Lactoferrin sequestration and its contribution to iron-deficiency anemia in Helicobacter pylori-infected gastric mucosa

• Published in: Journal of gastroenterology and hepatology Vol. 18; no. 8; pp. 980 - 985
• Main Authors: CHOE, YON HO, OH, YOO JOUNG, LEE, NA GYONG, IMOTO, ICHIRO, ADACHI, YUKIHIKO, TOYODA, NAGAHITO, GABAZZA, ESTEBAN C
• Format: Journal Article
• Language: English
• Published: Melbourne, Australia Blackwell Science Pty 01.08.2003
• Subjects: Adolescent; Anemia, Iron-Deficiency - etiology; Anemia, Iron-Deficiency - metabolism; Biopsy; Enzyme-Linked Immunosorbent Assay; Female; Gastric Mucosa - chemistry; Gastric Mucosa - microbiology; Gastroscopy; Helicobacter Infections - complications; Helicobacter Infections - metabolism; Helicobacter pylori; Humans; Immunoenzyme Techniques; iron-deficiency anemia; Lactoferrin - metabolism; lactoferrin sequestration; Male; Statistics, Nonparametric
• ISSN: 0815-9319; 1440-1746
• DOI: 10.1046/j.1440-1746.2003.03098.x

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/µg protein) in HPIDA, followed by 2.67 ± 1.79 ng/µg protein in HP, 0.59 ± 0.57 ng/µg protein in NL and 0.14 ± 0.10 ng/µg 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.