Erosive Esophagitis (EE) is the most common complication of gastroesophageal reflux disease. Patients with EE can be asymptomatic or present with severe symptoms such as dysphagia and gastrointestinal bleeding. Approximately 10-15% of patients with EE have refractory disease. Optimal management of EE requires understanding its pathophysiology, clinical presentation, and available evaluation and treatment modalities. While pharmacologic treatment of EE is often successful, procedural options such as surgery and endoscopic therapy may be necessary. This article presents an evidence-based and pragmatic approach to the management of EE, the most common complication of gastroesophageal reflux disease.

Inflammatory bowel disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract and is primarily referred to as ulcerative colitis and Crohn’s disease. As the number of patients suffering from IBD increases, diagnosis and treatment have become pressing yet challenging tasks. A major challenge is that patients with IBD do not exhibit characteristic symptoms, making it difficult to differentiate between IBD and other intestinal abnormalities. Endoscopy is the most conventional method used to diagnose IBD; however, this method is invasive and expensive. Therefore, affordable non-invasive techniques need to be developed for diagnosing IBD, highlighting the need to identify biomarkers specific to the disease. It is now established that the gut microbiome contributes significantly in the development of IBD, and changes in the abundance of various organisms in the gut have been widely explored to identify microbial signatures associated with IBD. This review discusses the current state of knowledge on biomarkers in IBD, with a primary focus on the gut microbiome, associated metabolic signatures, and their links with immunological biomarkers. These biomarkers can help propose an integrative model to better understand the pathophysiology of this complex disease. This integrated approach will also provide insights into potential therapeutic targets for designing appropriate treatment strategies for patients.

This study investigates upper gastrointestinal tract (UGIT) involvement in patients with ulcerative colitis (UC), a condition traditionally considered limited to the colon. Although extra-colonic manifestations of UC are well recognized, UGIT issues have received less attention. This research aimed to document the clinical, endoscopic, and histopathological UGIT findings in adults with UC and assess their association with disease severity and extent.

This descriptive cross-sectional study was conducted at Ain Shams University over one year. A total of 78 UC patients underwent comprehensive clinical evaluations, including assessments of gastrointestinal complaints, medication history, disease progression, surgeries, and physical examinations. Endoscopic assessments of both the UGIT and colon were performed, accompanied by biopsies for histopathological analysis.

The study population had a mean age of 35.26 years, with a nearly equal gender distribution. Endoscopic findings revealed significant UGIT involvement: 64% of patients had esophagitis and/or gastroesophageal reflux disease, 93% had gastritis, and 80% had duodenitis. Histopathological findings showed notable inflammation, basal cell hyperplasia, and ulcerations in the esophagus, with 51.3% of patients exhibiting chronic gastritis and 38.5% testing positive for Helicobacter pylori infection. Statistical analysis demonstrated a strong association between colonic disease severity and UGIT endoscopic (p < 0.0001 and p < 0.001 in the esophagus and stomach, respectively) and histopathological (p < 0.004, p < 0.001, and p <0.005 in the esophagus, stomach, and duodenum, respectively) findings, particularly in patients with UGIT symptoms.

This study concludes that UGIT endoscopic and histopathological changes are prevalent among Egyptian UC patients, suggesting a significant link between UC and these UGIT findings.

Gluten has multiple harmful effects that compromise human health, not only in gluten-dependent diseases but also in non-gluten-affected chronic inflammatory conditions. After consumption, the indigestible gluten peptides are modified by luminal microbial transglutaminase or transported through the gut epithelium to interact with the highly populated mucosal immune cells. As a disruptor of gut permeability, gluten peptides compromise tight junction integrity, allowing foreign immunogenic molecules to reach internal compartments. Gliadin peptides are distributed systemically to remote organs, where they encounter endogenous tissue transglutaminase. Following post-translational deamidation or transamidation, the peptides become immunogenic and pro-inflammatory, inducing organ dysfunction and pathology. Cross-reactivity and sequence homology between gluten/gliadin peptides and human epitopes may contribute to molecular mimicry in autoimmunity induction. A gluten-free diet can prevent these phenomena through various mechanisms. As proof of concept, gluten withdrawal alleviates disease activity in chronic inflammatory, metabolic, and autoimmune conditions, and even in neurodegeneration. We recommend combining the gluten-free and Mediterranean diets to leverage the advantages of both. Before recommending gluten withdrawal for non-gluten-dependent conditions, patients should be asked about gut symptomatology and screened for celiac-associated antibodies. The current list of gluten-induced diseases includes celiac disease, dermatitis herpetiformis, gluten ataxia, gluten allergy, and non-celiac gluten sensitivity. In view of gluten being a universal pro-inflammatory molecule, other non-celiac autoinflammatory and neurodegenerative conditions should be investigated for potential gluten avoidance.

The gastrointestinal microbiome remains an explosively increasing topic of study, assessing the potentially pivotal roles of the microbiome in maintaining health or causality in disease pathogenesis. Gastroesophageal reflux disease (GERD) has long been understood to be a result of direct acidic injury. However, emerging evidence suggests that GERD could also be caused by alterations in the esophageal microbiome, causing an induction of a submucosal inflammatory cytokine cascade, that has a retrograde effect on the luminal mucosa. This concept of a microbial shift/dysbiosis in the causality of GERD is clearly a paradigm shift and has led to possible treatment strategies beyond the traditional approach of acid-suppressive therapies. This review focuses on the current evidence surrounding GERD and the rationale for possible esophageal microbiome-directed treatment strategies.

Obesity is a complex disease resulting from excessive adipose tissue in the body, leading to various metabolic, mechanical, and psychological complications. The prevalence of obesity has increased exponentially in the past few decades to reach an epidemic proportion. Obesity can predispose to or aggravate the fatty liver. Metabolic dysfunction-associated fatty liver disease (MAFLD) represents fatty liver in individuals who are either overweight/obese, or have type 2 diabetes, or have normal weight with at least two metabolic risk factors. MAFLD pathogenesis is multifactorial and involves an interplay of genetics, lifestyle-related factors, gut dysbiosis, lipotoxicity, and oxidative stress. Besides hepatic complications, MAFLD also has systemic implications in the form of increased risk for various metabolic diseases, cardiovascular diseases, malignancies, and infectious diseases. If left untreated, MAFLD can progress to liver cirrhosis and end-stage liver disease. Many noninvasive strategies like serum-based markers and imaging help diagnose MAFLD at an early stage. Timely detection and appropriate intervention are crucial for preventing its progression to advanced liver disease and hepatocellular carcinoma. Though lifestyle modification remains the main pillar of management, with advances in the treatment of obesity, newer agents are being tried for patients with MAFLD. The current therapeutic strategies are limited, and future research is needed to identify the subset of patients with MAFLD who are at a higher risk of hepatic and systemic complications and to develop more effective and personalized therapies.