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©The Author(s) 2020.
World J Gastroenterol. Jul 28, 2020; 26(28): 4076-4093
Published online Jul 28, 2020. doi: 10.3748/wjg.v26.i28.4076
Published online Jul 28, 2020. doi: 10.3748/wjg.v26.i28.4076
Table 1 Non-gastric manifestations of Helicobacter pylori and their suggested mechanisms of pathophysiology
Non-gastric manifestation | Mechanisms of pathology suggested to be correlated | |
Allergic diseases | Hygiene hypothesis[9,96] | |
Alzheimer’s disease | Vitamin B12 deficiency leading to increased concentrations of homocysteine[109] | |
Anormal hyperphosphorylation of the TAU protein caused by H. pylori infection[109] | ||
ApoE polymorphism[110] | ||
Asthma | Treg pattern, suppressing Th-2-mediated allergic response[94] | |
Atherosclerosis and myocardial infarction | Stimulation of foam production inside macrophages, contributing to the magnification of the atherosclerotic plaque and arterial dysfunction[122] | |
B12 deficiency | Still to be clarified, but proven to be independent of gastric atrophy and bleeding that impair their dietary absorption[49] | |
Cholelithiasis | Presence of H. pylori infected bile[43,44] | |
Coronary arterial disease/systemic arterial stiffness | Increased levels of homocysteine[132]. | |
Gastroesophageal reflux disease | Hyperacidity[25] | |
Diabetes mellitus | Increased cytokine production; phosphorylation of serine residues from the insulin receptor substrate[136] | |
Hepatic carcinoma | Inflammatory, fibrotic and, consequently, necrotic process[37,38] | |
Idiopathic thrombocytopenic purpura (ITP) | CagA may stimulate the synthesis of anti-CagA antibodies that cross-react with platelet surface antigens causing ITP[74,75] | |
Inflammatory bowel disease | Reduced intestinal inflammation through release of IL-18 and development of FoxP3-positive regulatory T cells[16-18] | |
Neutrophil-activating protein reducing inflammation through Toll-like receptor 2 and IL-10 stimulation[19,20] | ||
Iron deficiency anemia | Still to be clarified, but proven to be independent of gastric atrophy and bleeding that impair their dietary absorption[49] | |
Relationship with growth disorders in children[52,53] | ||
Multiple sclerosis | Hygiene hypothesis[9] | |
Inhibitory induction of H. pylori over the Th1 and Th17 immune response[103] | ||
Non-alcoholic fatty liver disease | H. pylori induced insulin resistance[32] | |
Reduced production of adiponectin[33] | ||
Liver inflammation[34,35] | ||
Ophthalmic manifestations | Systemic inflammatory status; increased oxidative stress; mitochondrial dysfunction; damage to DNA[82] | |
Parkinson’s disease | Increased synthesis of 1-methyl-4-phenyl-1,2,36-tetrahydropyridine[118] | |
Reduced levodopa absorption[118] |
- Citation: Santos MLC, de Brito BB, da Silva FAF, Sampaio MM, Marques HS, Oliveira e Silva N, de Magalhães Queiroz DM, de Melo FF. Helicobacter pylori infection: Beyond gastric manifestations. World J Gastroenterol 2020; 26(28): 4076-4093
- URL: https://www.wjgnet.com/1007-9327/full/v26/i28/4076.htm
- DOI: https://dx.doi.org/10.3748/wjg.v26.i28.4076