title: Lactoferrin sequestration and its contribution to iron-deficiency anemia in Helicobacter pylori-infected gastric mucosa.
abstract: OBJECTIVE
  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/microg protein) in HPIDA, followed by 2.67 +/- 1.79 ng/microg protein in HP, 0.59 +/- 0.57 ng/microg protein in NL and 0.14 +/- 0.10 ng/microg 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. cyh@smc.samsung.co.kr
authors.forename: Yon Ho
authors.initials: YH
authors.lastname: Choe
authors.forename: Yoo Joung
authors.initials: YJ
authors.lastname: Oh
authors.forename: Na Gyong
authors.initials: NG
authors.lastname: Lee
authors.forename: Ichiro
authors.initials: I
authors.lastname: Imoto
authors.forename: Yukihiko
authors.initials: Y
authors.lastname: Adachi
authors.forename: Nagahito
authors.initials: N
authors.lastname: Toyoda
authors.forename: Esteban C
authors.initials: EC
authors.lastname: Gabazza
mesh_terms: D000293:Adolescent; D018798:Anemia, Iron-Deficiency / Q000209:etiology / Q000378:metabolism*; D001706:Biopsy; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005753:Gastric Mucosa / Q000737:chemistry* / Q000382:microbiology; D005773:Gastroscopy; D016481:Helicobacter Infections / Q000150:complications / Q000378:metabolism*; D016480:Helicobacter pylori; D006801:Humans; D007124:Immunoenzyme Techniques; D007781:Lactoferrin / Q000378:metabolism*; D008297:Male; D018709:Statistics, Nonparametric
chemical_list: D007781:Lactoferrin