Lactoferrin Sequestration and Its Contribution to Iron Deficiency Anemia in Helicobacter pylori Infected Gastric Mucosa.
- Author:
Kwang Bin MOON
1
;
Chang Kyu KANG
;
Yon Ho CHOE
;
Hye Seung HAN
;
Sun Uk SONG
Author Information
1. Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University, School of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Helicobacter pylori;
Iron-deficiency anemia;
Lactoferrin sequestration
- MeSH:
Adolescent;
Anemia, Iron-Deficiency*;
Biopsy;
Epithelium;
Gastric Mucosa*;
Gastritis;
Helicobacter pylori*;
Helicobacter*;
Humans;
Immunoassay;
Immunohistochemistry;
Inflammation;
Iron*;
Lactoferrin*;
Neutrophils
- From:Korean Journal of Pediatric Gastroenterology and Nutrition
2002;5(1):11-18
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: It is known that lactoferrin serves as a source of iron for H. pylori in gastric mucosa. This 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: Fifty-five adolescents that underwent gastroduodenoscopy were divided into three groups: NL (n=19) for normal controls, HP (n=15) for patients with H. pylori, and IDA (n=21) for patients with H. pylori gastritis and coexisting iron-deficiency anemia. Histopathologic features were graded from null to marked on the basis of the Updated Sydney System. 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: Lactoferrin levels in the antrum increased significantly, in proportion to, H. pylori density, polymorphonuclear cell infiltration, and chronic inflammation in the histologic specimens. Patients in the HP and IDA groups showed significantly increased mucosal levels of lactoferrin compared with that observed in the normal group (p=0.0001). The lactoferrin level in IDA group tended to be higher than that in the HP group (p=0.2614). The major sites of lactoferrin expression by immunohistochemistry were in glands and neutrophils within epithelium. Lactoferrin was stained weakly in NL, and strongly in HP and IDA. CONCLUSION: The lactoferrin sequestration in the gastric mucosa of IDA 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.
