Barrett’s esophagus (BE) is a premalignant lesion that can develop into esophageal adenocarcinoma (EAC). The development of Barrett’s esophagus is caused by biliary reflux, which causes extensive mutagenesis in the stem cells of the epithelium in the distal esophagus and gastro-esophageal junction. Other possible cellular origins of BE include the stem cells of the mucosal esophageal glands and their ducts, the stem cells of the stomach, residual embryonic cells and circulating bone marrow stem cells. The classical concept of healing a caustic lesion has been replaced by the concept of a cytokine storm, which forms an inflammatory microenvironment eliciting a phenotypic shift toward intestinal metaplasia of the distal esophagus. This review describes the roles of the NOTCH, hedgehog, NF-κB and IL6/STAT3 molecular pathways in the pathogenesis of BE and EAC.

Eosinophilic esophagitis (EoE) is an immune-mediated disease that presents with dysphagia and esophageal bolus obstruction and is characterized by predominant intraepithelial eosinophilic infiltration at histology. The aim of our literature review was to delineate clinical and morphological EoE features in terms of differential diagnosis with other esophageal diseases, i.e., gastroesophageal reflux disease (GERD), inflammatory bowel diseases (IBDs), autoimmune diseases, and rare esophageal disorders. Clinical features of dysphagia and esophageal bolus obstruction and endoscopic criteria (according to EREFS) are typical of EoE. Nevertheless, eosinophilia of the esophageal mucosa is not a specific marker of mucosal injury and is not sufficient for EoE diagnosis. Therefore, eosinophilic esophagitis histological scoring system (EoEHSS) was developed. It involves assessment of intraepithelial eosinophilic infiltration, basal zone hyperplasia, eosinophilic abscesses, eosinophil surface layering, dilated intercellular spaces, surface epithelial alteration, dyskeratotic epithelial cells, and lamina propria fibrosis. Complex clinical, endoscopic, and histological evaluation allows accurate diagnosis of EoE and other causal factors of esophageal eosinophilia. Keywords: eosinophilic esophagitis, esophageal eosinophilia, gastroesophageal reflux disease, celiac disease, inflammatory bowel diseases, achalasia, atopy

Патоморфологические и молекулярно-генетические особенности диффузного типа рака желудка

Since inflammatory diseases and precancerous lesions of esophagus require clinico-morphological diagnostics, it includes histological verification of endoscopic lesions in line with specific protocols of biopsy taking according to endoscopic findings and expected diagnosis. This review elucidates pathogenesis of gastroesophageal reflux disease (GERD) specter and focuses on detailed features of histologic diagnostics of Barrett’s esophagus and Barrett’s dysplasia. Precise histologic diagnosis in this group of patients implies appropriate treatment and defines prognosis.

Introduction. Cystic fibrosis is a severe systemic multiorgan exocrinopathy, the severity of the condition in 95% cases is caused by the depth of respiratory organ damage. Symptom management drugs that were developed over more than 50 years allowed to improve survival, but average life expectancy in cystic fibrosis (CF) remains well below the general population average. Targeted therapy is the most promising treatment, which restores the chloride channel function. Lumacaftor/ivacaftor is the first targeted therapy drug authorized in Russia.Aim. To evaluate the effect of lumacaftor/ivacaftor therapy on the respiratory function, microbiological profile, nutritional and oxygen status, as well as the rescue antibiotic therapy coverage in adult patients with CF.Materials and methods. 39 adult patients with CF received lumacaftor/ivacaftor for one year. The therapy effectiveness endpoints included the changes in indices of the pulmonary function tests: FEV₁, FVC, FEV₁/FVC, sweat test results, nutritional and oxygen status, antibiotic therapy coverage. The tolerability of the drug was assessed. The median age of patients was 28.9 (11.3) years. 6 patients (15.4%) discontinued therapy due to different adverse reactions.Results. The median increase in FVC was 2.9 (4.1)%, in FEV₁ – 3.1 (4.1)%, sweat chloride decreased by 21 (27) mmol/l during 1–1.5-month lumacaftor/ivacaftor therapy. After 12-month therapy, the median increase in FVC was 2.3 (3.6)%, in FEV₁ – 2.4 (3.8)%, BMI increased by 0.6 (0.6) kg/m² and the frequency of rescue antibiotic therapy decreased by half. The patients showed a significant increase in FVC and FEV¹ indices and a decrease in sweat chloride after 1-month therapy and an increase in FEV₁ indices, BMI vales as well as a reduced need for rescue antibiotic therapy after 12-month therapy.Conclusion. The first experience with a long-term pathogenetic therapy with lumacaftor/ivacaftor in adult patients with CF in Russia demonstrated the expected positive effect on the respiratory function and changes in nutritional status, a reduced need for rescue antibiotic therapy, and low rates of adverse reactions.

The anatomy of the male mammary gland, both normal and pathological, has not been sufficiently described. Male breast cancer is a rare pathology and presents a particular scientific interest to pathologists, geneticists, and clinicians. Due to its rare occurrence, there are few studies describing clinical and laboratory aspects, and even less research focuses on pathomorphological tissue examination of the affected male mammary gland. The article presents a clinical case of male breast cancer in a deceased elderly patient, which was detected on autopsy examination. Keywords: mamma virilis, elderly patient, normal anatomy, pathological anatomy, immunohistochemical diagnosis