Dietary Composition Influences Incidence of Helicobacter pylori-Induced Iron Deficiency Anemia and Gastric Ulceration.
Epidemiologic studies have provided conflicting data regarding an association between Helicobacter pylori infection and iron deficiency anemia (IDA) in humans. Here, a Mongolian gerbil model was used to investigate a potential role of H. pylori infection, as well as a possible role of diet, in H. pylori-associated IDA. Mongolian gerbils (either H. pylori infected or uninfected) received a normal diet or one of three diets associated with increased H. pylori virulence: high-salt, low-iron, or a combination of a high-salt and low-iron diet. In an analysis of all infected animals compared to uninfected animals (independent of diet), H. pylori-infected gerbils had significantly lower hemoglobin values than their uninfected counterparts at 16 weeks postinfection (P < 0.0001). The mean corpuscular volume (MCV) and serum ferritin values were significantly lower in H. pylori-infected gerbils than in uninfected gerbils, consistent with IDA. Leukocytosis and thrombocytosis were also detected in infected gerbils, indicating the presence of a systemic inflammatory response. In comparison to uninfected gerbils, H. pylori-infected gerbils had a higher gastric pH, a higher incidence of gastric ulcers, and a higher incidence of fecal occult blood loss. Anemia was associated with the presence of gastric ulceration but not gastric cancer. Infected gerbils consuming diets with a high salt content developed gastric ulcers significantly more frequently than gerbils consuming a normal-salt diet, and the lowest hemoglobin levels were in infected gerbils consuming a high-salt/low-iron diet. These data indicate that H. pylori infection can cause IDA and that the composition of the diet influences the incidence and severity of H. pylori-induced IDA.
Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Amber C
AC
Beckett
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
M Blanca
MB
Piazuelo
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Jennifer M
JM
Noto
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Richard M
RM
Peek
Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
M Kay
MK
Washington
Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.|Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.|Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee, USA.
Holly M Scott
HM
Algood
Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA timothy.l.cover@vanderbilt.edu.|Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.|Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee, USA.
Timothy L
http://orcid.org/0000-0001-8503-002X
TL
Cover
D018798:Anemia, Iron-Deficiency / Q000209:etiology* / Q000517:prevention & control; D000821:Animal Feed / Q000032:analysis*; D000818:Animals; D004032:Diet; D005849:Gerbillinae; D016481:Helicobacter Infections / Q000150:complications* / Q000382:microbiology; D016480:Helicobacter pylori / Q000472:pathogenicity*; D007249:Inflammation / Q000209:etiology / Q000473:pathology; D013276:Stomach Ulcer / Q000382:microbiology* / Q000517:prevention & control