Basic Study
Copyright ©The Author(s) 2018.
World J Gastroenterol. Mar 7, 2018; 24(9): 971-981
Published online Mar 7, 2018. doi: 10.3748/wjg.v24.i9.971
Table 1 Polymerase chain reaction primers used in this study
PrimerPrimer sequenceGeneProduct size (bp)
CAGA-F5’-GATAACAGGCAAGCTTTTGATG-3’cagA349
CAGA-R5’-CTGCAAAAGATTGTTTGGCAGA-3’
VA1-F5’- ATGGAAATACAACAACAAACACAC-3’vacA signal region259/286 (s1/s2)
VA1-R5’ – CTGCTTGAATGCGCCAAAC-3’
VAG-F5’ – CAATCTGTCCAATCAAGCGAG-3’vacA middle region567/642 (m1/m2)
VAG-R5’- GCTTCAAAATAATTCCAAGG-3’
Table 2 Demographic and clinical characteristics of Helicobacter pylori-infected patients included in the study
Number of gastric biopsy specimens n (%)
All patients 165 (100)Treatment Naïve 105 (63.6)Previously treated 60 (36.4)
Gender
Female69 (41.8)31 (29.5)38 (63.3)
Male96 (58.2)74 (70.5)22 (36.7)
Age
mean ± SD49.2 ± 15.850.3 ± 16.347.4 ± 14.7
Histology findings
Chronic gastritis130 (78.8)78 (74.3)52 (86.7)
Intestinal metaplasia23 (13.9)16 (15.2)7 (11.7)
No data available11 (6.7)10 (9.5)1 (1.7)
Normal mucosa1 (0.6)1 (1.0)0 (0.0)
Endoscopic findings
Gastritis92 (55.8)57 (54.3)35 (58.3)
Normal32 (19.4)19 (18.1)13 (21.7)
Gastric/duodenal ulcer21 (12.7)15 (14.3)6 (10.0)
No data available17 (10.3)11 (10.5)6 (10.0)
Atrophic mucosa1 (0.6)1 (1.0)0 (0.0)
Other12 (1.2)2 (1.9)0 (0.0)
Table 3 Clarithromycin resistance rates and the distribution of resistance-mediating mutations
GenotypeNumber of gastric biopsy specimens n (%)
P value1
All patients 165 (100)Treatment Naïve 105 (63.6)Previously treated 60 (36.4)
ClarithromycinS (WT)65 (39.4)52 (49.5)13 (21.7)< 0.001
ClarithromycinR100 (60.6)53 (50.5)47 (78.3)
Point mutations
A2147G78 (78)44 (83)34 (72.3)NS
A2146G8 (8)3 (5.7)5 (10.6)NS
A2146C6 (6)3 (5.7)3 (6.4)NS
A2146C + A2147G5 (5)3 (5.7)2 (4.3)NS
A2146G + A2147G2 (2)0 (0)2 (4.3)NS
A2146G + A2146C1 (1)0 (0)1 (2.1)NS
Table 4 Fluoroquinolone resistance rates and the distribution of resistance-mediating mutations
GenotypeNumber of gastric biopsy specimens n (%)
P value1
All patients 165 (100)Treatment Naïve 105 (63.6)Previously treated 60 (36.4)
FluoroquinoloneS (WT)132 (80.0)89 (84.8)43 (71.7)
FluoroquinoloneR33 (20.0)16 (15.2)17 (28.3)NS
Point mutations
gyr91 D91Y18 (54.5)10 (62.5)8 (47.1)NS
gyr91 D91N6 (18.2)2 (12.5)4 (23.5)NS
gyr91 D91G2 (6.1)0 (0.0)2 (11.8)NS
gyr91 D91N + gyr91 D91G2 (6.1)1 (6.3)1 (5.9)NS
gyr91 D91N +gyr91 D91Y2 (6.1)1 (6.3)1 (5.9)NS
gyr87 N87K1 (3.0)1 (6.3)0 (0.0)NS
gyr87 N87K + gyr91 D91N + gyr91 D91G1 (3.0)0 (0.0)1 (5.9)NS
gyr87 N87K + gyr91 D91N + gyr91 D91G + gyr91 D91Y1 (3.0)1 (6.3)0 (0.0)NS
Table 5 Antimicrobial susceptibility results for both clarithromycin and fluoroquinolone
GenotypeNumber of gastric biopsy specimens n (%)
P value1
All patients 165 (100)Treatment Naïve 105 (63.6)Previously treated 60 (36.4)
Susceptible (to both)60 (36.4)49 (46.6)11 (18.3)< 0.05
Resistant (to at least one)105 (63.6)56 (53.3)49 (81.6)
Susceptible/resistant to one137 (83.0)92 (87.6)45 (75.0)
Resistant to both28 (17.0)13 (12.4)15 (25.0)0.05
Table 6 Distribution of Helicobacter pylori virulence-factor genotypes among infected patients in Ireland n (%)
GenotypeOverall (n = 165)Treatment naïve (n = 105)Previous treatment (n = 60)P value1
cagA status
Positive37 (22.4)25 (23.8)12 (20)NS
Negative128 (77.6)80 (76.2)48 (80)
vacA allele
S1113 (68.5)78 (74.3)35 (58.3)
S252 (31.5)27 (25.7)25 (41.7)< 0.05
M147 (28.5)31 (29.5)16 (26.7)
M2118 (71.5)74 (70.5)44 (73.3)NS
S1/M139 (23.6)26 (24.8)13 (21.7)NS
S1/M274 (44.8)52 (49.5)22 (36.7)NS
S2/M18 (4.8)5 (4.8)3 (5.0)NS
S2/M244 (26.7)22 (21.0)22 (36.7)< 0.05