Metabolic consequences of Helicobacter pylori infection and eradication.
Helicobacter pylori (H. pylori) is still the most prevalent infection of the world. Colonization of the stomach by this agent will invariably induce chronic gastritis which is a low-grade inflammatory state leading to local complications (peptic ulcer, gastric cancer, lymphoma) and remote manifestations. While H. pylori does not enter circulation, these extragastric manifestations are probably mediated by the cytokines and acute phase proteins produced by the inflammed mucosa. The epidemiologic link between the H. pylori infection and metabolic changes is inconstant and controversial. Growth delay was described mainly in low-income regions with high prevalence of the infection, where probably other nutritional and social factors contribute to it. The timely eradication of the infection will lead to a more healthy development of the young population, along with preventing peptic ulcers and gastric cancer An increase of total, low density lipoprotein and high density liporotein cholesterol levels in some infected people creates an atherogenic lipid profile which could promote atherosclerosis with its complications, myocardial infarction, stroke and peripheral vascular disease. Well designed and adequately powered long-term studies are required to see whether eradication of the infection will prevent these conditions. In case of glucose metabolism, the most consistent association was found between H. pylori and insulin resistance: again, proof that eradication prevents this common metabolic disturbance is expected. The results of eradication with standard regimens in diabetics are significantly worse than in non-diabetic patients, thus, more active regimens must be found to obtain better results. Successful eradication itself led to an increase of body mass index and cholesterol levels in some populations, while in others no such changes were encountered. Uncertainities of the metabolic consequences of H. pylori infection must be clarified in the future.
György Miklós Buzás, Department of Gastroenterology, Ferencváros Health Centre, 1095 Budapest, Hungary.
György Miklós
GM
Buzás
D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000453:epidemiology / Q000382:microbiology; D050171:Dyslipidemias / Q000097:blood* / Q000453:epidemiology / Q000382:microbiology; D016481:Helicobacter Infections / Q000097:blood* / Q000188:drug therapy* / Q000453:epidemiology / Q000382:microbiology; D016480:Helicobacter pylori / Q000187:drug effects* / Q000254:growth & development; D054884:Host-Pathogen Interactions; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D024821:Metabolic Syndrome / Q000097:blood* / Q000453:epidemiology / Q000382:microbiology; D012307:Risk Factors; D016896:Treatment Outcome
D000900:Anti-Bacterial Agents; D001786:Blood Glucose; D018836:Inflammation Mediators; D008055:Lipids
Cytokines; Diabetes mellitus; Glucose homeostasis; Growth; Helicobacter pylori; Interleukins; Lipid metabolism; Metabolic syndrome