Randomized Controlled Trial
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World J Gastroenterol. Sep 14, 2014; 20(34): 12308-12312
Published online Sep 14, 2014. doi: 10.3748/wjg.v20.i34.12308
Helicobacter pylori infection in Mongolian gerbils does not initiate hematological diseases
Chuan Xie, Li-Yao Xu, Wei Li, Zhen Yang, Nong-Hua Lu
Chuan Xie, Li-Yao Xu, Wei Li, Zhen Yang, Nong-Hua Lu, Department of Gastroenterology, the First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China
Author contributions: Xie C, Xu LY, Li W, Yang Z and Lu NH designed the study; Xie C, Xu LY and Li W performed the study; Xie C and Yang Z analyzed the data; Xie C and Lu NH wrote the paper.
Supported by National Natural Science Foundation of China, No. 81060038 and No. 81270479; Grants from Jiangxi Province Talent 555 Project; National Science and Technology Major Projects for “Major New Drug Innovation and Development” of China, No. 2011ZX09302-007-03; and Graduate Innovative Foundation of Jiangxi Province, China, No. YC2013-B004
Correspondence to: Nong-Hua Lu, MD, Department of Gastroenterology, the First Affiliated Hospital of Nanchang University, No. 17, Yongwaizheng Street, Nanchang 330006, Jiangxi Province, China. lunonghua@ncu.edu.cn
Telephone: +86-791-88692706 Fax:+86-791-886223153
Received: March 5, 2014
Revised: April 14, 2014
Accepted: May 26, 2014
Published online: September 14, 2014
Processing time: 197 Days and 9.5 Hours
Abstract

AIM: To investigate whether Helicobacter pylori (H. pylori) infection contributes to idiopathic thrombocytopenic purpura (ITP) or iron-deficiency anemia (IDA) onset in gerbils.

METHODS: A total of 135 Mongolian gerbils were randomly divided into two groups: an H. pylori infection group and a control group. Both groups were fed the same diet and the same amount of food. Each group was then divided into three subgroups, which were sacrificed at 6, 12, or 18 mo for analysis. At each time point, arterial blood was collected from the abdominal aorta and a complete blood cell count was analyzed in the clinical laboratory in the First Affiliated Hospital of Nanchang University.

RESULTS: There were no significant differences in platelet counts (938.00 ± 270.27/L vs 962.95 ± 162.56 × 109/L), red blood cell counts (8.11 ± 1.25/L vs 8.44 ± 1.48 × 1012/L), or hemoglobin levels (136.9 ± 8.76 g/L vs 123.21 ± 18.42 g/L) between the control and the H. pylori groups, respectively, at 18 mo. With the exception of the mean corpuscular volume (MCV), all other indicators, including white blood cell counts, hematocrit, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, red blood cell distribution width, mean platelet volume, platelet distribution width, lymphocyte count, and lymphocyte count percentage, showed no significant differences between the control and H. pylori infection groups at each time point. The MCV in the H. pylori infection group (52.32 f/L ± 2.86 f/L) was significantly lower than the control group (55.63 ± 1.89 f/L) at 18 mo (P = 0.005), though no significant differences were observed at 6 (54.40 ± 2.44 f/L vs 53.30 ± 1.86 f/L) or 12 mo (53.73 ± 2.31 f/L vs 54.80 ± 3.34 f/L).

CONCLUSION: A single H. pylori infection is insufficient to cause onset of ITP or IDA and other factors may be required for disease onset.

Keywords: Helicobacter pylori; Extragastric diseases; Idiopathic thrombocytopenic purpura; Iron-deficiency anemia; Chronic inflammation

Core tip: This is the first study designed to investigate the relationship between Helicobacter pylori (H. pylori) infection and idiopathic thrombocytopenic purpura (ITP) and iron-deficiency anemia (IDA) hematological diseases in a Mongolian gerbil model. Although there were no significant differences between the H. pylori infection and control groups, this study may help us better understand the relationships between H. pylori and extragastric diseases. While a single H. pylori infection is not sufficient to cause ITP or IDA, the precise role of H. pylori infection in extragastric disease pathogenesis remains to be further elucidated.