Influence of bacterial CagA status on gastritis, gastric function indices, and pattern of symptoms in H. pylori-positive dyspeptic patients.
OBJECTIVE
To date, little is known about a possible relationship between H. pylori-related disturbances of gastric function and the bacterial virulence. The aim of this study was to assess whether certain gastric function indices as well as the pattern of symptoms in nonulcer dyspepsia (NUD) are related to CagA status.


METHODS
A total of 56 consecutive patients with NUD (38 H. pylori-positive and 18 H. pylori-negative) were studied. Dyspeptic symptoms were categorized according to the predominant complaints and scored for severity and frequency. In all subjects, basal and pentagastrin-stimulated acid secretion, fasting and meal-induced gastrin release, fasting serum pepsinogen I (PG I) levels, and gastric emptying of solids were determined. CagA status was determined by assaying serum CagA IgG antibodies by western blotting.


RESULTS
Eighteen of 38 (47%) H. pylori-positive dyspeptics were CagA seropositive. Type and severity of dyspeptic symptoms did not significantly differ between CagA-positive and CagA-negative dyspeptics nor between H. pylori-positive and negative patients. Among the gastric function indices studied, only meal-stimulated gastrin was significantly influenced by CagA status (peak gastrin 129.9 [44.1] vs 99.1 [48.6] pg/ml in CagA-positive and negative NUD, respectively), but this was not accompanied by any significant modification of basal or stimulated acid secretion or gastric emptying of solids. The activities of both antral and corpus gastritis in NUD harboring CagA-positive strains were significantly higher than those of CagA-negative NUD. Accordingly, serum PG I levels were significantly higher in CagA-positive than CagA-negative or H. pylori-negative dyspeptics.


CONCLUSIONS
These findings support a role for CagA status in influencing the activity and perhaps the distribution of gastritis in NUD, as well as the degree of gastrin response to a meal; however, this is not accompanied by disturbances of acid secretion or gastric emptying or by differences in the type and severity of symptoms.
Parente
F
F
Department of Gastroenterology and Pathology Service, L. Sacco University Hospital, Milan, Italy.
Imbesi
V
V
Maconi
G
G
Cucino
C
C
Sangaletti
O
O
Vago
L
L
Bianchi Porro
G
G
D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial / Q000032:analysis*; D001426:Bacterial Proteins / Q000032:analysis* / Q000097:blood; D015153:Blotting, Western; D004415:Dyspepsia / Q000382:microbiology* / Q000503:physiopathology; D004435:Eating / Q000502:physiology; D005215:Fasting / Q000502:physiology; D005260:Female; D005744:Gastric Acid / Q000378:metabolism; D005746:Gastric Emptying / Q000502:physiology; D005755:Gastrins / Q000378:metabolism; D005756:Gastritis / Q000382:microbiology* / Q000503:physiopathology; D016481:Helicobacter Infections / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000276:immunology / Q000472:pathogenicity / Q000502:physiology*; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D008297:Male; D008875:Middle Aged; D010418:Pentagastrin; D010435:Pepsinogens / Q000097:blood; D011706:Pyloric Antrum / Q000382:microbiology; D013270:Stomach / Q000503:physiopathology*; D014774:Virulence
D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D005755:Gastrins; D007074:Immunoglobulin G; D010435:Pepsinogens; C080866:cagA protein, Helicobacter pylori; D010418:Pentagastrin