Gastric permeability is not increased in children colonized by CagA-positive strains of Helicobacter pylori.
BACKGROUND
Sucrose permeability has been used as a marker to detect gastric lesions in children. As CagA status of Helicobacter pylori is an important factor in determining the evolution of the gastric lesion, CagA-positive strains being more frequently associated with severe mucosal lesions, the aim of this study was to determine the prevalence of CagA-positive strains in Helicobacter pylori-colonized children and to evaluate whether the sucrose permeability test might discriminate between colonization by CagA-positive or negative strains.


METHODS
A series of 38 children (11.1+/-3.6 years) who required upper endoscopy for diagnostic purposes were included in the study. Endoscopy was carried out after the sucrose permeability test, and gastric biopsies were obtained for histologic examination, Helicobacter pylori detection by Giemsa staining and CLO-test, and determination of CagA status of the colonizing Helicobacter pylori strains by polymerase chain reaction.


RESULTS
Helicobacter pylori was detected in 26 subjects (68.4%) and of these, 16 (61.5%) were colonized by CagA-positive strains. The intensity of the histologic findings was significantly associated with the presence of Helicobacter pylori and with CagA status of the infecting strains (chi2=21.2, p=0.0017). However no significant difference in the urinary excretion of sucrose between children not colonized and children with CagA- negative or positive strains was observed (0.027% [0.012-0.035%]; 0.027% [0.016-0.047%] and 0.026% [0.016-0.038], median [range], respectively; Kruskal-Wallis analysis of variance F=0.75, p=0.69).


CONCLUSIONS
These results indicate that in Chile, about 60% of the Helicobacter pylori infected children are colonized by CagA-positive strains, in association with more intense lesions of the gastric mucosa, but that gastric permeability to sucrose does not discriminate between colonization by CagA-negative and positive strains of Helicobacter pylori.
Gotteland
M
M
Gastroenterology Unit, Institute of Nutrition and Food Technology, University of Chile, Santiago. mgottela@uec.inta.uchile.cl
Corvalan
A
A
Sarmiento
F
F
Chavez
E
E
Backouse
C
C
Palma
M
M
Kakarieka
E
E
Vial
M T
MT
Figueroa
G
G
D015746:Abdominal Pain / Q000378:metabolism / Q000382:microbiology; D000293:Adolescent; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D002648:Child; D002675:Child, Preschool; D016099:Endoscopy, Gastrointestinal; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism*; D005767:Gastrointestinal Diseases / Q000175:diagnosis / Q000378:metabolism* / Q000382:microbiology; D016481:Helicobacter Infections / Q000175:diagnosis / Q000378:metabolism*; D016480:Helicobacter pylori / Q000502:physiology; D006801:Humans; D008297:Male; D010539:Permeability; D013395:Sucrose / Q000652:urine
D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori; D013395:Sucrose