Malaria and Peptic Ulcer Disease: Exploring Potential Pathophysiological Links and Clinical Implications
Jamel Khabat
Department of Biomedical Science, Faculty of Science and Engineering, University of Wolverhampton, Wulfruna Street, Wolverhampton WV1 1LY, UK.
Tunde O. Egunjobi
*
Department of Medical Microbiology, School of Basic Clinical Sciences, College of Health Sciences, Igbinedion University Okada, Edo State, Nigeria and College of Nursing Sciences, Igbinedion University Teaching Hospital, Okada, Edo State, Nigeria.
Imesidayo O. Eboreime-Oikeh
Department of Medicine, College of Health Sciences, Igbinedion University Okada, Edo State, Nigeria.
Daniel O. Ugbomoiko
Department of Medical Laboratory Science, College of Health Sciences, Igbinedion University Okada, Edo State, Nigeria.
Anthony C. Nwaobi
Department of Chemical Pathology, College of Health Sciences, Igbinedion University Okada, Edo State, Nigeria.
Harmony U. Ibezim
Department of Medicine, College of Health Sciences, Igbinedion University Okada, Edo State, Nigeria and Department of Biochemistry, College of Health Sciences, Igbinedion University Okada, Edo State, Nigeria.
*Author to whom correspondence should be addressed.
Abstract
Background: Malaria and peptic ulcer disease (PUD) remain major causes of illness in many tropical and subtropical areas, where both diseases occur in the same populations and share similar epidemiological and socioeconomic factors. Although malaria has traditionally been considered a parasitic disease affecting the whole body, growing evidence shows that its effects go beyond the destruction of red blood cells to involve vascular, inflammatory, and metabolic disturbances that can interfere with the normal function of the gastrointestinal tract. The present review examines the existing evidence regarding the biological relationship between malaria and PUD, with a focus on the mechanisms that may damage the integrity of the gastric mucosa.
Methods: A structured narrative review was conducted using peer-reviewed publications indexed in PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar between January 2000 and March 2026. Experimental, observational, clinical, and translational studies addressing malaria pathophysiology, gastric mucosal injury, Helicobacter pylori infection, oxidative stress, endothelial dysfunction, intestinal barrier impairment, gut microbiota alterations, and antimalarial therapy were assessed and incorporated into a mechanistic framework.
Results: The available evidence shows that malaria can affect mucosal homeostasis through several closely linked biological pathways. These pathways involve the sequestration of parasitised erythrocytes in the microvasculature, activation of the endothelium, reduced tissue perfusion, the release of inflammatory cytokines, oxidative stress, depletion of nitric oxide associated with haemolysis, and tissue hypoxia resulting from anaemia.
Conclusion: The available evidence indicates a biologically plausible interaction between malaria and peptic ulcer disease rather than establishing a definite causal link. This review, by combining results from the fields of vascular biology, immunology, gastroenterology, oxidative stress research, and microbiome science, offers a comprehensive mechanistic view that could enhance understanding of the gastrointestinal complications associated with malaria.
Keywords: Malaria, peptic ulcer disease, Plasmodium falciparum, gastric mucosa, oxidative stress, endothelial dysfunction, inflammation, Helicobacter pylori