N. Matsukura et al., ROLE OF HELICOBACTER-PYLORI INFECTION IN PERFORATION OF PEPTIC-ULCER - AN AGE-MATCHED AND GENDER-MATCHED CASE-CONTROL STUDY, Journal of clinical gastroenterology, 25, 1997, pp. 235-239
Evidence showed a marked decrease in recurrence rate of peptic ulcer a
fter eradication of Helicobacter pylori infection. However, whether H.
pylori infection is etiologically related to perforation of peptic ul
cer remains to be clarified. We therefore conducted an age-and gender-
matched case-control study between perforated and nonsurgical peptic u
lcers in H. pylori infection and examined differences in the cytotoxin
genes cagA and vacA. Serum H. pylori IgG antibody (ELISA) was positiv
e in 20/21 (95%) of perforated vs. 37/40 (93%) of nonsurgical duodenal
ulcers and in 5/5 (100%) of perforated vs. 24/28 (86%) of nonsurgical
gastric ulcer patients, Positivity of H. pylori DNA in gastric juice,
which was amplified by PCR and identified by Southern blot hybridizat
ion, was 17/23 (74%) of perforated vs. 32/45 (71%) in the nonsurgical
duodenal ulcer group. Positivity of the cytotoxin genes cagA and vacA
in H. pylori DNA-positive gastric juice was as follows: perforated vs.
nonsurgical duodenal ulcer, cagA 11/13 (85%) vs. 24/27 (89%); vacA1:
9/13 (69%) vs. 22/27 (82%); vacA2 8/13 (62%) vs, 21/27 (78%). There we
re no significant differences between the perforated and nonsurgical p
eptic ulcer groups for these H. pylori serum and gene markers. It is a
ssumed that H. pylori infection is not etiologically related to perfor
ation of peptic ulcer.