Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently
A Hackelsberger
a Department of Gastroenterology, Hepatology, and
Infectious Diseases, b Department of Pathology, Otto-von-Guericke
University, Magdeburg, Germany
Correspondence to: Professor P Malfertheiner,
Department of Gastroenterology, Hepatology, and Infectious Diseases,
Otto-von-Guericke-University, Leipziger Strasse 44, 39120 Magdeburg,
Germany. Accepted for publication 23 March 1998 Background Keywords:
gastric mucosal defence;
surface hydrophobicity;
aging;
Helicobacter pylori
Gastric mucosal surface hydrophobicity
(GMSH) is an essential component of the mucosal defence system that is
decreased by Helicobacter pylori and non-steroidal
anti-inflammatory drugs (NSAIDs). Gastric ulcers occur predominantly in
elderly subjects, and may thus reflect diminished mucosal resistance.
Aims
To investigate whether aging decreases GMSH.
Patients
One hundred and twenty patients without
peptic ulcer disease were divided into three age groups: I (41 years or
below); II (41-64 years); and III (65 years or above).
Methods
Biopsy specimens were taken from the
antrum, corpus, and cardia for histology (Sydney system), urease
testing for H pylori, and for contact angle measurement of
GMSH with a goniometer. The presence of specific H pylori
antibodies was checked by immunoblotting.
Results
Fifty two patients (43%) were infected,
and 68 were uninfected with H pylori. GMSH at all biopsy
sites was lower in H pylori infected subjects (p=0.0001),
but also decreased with age independently of infection status
(p=0.0001). The most notable decrease in GMSH occurred between age
groups I and II in those with, and between age groups II and III in
those without, H pylori infection. GMSH was greater in
antral than in corpus mucosa in both infected (p=0.0001) and uninfected
patients (p=0.0003).
Conclusions
A physiological decrease in GMSH with
aging may contribute to the risk of ulcer development in the elderly,
and may act synergistically with H pylori and/or NSAIDs on
gastric mucosal defence.
(GUT 1998;43:465-469)
© 1998 by Gut
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