Pelin Ergun, Sezgi Kipcak, Nur S Gunel, Serhat Bor, and Eser Y Sozmen. J Neurogastroenterol Motil 2024;30:290-302. https://doi.org/10.5056/jnm22186

Barrett’s esophagus (BE) is a disease entity that is a sequela of chronic gastroesophageal reflux disease that may result in esophageal adenocarcinoma (EAC) due to columnar epithelial dysplasia. The histological degree of dysplasia is the sole biomarker frequently utilized by clinicians. However, the cost of endoscopy and the fact that the degree of dysplasia does not progress in many patients with BE diminish the effectiveness of histological grading as a perfect biomarker. Multiple or more quantitative biomarkers are required by clinicians since early diagnosis is crucial in esophageal adenocancers, which have a high mortality rate. The presence of epigenetic factors in the early stages of this neoplastic transformation holds promise as a predictive biomarker. In this review, current studies on DNA methylations, histone modifications, and noncoding RNAs (miRNAs) that have been discovered during the progression from BE dysplasia to EAC were collated.

Goal: The aim of this study was to investigate the pepsin values and pH results of gastric juice among the subtypes of gastroesophageal reflux disease (GERD) and functional heartburn. Background: The major destructive agents of GERD on the esophageal epithelium are gastric acid and pepsin. No precise information about pepsin concentration in gastric juice exists. Study: Ninety patients with GERD, 39 erosive reflux disease (ERD) Los Angeles (LA) grade A/B, 13 ERD LA grade C/D, 19 nonerosive reflux disease (NERD), 8 esophageal hypersensitivity, 11 functional heartburn, and 24 healthy controls were included in the study. During endoscopy gastric juices from the patients were aspirated and their pH readings immediately recorded. Gastric juice samples were analyzed using Peptest, a lateral flow device containing 2 unique human monoclonal antibodies to detect any pepsin present in the gastric juice sample. Results: The highest mean gastric pepsin concentration (0.865 mg/mL) and the lowest median gastric pH (1.4) was observed in the LA grade C/D group compared with the lowest mean gastric pepsin concentration (0.576 mg/mL) and the highest median gastric pH (2.5) seen in the NERD group. Comparing pH, the NERD patient group was significantly higher (P=0.0018 to P=0.0233) when compared with all other GERD patient groups. Conclusions: The basal gastric pepsin level in the healthy control group was comparable to literature values. There was good correlation and a significant linear relationship between the gastric pepsin level and gastric pH within the patient groups. The severity of the GERD disease is related to the lowest pH and the highest pepsin concentration in gastric juice.

Introduction: Maffucci’s syndrome (MS) is a congenital non-hereditary mesodermal dysplasia characterised by numerous mesenchymal neoplasias in the form of enchondromas with secondary bone deformities and multiple soft tissue haemangiomas that may have phlebolitis. Clinical Picture: A 23-year-old male patient presented with non-productive cough, dyspnoea, chest pain and back pain. Chest X-ray showed unilateral pleural effusion and multiple enchondromas of the ribs. On physical examination, there were mobile, multiple, bluish-coloured lesions probably cavernous haemangiomas on bilateral chest walls. In addition, there were multiple nodular lesions on the extremities especially accumulated on the fingers. The patient was diagnosed as Maffucci’s syndrome according to computed tomography (CT) of the thorax, conventional radiography of the skeletal system, magnetic resonance (MR) imaging, Th4-Th11 intercostal and right upper extremity angiography and physical examination findings. Treatment: As the patient rejected any diagnostic intervention, he was monitored with CT. Outcome: During the last 6 years of follow-up, the lesion that was detected on the rib adjacent to the basal segments of the left lung showed significant progression and was accepted as chondrosarcoma. Conclusion: To our knowledge, this is the first case of Maffucci’ s syndrome with pleural effusion. In this case report, the probable mechanism of pleural effusion was discussed.

Breakthrough symptoms are thought to occur in roughly half of all gastroesophageal reflux disease (GERD) patients despite maximal acid suppression (proton pump inhibitor, PPI) therapy. Topical alginates have recently been shown to enhance mucosal defense against acid-pepsin insult during GERD. We aimed to examine potential alginate protection of transcriptomic changes in a cell culture model of PPI-recalcitrant GERD. Immortalized normal-derived human esophageal epithelial cells underwent pretreatment with commercial alginate-based anti-reflux medications (Gaviscon Advance or Gaviscon Double Action), a matched-viscosity placebo control, or pH 7.4 buffer (sham) alone for 1 min, followed by exposure to pH 6.0 + pepsin or buffer alone for 3 min. RNA sequencing was conducted, and Ingenuity Pathway Analysis was performed with a false discovery rate of ≤0.01 and absolute fold-change of ≥1.3. Pepsin-acid exposure disrupted gene expressions associated with epithelial barrier function, chromatin structure, carcinogenesis, and inflammation. Alginate formulations demonstrated protection by mitigating these changes and promoting extracellular matrix repair, downregulating proto-oncogenes, and enhancing tumor suppressor expression. These data suggest molecular mechanisms by which alginates provide topical protection against injury during weakly acidic reflux and support a potential role for alginates in the prevention of GERD-related carcinogenesis.