Clinical variants of esophageal stenosis caused by infectious esophagitis in children

Infectious esophagitis (IE) is commonly seen in immunocompromised patients. IE may be the first symptom of immunodeficiency state, also can be complication of immunosuppressive therapy in patients with hematological and oncological diseases. Severe complication of IE is esophageal stenosis. Patient management tactics continue to be discussed. A purpose of our publication is to demonstrate our experience in the management of patients with infectious esophageal stenosis. The etiology, features of the clinical and endoscopic picture, as well as the effectiveness of drug therapy and endoscopic methods of treatment have been analyzed. The study was approved by the Independent Ethics Committee and the Scientific Council of the D. Rogachev NMRCPHOI. In each case, parents gave their consent to the use of their child’s data, including photographs, for research purposes and in publications.

Prevention Effect of TGF-β Type I Receptor Kinase Inhibitor in Esophageal Stricture Formation after Corrosive Burn

Corrosive burns lead to progressive esophageal stricture and dysphagia. There are many trials to prevent esophageal stricture formation after corrosive burn. EW-7197 has been proven in several animal models of fibrosis to have antifibrotic and antiproliferative effect. This study aimed to assess the effects of EW-7197 on prevention for esophageal stricture formation after corrosive esophageal burn. An animal study was carried out, where the animals were divided into three groups: a healthy group, a control group (corrosive burn without EW-7197), and a treatment group (corrosive burn with EW-7197). Corrosive esophageal burns were induced using 30% NaOH on the lower esophagus. For 3 weeks, the control group received vehicle and the treatment group received 20 mg/kg/day EW-7197. Treatment efficacy was assessed by measuring the stenosis ratio by esophagogram with contrast media on day 21. Histologic staining was performed to evaluate the fibrosis area ratio, and Western blotting was performed to evaluate fibrotic markers. Among 20 rats that underwent surgery, 14 survived. Three in the treatment group died because of esophageal perforation, and three in the control group died due to their debilitating status. The esophageal stenosis ratio was significantly lower in the treatment group than in the control group (12.1 ± 9.5% and 42.2 ± 8.3%, respectively; p = 0.001). The histologic fibrosis area ratio was also significantly lower in the treatment group (12.5 ± 3.0% and 21.6 ± 2.1%, respectively; p = 0.001). The treatment group showed lower expressions of profibrogenic proteins such as TGF-β1, pSmad3, and α-SMA. EW-7197 may be a good alternative for the prevention esophageal stricture formation after corrosive burn.

Prevention Effect of TGF-β Type I Receptor Kinase Inhibitor in Esophageal Stricture Formation after Corrosive Burn

Corrosive burns lead to progressive esophageal stricture and dysphagia. There are many trials to prevent Esophageal stricture formation after corrosive burn. This study aimed to access the effects of EW-7197 on prevention for esophageal stricture formation after corrosive esophageal burn. animal study were classified divided into three groups: a healthy group, a control group (corrosive burn without EW-7197), and a treatment group (corrosive burn with EW-7197). Corrosive esophageal burns were produced using 30% NaOH on the lower esophagus. For 3 weeks, the control group received vehicle and the treatment group received 20 mg/kg/day EW-7197. Treatment efficacy was assessed by measuring the stenosis ratio by esophagogram with contrast media on day 21. histologic staining was performed to evaluate the fibrosis area ratio, and western blotting was performed to evaluate fibrotic markers. Among 20 rats that underwent surgery, 14 survived. Three in the treatment group died because of esophageal perforation, and three in the control group died due to their debilitating status. The esophageal stenosis ratio was significantly lower in the treatment group than in the control group (12.1 ± 9.5% and 42.2 ± 8.3%, respectively; p = 0.001). The histologic fibrosis area ratio was also significantly lower in the treatment group (12.5 ± 3.0% and 21.6 ± 2.1%, respectively; p = 0.001). The treatment group showed lower expressions of profibrogenic proteins such as TGF-β1, pSmad3, and α-SMA. EW-7197 may be a good alternative for the prevention esophageal stricture formation after corrosive burn.

Esophageal Stenosis in a Patient with Breast Cancer after Chemotherapy: A Case Report and Review of Literature

Introduction: Esophageal stenosis after chemotherapy in breast cancer patients is rare. It is important to distinguish esophageal stenosis from esophageal metastasis caused by breast cancer.Case presentation: We present the case of a 62-year-old woman who was diagnosed with breast cancer 4 months prior, had dysphagia and was referred to our department for further treatment after 2 cycles of chemotherapy. She suffered from severe mouth ulcers, painful swallowing and large areas of skin pigmentation with overlying scaliness after every chemotherapy session. Endoscopy revealed that the lumen of the lower esophagus was obviously narrow with ulceration above the stenosis. Histological results demonstrated inflammatory fibrinous necrosis and granulation tissue, with no clear neoplastic component. Conclusion: Short-term esophageal stenosis after chemotherapy may be caused by local mucosal injury, but malignant tumors need to be excluded.

Eosinophilic Esophagitis: Atopy Conditions of the Esophagus

Eosinophilic esophagitis is an immune-allergic pathology of multifactorial etiology(genetic and environmental) characterized by major symptoms of esophagealdysphagia and eosinophil-predominant inflammation of the esophageal mucosathat affects both pediatric and adult patients. EoE is an immune-mediated diseaseby which environmental and food antigens stimulate the Th2 inflammatorycascade. It is correlated with food allergy and atopy condition such as asthma, atopydermatitis, rhinitis allergic and often in conjunction with Gastroesophageal RefluxDisease (GERD). Eosinophilic esophagitis (EoE) was first described in the 1990s,showing an increasing incidence and prevalence since then, in the United States isestimated to be approximately 57 per 100,000 persons being the leading cause offood impaction and the major cause of dysphagia. Its symptoms, which includeheartburn, regurgitation, and esophageal stenosis. This symptomps similar to thoseof gastroesophageal reflux disease, causing delays in diagnosis and treatment. Theendoscopic findings such as furrows, esophageal mucosa trachealization, andwhitish exudates, this diagnosis should be confirmed histologically confirmed bybiopsy on the presence of more than 15 eosinophils per high-power field and theexclusion of other causes of eosinophilia. Management includes medications, diet,and surgical dilatation.