Thalassemia, a genetic condition characterized by defective hemoglobin synthesis, is often managed with transfusion therapy, which can lead to iron overload—a significant contributor to morbidity and mortality due to organ damage and pathogenic infections. Iron chelation therapy, the cornerstone of managing iron toxicity, may inadvertently influence the gut microbiome, a critical modulator of immunity and metabolism. This review provides new insights into the interplay between iron chelation therapy and gut microbiome dynamics in thalassemia patients. It synthesizes findings on how chelators such as deferoxamine, deferasirox, and deferiprone influence microbial composition, iron availability, and systemic inflammation. Emerging evidence highlights alterations in gut microbial diversity, with reduced beneficial taxa and increased pathogenic populations, driven by changes in luminal iron levels. This imbalance contributes to immune dysregulation, systemic inflammation, and susceptibility to infections. The review advocates for tailored treatment strategies that integrate microbiome-targeted interventions alongside traditional chelation therapy to improve patient outcomes. By combining genetic profiling, dietary adjustments, and microbiome modulation, this approach offers a promising avenue for personalized medicine in thalassemia care.

Enteric viruses are commonly found obligate parasites in the gastrointestinal (GI) tract. These viruses usually follow a fecal-oral route of transmission and are characterized by their extraordinary stability as well as resistance in high-stress environments. Most of them cause similar symptoms including vomiting, diarrhea, and abdominal pain. In order to come in contract with mucosal surfaces, these viruses need to pass the three main lines of defense: mucus layer, innate immune defenses, and adaptive immune defenses. The following atypical gastrointestinal infections are discussed: SARS-CoV2, hantavirus, herpes simplex virus I, cytomegalovirus, and calicivirus. Dysbiosis represents any modification to the makeup of resident commensal communities from those found in healthy individuals and can cause a patient to become more susceptible to bacterial and viral infections. The interaction between bacteria, viruses, and host physiology is still not completely understood. However, with growing research on viral infections, dysbiosis, and new methods of detection, we are getting closer to understanding the nature of these viruses, their typical and atypical characteristics, long-term effects, and mechanisms of action in different organ systems.

In recent years, it has been shown that gastrointestinal microflora has a substantial impact on the development of a large number of chronic diseases. The imbalance in the number or type of microbes in the gastrointestinal tract can lead to diseases and conditions, including autism spectrum disorder, celiac disease, Crohn’s disease, diabetes, and small bowel cancers. This can occur as a result of genetics, alcohol, tobacco, chemotherapeutics, cytostatics, as well as antibiotic overuse. Due to this, essential taxa can be lost, and the host’s metabolism can be severely affected. A less known condition called small intestine bacterial overgrowth (SIBO) can be seen in patients who suffer from hypochlorhydria and small intestine cancers. It is characterized as a state in which the bacterial population in the small intestine exceeds 105–106 organisms/mL. The latest examination methods such as double-balloon enteroscopy and wireless capsule endoscopy have the potential to increase the accuracy and precision of diagnosis and provide better patient care. This review paper aims to summarize the effect of the gastrointestinal environment on chronic disease severity and the development of cancers.

Celiac Disease (CD) represents an immune-mediated disorder that involves the body’s inability to digest gluten prop-erly. After contact with gluten, patients of all ages might experience symptoms such as bloating, diarrhea, gas, growth issues