Background/Aim: H. pylori infection can promote a systemic inflammatory syndrome, eventually leading to intestinal metaplasia and gastric cancer. The aim of our study was to investigate the possible association between dyslipidemia and histopathological features of H. pylori gastritis. Patients and Methods: An observational, retrospective study was conducted over the period 2017-2022 on symptomatic patients with a positive rapid urease test. A total of 121 patients who underwent upper gastrointestinal endoscopy with stomach biopsy were enrolled in this study. Based on the updated Sydney System, we investigated the association between neutrophils, mononuclear cells, intestinal metaplasia, or gastric atrophy and altered lipid profiles. Results: A high prevalence of H. pylori infection was noticed in the studied group upon the application of the rapid urease test, being associated with dyslipidemia regardless of patient sex. All the endoscopic diagnoses (acute, chronic, or atrophic chronic gastritis, metaplasia) correlated with the histopathological features. Mononuclear cells and metaplasia were more likely to be found in H. pylori-positive patients with dyslipidemia, which is consistent with acute and chronic inflammation caused by H. pylori in the gastric mucosa. Conclusion: Although our study was conducted on a small scale, it offers new insights and details regarding H. pylori infection and histopathological features. Mononuclear cells and metaplasia were associated with an altered lipid profile in H. pylori-positive patients. These findings warrant future investigation, such as the evolution of gastric biopsies and lipid profiles before and after eradication. H. pylori is a genetically diversified pathogen with a constrained host and target organ range (1). It is estimated that 50% of the world's population is infected with H. pylori (2). The percentage is lower in developed countries and higher in developing ones, and it is more frequent in men than in women (3). It is a gram-negative bacterium that causes chronic gastritis, peptic ulcers, and stomach cancer (4, 5). Chronic and ongoing inflammation caused by H. pylori infection leads to the production of cytokines, such as tumor necrosis factor, interleukin (IL)-6, and IL-8 (6, 7). Consequently, a chronic inflammatory syndrome and extragastric diseases may develop, including non-alcoholic fatty liver disease, dyslipidemia, and coronary heart disease (8)(9)(10)(11). By preventing the release of pro-inflammatory cytokines, H. pylori eradication therapy may improve lipid profiles in patients with dyslipidemia (12-14). In addition, H. pylori chronic inflammation may prevent proper lipid absorption (15). Furthermore, more changes in the metabolism of lipids and lipoproteins, induced by this infection, may allow transfer of nutrients to cells, which is crucial for tissue healing or host defense (16). Since H. pylori cannot produce cholesterol on its own, it must obtain exogenous cholesterol from the host (17). Glycosylated cholesterol (8), a significant constituent...