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Lactoferrin sequestration and its contribution to iron-deficiency anemia in Helicobacter pylori-infected gastric mucosa
被引:46
作者:
Choe, YH
Oh, YJ
Lee, NG
Imoto, I
Adachi, Y
Toyoda, N
Gabazza, EC
机构:
[1] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pediat, Seoul 135710, South Korea
[2] Sejong Univ, Coll Engn, Dept Biosci & Biotechnol, Seoul, South Korea
[3] Mie Univ, Sch Med, Dept Internal Med 3, Tsu, Mie 514, Japan
关键词:
Helicobacter pylori;
iron-deficiency anemia;
lactoferrin sequestration;
D O I:
10.1046/j.1440-1746.2003.03098.x
中图分类号:
R57 [消化系及腹部疾病];
学科分类号:
摘要:
Background and Aim: It is known that lactoferrin serves as a source of iron for Helicobacter pylori in gastric mucosa. The present study was undertaken to investigate the relationship between lactoferrin and H. pylori infection coexistent with iron-deficiency anemia by determining the lactoferrin levels in gastric biopsy specimens, and by locating the major sites of lactoferrin expression, according to the presence or absence of iron-deficiency anemia. Methods: One hundred and one adolescents who underwent gastroduodenoscopy were divided into four groups: controls without H. pylori infection (NL; n = 43); patients with H. pylori infection (HP; n = 26); patients with iron-deficiency anemia (IDA; n = 6); and patients with H. pylori gastritis and coexisting iron-deficiency anemia (HPIDA; n = 26). The gastric mucosal levels of lactoferrin were measured by immunoassay. Immunohistochemical technique was used to allow identification of the location and quantification of the lactoferrin expression. Results: The mucosal level of lactoferrin was highest (3.93 +/- 2.73 ng/mug protein) in HPIDA, followed by 2.67 +/- 1.79 ng/mug protein in HP, 0.59 +/- 0.57 ng/mug protein in NL and 0.14 +/- 0.10 ng/mug protein in IDA. Their multiple comparisons were statistically significant at the 0.05 level. After the eradication of H. pylori in 12 HPIDA patients who underwent follow-up endoscopy, the mean mucosal level of lactoferrin decreased significantly, while the blood hemoglobin level correspondingly increased. The major sites of lactoferrin expression by immunohistochemistry were in glands and neutrophils within epithelium. Lactoferrin was stained weakly in NL and IDA, and strongly in HP and HPIDA. Conclusion: The lactoferrin sequestration in the gastric mucosa of HPIDA was remarkable, and this finding seems to give a clue that leads to the clarification of the mechanism by which H. pylori infection contributes to iron-deficiency anemia. (C) 2003 Blackwell Publishing Asia Pty Ltd.
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页码:980 / 985
页数:6
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