Key
Takeaways
-
The
role
of
H.
pylori
in
colorectal
cancer
is
controversial,
despite
a
growing
body
of
evidence
supporting
an
association. -
Based
on
estimates
from
43
studies,
H.
pylori
exposure
was
associated
with
a
1.59-fold
higher
risk
of
colorectal
cancer. -
In
limited
observational
studies,
eradication
of
H.
pylori
was
associated
with
a
reduced
risk
of
colorectal
cancer,
but
only
after
10
years
of
follow-up.
Exposure
to
Helicobacter
pylori,
known
for
its
role
in
gastric
cancer,
may
also
play
a
role
in
colorectal
cancer
(CRC),
according
to
results
from
a
risk-attribution
modeling
study.
Based
on
estimates
from
43
studies,
H.
pylori
exposure
was
associated
with
a
1.59-fold
higher
risk
of
CRC
(95%
CI
1.36-1.87),
reported
Shailja
C.
Shah,
MD,
MPH,
of
the
University
of
California
San
Diego,
and
colleagues
in
eGastroenterology.
Under
the
pooled
risk-attribution
model
based
on
estimates
from
the
43
studies,
an
estimated
22%
(95%
uncertainty
interval
[UI]
14.7-29.4)
of
global
CRC
cases
were
potentially
related
to
H.
pylori
exposure.
However,
that
proportion
decreased
to
11.9%
(95%
UI
0.7-22.8)
when
risk
estimates
were
derived
from
14
population-based
and
cohort
studies.
In
limited
observational
studies,
eradication
of
H.
pylori
was
associated
with
a
reduced
risk
of
CRC,
but
only
after
10
years
of
follow-up.
“The
findings
of
this
study
should
be
considered
exploratory
and
motivational,
as
the
true
clinical
implications
hinge
on
future
well-designed
studies
aiming
to
establish
a
causal
association
between
H.
pylori
and
CRC,”
the
authors
wrote.
However,
“these
findings
are
noteworthy
in
the
context
of
the
clear
successes
of
population-level
H.
pylori
screen-and-
eradicate
programs
for
gastric
cancer
prevention
and
underscore
the
potential
dual
benefit
of
H.
pylori
eradication
on
CRC
risk,
particularly
in
high
H.
pylori
prevalence
and
resource-constrained
settings,”
they
added.
Because
of
its
causal
association
with
gastric
cancer,
the
International
Agency
for
Research
on
Cancer
has
categorized
H.
pylori
as
a
group
1
human
carcinogen.
However,
its
role
in
CRC
is
controversial,
despite
a
growing
body
of
evidence
supporting
an
association.
For
example,
a
previous
large
retrospective
cohort
study
of
U.S.
military
veterans
suggested
that
H.
pylori
increased
the
likelihood
of
developing
CRC
by
18%
and
the
risk
of
dying
of
CRC
by
12%
versus
no
history
of
the
infection.
Even
so,
“to
date,
evidence
for
a
clear
exposure-response
remains
incomplete,”
Shah
and
team
noted.
Thus,
the
goal
of
their
study
was
to
“provide
evidence
to
inform
public
health
and
research
prioritization,
and
to
guide
infection-targeted
cancer
prevention
strategies
at
both
global
and
regional
levels
that
complement
and
extend
beyond
H.
pylori
eradication
for
gastric
cancer
prevention,”
they
wrote.
They
used
data
from
systematic
reviews
and
meta-analyses,
stratified
by
region,
diagnostic
method,
and
eradication
status,
among
others.
Estimates
of
CRC
cases
were
derived
from
the
Global
Cancer
Observatory.
Estimated
proportions
of
CRC
cases
related
to
H.
pylori
exposure
varied
when
stratified
by
sex,
age,
region,
and
country.
When
stratified
by
sex,
women
had
higher
estimated
proportions
of
CRC
cases
potentially
related
to
H.
pylori
exposure
compared
with
men
(24.8%
vs
19.9%).
In
addition,
the
proportion
of
CRC
cases
linked
to
H.
pylori
exposure
was
greater
among
those
born
more
recently,
increasing
from
9.5%
in
those
born
before
1947
to
10.2%
among
those
born
in
1948
to
1962,
and
15%
among
those
born
in
1963
to
1977.
The
highest
age-standardized
incidence
rates
of
CRC
potentially
related
to
H.
pylori
exposure
were
observed
in
Japan
(9.0
per
100,000),
Portugal
(8.4
per
100,000),
and
South
Korea
(7.8
per
100,000).
The
age-standardized
incidence
rate
for
the
U.S.
was
2.5
per
100,000.
The
Western
Pacific
and
Mongolia
had
the
highest
estimated
proportions
of
CRC
cases
potentially
linked
to
H.
pylori
exposure
(25%
and
36%,
respectively).
While
there
was
a
similarly
high
prevalence
of
H.
pylori
in
Africa,
South-East
Asia,
and
the
Eastern
Mediterranean,
those
regions
had
lower
estimated
proportions
of
CRC
cases
potentially
attributable
to
H.
pylori
exposure.
Shah
and
team
acknowledged
that
“evidence
directly
evaluating
H.
pylori
eradication
and
subsequent
CRC
risk
remains
sparse
and
largely
observational,”
and
is
often
limited
by
short
follow-up
and
potential
confounders.
“Therefore
our
findings
should
be
interpreted
as
hypothesis-generating,
and
further
prospective
and
interventional
studies
are
needed,”
they
wrote.
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