESD.

Evaluation of systemic oxidative status and mononuclear leukocytes DNA damage in children with caustic esophageal stricture.

Esophageal stricture (ES) due to accidentally caustic digestions is a common problem in children. Mucosal damage and repeated dilatations lead to chronic inflammation and finally ES. We investigated the oxidative status and DNA damage of children with ES. Five children with ES were compared with the same age- and sex-matched healthy subjects. Oxidative status of plasma was evaluated by measuring myeloperoxidase (MPO) activity, and total peroxide (TP) level. Anti-oxidative status of the plasma was evaluated by measuring catalase (CAT) activity, and total antioxidant response (TAR). We used the Single Cell Gel Electrophoresis (also called Comet Assay) to measure DNA strand break in peripheral blood mononuclear leukocytes. Mean MPO activity and TP levels in the ES group were significantly higher than the control group (0.83 +/- 0.35, 0.09 +/- 0.03 and 0.98 +/- 0.38, 0.34 +/- 0.20, P = 0.009 and P = 0.047 respectively). There was no significant difference in CAT activity and TAR levels between the two groups (P = 0.347). DNA damage in patients with ES was increased compared to control subjects (108.8 +/- 51.2 and 57.6 +/- 31.2 arbitrary units, respectively), but this difference was not significant statistically (P= 0.09). This study shows that systemic oxidative stress and alteration at the nuclear level occur in patients with ES, as a result of multiple dilatations and tissue injury. On the other hand, these results support that patients with ES may benefit from antioxidant treatment.

Montelukast reduces peripheral blood eosinophilia but not tissue eosinophilia or symptoms in a patient with eosinophilic gastroenteritis and esophageal stricture.

BACKGROUND: Eosinophilic gastroenteritis (EG) is an uncommon entity of which the pathogenesis is unclear. As no controlled treatment trials exist, treatment of EG remains largely empiric. Limited results have been achieved with oral cromolyn, ketotifen, and other antihistamines. Oral corticosteroids are effective, but long-term use is complicated by side effects including growth retardation, diabetes, and osteoporosis. OBJECTIVES: We sought to determine whether treatment with montelukast would improve symptoms and decrease both peripheral blood and tissue eosinophilia (TE) in a patients with steroid-dependent EG for 20 years complicated by esophageal stricture. METHODS: In an unblinded, n = 1 trial, we treated the patient for 5 months with montelukast (20 to 30 mg daily) while his baseline dose of prednisone (10 mg daily) was continued. Complete blood counts and symptoms were monitored weekly. Esophageal biopsies were obtained before and after 5 months of therapy with montelukast. After the posttreatment biopsy was obtained, montelukast was discontinued. Outcome measures included patient symptoms and peripheral and tissue eosinophil counts. RESULTS: During treatment with montelukast, the mean peripheral blood eosinophil count fell from 5,064 cells/microL (average 28 determinations over 20 years; range 1,408 to 12,500 cells/microL) to 1,195 cells/microL (average 14 determinations over 16 weeks; range 556 to 2,193 cells/microL), a 76% reduction. The corresponding TE as calculated from esophageal biopsies was 31 eosinophils/high power field before and 70 eosinophils/high power field after treatment. The patient noted no appreciable improvement in esophageal symptoms. CONCLUSIONS: Montelukast dramatically reduced peripheral blood eosinophilia, but did not affect TE or symptoms in this patient with severe, long-standing EG complicated by esophageal stricture.