The bacteria seen in the stomach's inner lining known as H. PYLORI was discovered in 1982. It's widespread globally, infecting over half of the world's population, particularly in areas with poor sanitation [1]. H. PYLORI can cause gastritis (inflammation of the stomach lining), and peptic ulcers, and is a significant risk factor for stomach cancer. H. PYLORI causes various diseases through several distinct mechanisms. Initial infection typically results in chronic gastritis due to immune responses and bacterial toxins like VacA and CagA, which damage the stomach lining [2]. This chronic inflammation can progress to peptic ulcers, where H. PYLORI weakens the mucous barrier of the stomach, allowing acid and digestive juices to create sores. Long-term infection with virulent strains increases the risk of gastric cancer by inducing persistent inflammation and genetic mutations in stomach cells [3]. Additionally, H. PYLORI infection is linked to the development of MALT lymphoma, a type of lymphoma originating from mucosal lymphoid tissue stimulated by chronic inflammation [4]. These diseases represent a spectrum of H. PYLORI-related pathologies, each driven by the bacterium's ability to adhere to gastric epithelial cells, evade immune detection, produce toxins that disrupt cell function, and induce prolonged inflammation in the stomach lining. Understanding these pathogenic pathways is crucial for effective management and treatment strategies against H. PYLORI-associated diseases [5]. Common symptoms of H. PYLORI infection include a burning sensation or discomfort in the upper abdomen, bloating, frequent burping, and loss of appetite, which can lead to weight loss. Nausea, vomiting, indigestion, and heartburn are also frequent. In severe cases, the infection may cause peptic ulcers, leading to persistent abdominal pain, vomiting blood, or passing dark, tarry stools, indicating significant damage to the stomach lining or upper gastrointestinal tract [6]. H. PYLORI can be diagnosed using non-invasive tests like the urea breath test, stool antigen test, and serology, or invasive methods such as endoscopy with biopsy followed by rapid urease test, histology, culture, and PCR. Non-invasive tests are less intrusive, while invasive tests provide direct evidence from biopsy samples and allow for further analysis like antibiotic susceptibility testing [7]. The global prevalence of H. PYLORI in adults has dropped from 52.6 % before 1990 to 43.9 % between 2015 and 2022. However, it remains high in children and adolescents at 35.1 % during the same period. A significant decline of 15.9 % in H. PYLORI prevalence was noted in adults over the past 30 years, particularly in the Western Pacific, Southeast Asia, and Africa, but not in younger populations [8].