Role of Helicobacter pylori virulence factor and genotypes in non-ulcer dyspepsia.
OBJECTIVE
The role of Helicobacter pylori (HP) in non-ulcer dyspepsia is debatable. Eradicating HP will help a small group of non-ulcer dyspeptic patients. However, it is unclear which subgroup of patients will benefit from eradication therapy. The aim of the present study was to compare the cagA and cagE status, as well as vacA genotypes, of HP in non-ulcer dyspeptic patients who responded successfully to eradication therapy compared with those patients who did not.


METHODS
Consecutive patients with moderate to severe (Likert 2 or 3) non-ulcer dyspepsia with HP were recruited prospectively. Gastric biopsies were taken, DNA extracted and polymerase chain reaction performed to determine the cagA and cagE status and vacA alleles. Eradication therapy was offered until HP was eradicated successfully. The HP status was checked 1 month after eradication therapy using the [(13)C]-urea breath test. All patients were assessed by one interviewer using Gastrointestinal Symptom Rating Scale (GSRS), a four-point Likert scale, and SF-36 for quality of life over 12 months. Treatment success was defined as minimal or no symptoms (Likert 1 or 0). The cagA, cagE and vacA status was blinded to the investigators until completion of the study.


RESULTS
Seventy-three patients (36 males, 37 females) were recruited to the study. The mean+/-SD patient age was 53.38+/-12.09 years. When the 36 patients who improved (group A) were compared with the 37 (group B) who did not, no significant difference was found in the cagE positive rate (55.6 vs 43.2%, respectively; P=0.638), cagA positive rate (83.1 vs 73.0%, respectively; P=0.247), vacA m1 versus m2 subtype (84.0 vs 55.6%, respectively; P=0.472) or vacA s1a versus s1c (39.4 vs 57.1%, respectively; P=0.166). There was also no significant difference noted in the SF-36 scores between the two groups after the conclusion of eradication therapy.


CONCLUSIONS
Stratification of HP genotypes and virulence factor has no significant impact on the treatment success of non-ulcer dyspepsia.
Tan
Huck Joo
HJ
Sunway Medical Center, Selangor, Malaysia. hucktan@hotmail.com
Rizal
Abdul Manaf
AM
Rosmadi
Mohamed-Yusoff
MY
Goh
Khean-Lee
KL
D000658:Amoxicillin / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D000942:Antigens, Bacterial / Q000235:genetics*; D001426:Bacterial Proteins / Q000235:genetics*; D017291:Clarithromycin / Q000627:therapeutic use; D004415:Dyspepsia / Q000188:drug therapy* / Q000382:microbiology; D005260:Female; D005838:Genotype; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000382:microbiology; D016480:Helicobacter pylori / Q000235:genetics* / Q000472:pathogenicity; D006801:Humans; D008297:Male; D008875:Middle Aged; D009853:Omeprazole / Q000627:therapeutic use; D016896:Treatment Outcome; D014774:Virulence; D037521:Virulence Factors / Q000235:genetics*
D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C103937:PicB protein, Helicobacter pylori; C074689:VacA protein, Helicobacter pylori; D037521:Virulence Factors; C080866:cagA protein, Helicobacter pylori; D000658:Amoxicillin; D017291:Clarithromycin; D009853:Omeprazole