Lahat et al.

BMC Gastroenterology (2017) 17:27

DOI 10.1186/s12876-017-0588-7

RESEARCH ARTICLE Open Access

Helicobacter pylori prevalence and clinical

significance in patients with quiescent
Crohn’s disease
Adi Lahat1,2*, Uri Kopylov1,2, Sandra Neuman1,2, Nina Levhar1,2, Doron Yablecovitch1,2, Benjamin Avidan1,2,
Batia Weiss2,3, Shomron Ben-Horin1,2†, Rami Eliakim1,2† and on behalf of the Israeli IBD research Network (IIRN)

Abstract
Background: Helicobacter pylori (HP) infection is present in about 50% of the global population, and is associated
with chronic gastritis, peptic disease and gastric malignancies. HP prevalence in Crohn’s disease (CD) patients was
shown to be low compared to the general population, and its influence on disease activity is yet to be determined.
Our aims were to determine the prevalence of HP in a selected group of CD patients with quiescent disease, and
to assess the influence of its eradication on disease activity and endoscopic and laboratory activity measures.
Methods: Consecutive CD patients with quiescent disease underwent meticulous disease evaluation with MR
enterography (MRE), video capsule endoscopy (VCE), CRP, fecal calprotectin and CDAI. All patients were tested for
the presence of HP using stool antigen detection kit. Patients infected with HP were offered eradication treatment
with sequential therapy. HP eradication was confirmed using urease breath test and stool antigen test. The influence of
HP eradication on disease activity was assessed.
Results: Out of 56 patients enrolled, six patients (10.7%) had HP infection. Of them, five patients had gastro- duodenitis
per VCE. All HP positive patients were offered eradication treatment and underwent successful eradication.
Notably, 23 (50%) of patients had proximal disease per VCE, most of them (78%) were HP negative.
CDAI, CRP, fecal calprotectin and VCE Lewis inflammatory score did not change significantly following HP
eradication, Gastric findings on VCE were not impacted by HP eradication.
Conclusions: The prevalence of HP infection in patients with quiescent CD is relatively low. Eradication of the
bacteria did not significantly change neither disease activity measures nor the presence of gastro- duodenitis per VCE,
suggesting it might be part of proximal CD. The influence of HP on CD activity merits further investigation.
Keywords: Crohn’s disease, Helicobacter pylori, Video capsule endoscopy, Prevalence, Eradication

Background and metaplastic changes. Thus, HP infection is associ-

Helicobacter pylori (HP) infection is one of the most ated with chronic gastritis, peptic disease and gastric
prevailing global pathogens in humans, and can be malignancies [2, 3]. Crohn’s disease (CD) is a chronic in-
detected in 50% of the world’s population [1]. Its preva- flammatory condition that can affect the gastrointestinal
lence varies considerably in association by geography, system from the mouth to the anus. Inflammation is
ethnicity, age, and socioeconomic factors. transmural, and therefore may be cause internal ab-
This Gram- negative bacterium causes chronic inflam- scesses, fistula between adjacent organs, spontaneous
mation in the gastric mucosa, which leads to atrophic viscous perforations and fibrotic strictures.. The disease
may cause significant morbidity and diminished life
* Correspondence: [email protected]
†
quality [4–8]. Disease behavior is characterized by periods
Equal contributors
1
Department of Gastroenterology, Sheba Medical Center, Tel Hashomer, Tel
of flare-ups with active symptomatic disease and periods
Hashomer, Israel of remission [9]. Over the years, many epidemiological
2
Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel
Full list of author information is available at the end of the article

© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver
(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Lahat et al. BMC Gastroenterology (2017) 17:27 Page 2 of 6

studies showed low incidence of HP infection in patients previously described protocol [25]. A patency capsule
with CD [10–18]. (PC) test was performed in all patients with active
A recent meta-analysis demonstrated negative associ- small bowel disease detected on MRE. If the PC was
ation between HP infection and CD with OR of 0.38 not expelled from the small bowel within 30 h, the
(95% CI 0.31 to 0.47, p value <1e-10) [19]. patient was withdrawn from the study. Mucosal in-
The reason for that negative association is yet to flammation was quantified using the Lewis inflam-
be determined. One hypothesis suggests that medica- matory score (LS). Active inflammation was defined
tions used for CD treatment may eradicate HP. An- as a segmental Lewis score of ≥135 [26]. A board-
other suggestion along the same line is that CD certified gastroenterologist with over 10 years of
mucosal alterations might prevent HP colonization experience in capsule endoscopy read the capsule
[14, 15, 18–22]. An alternative argument suggests a videos. Gastric and duodenal findings were described
protective effect for HP infection from the occur- for each study.
rence of CD.
CD is categorized by selectively activation of type 1 T
helper lymphocyte (Th1) and Th17-related cytokines in- Inflammatory biomarkers and disease activity measures
volved in innate immunity (interleukin (IL) 12, IL-23, Fecal calprotectin, CRP and complete blood count
IL-27) [23]. HP was shown to produce IL-18 which (CBC) were measured routinely every 3 months.
causes accumulation of tolerogenic dendritic cells and Fecal calprotectin levels were measured using the
highly suppressive regulatory T cells (Tregs) that help Quantum blue calprotectin kit (BÜHLMANN Labo-
suppress the inflammatory process [24]. ratories AG, Basel, Switzerland). The reported value
High frequency of gastritis and duodenitis was range is 30 to 300 μg/g. Levels above 100 μg/g were
described in CD patients with no association to HP in- considered positive. CRP levels were considered ele-
fection [20–22]. However, data assessing the effect of HP vated if > 5 mg/l.
infection and eradication on proximal disease and on Patients underwent physician’s evaluation and CDAI
disease activity in patients with CD is scarce. assessment for disease activity every 3 months.
Thus, in our study we focused on patients with known
quiescent Crohn’s disease that were prospectively evalu-
ated for disease activity measures before and after HP HP assessment and treatment
eradication. All patients were tested for the presence of HP using
stool antigen detection kit as part (CerTest H. pylori
Methods one step card test, Certest Biotec S.L. Zaragoza, Spain).
Patient population Stool antigen test was chosen for HP detection since
Study population consisted of adult (>18 years) CD this method is noninvasive and most importantly is
patients with known small bowel Crohn’s disease in not influenced by antibiotics or Proton Pump Inhibi-
clinical remission, as determined by the validated tors (PPI) treatment. This kit has a sensitivity of >94%,
Crohn’s disease activity index (CDAI) of <150, or pa- pecificity of >99% and Positive predictive value (PPV)
tients suffering from mild disease symptoms, pre- of >99% for HP detection. Patients infected with HP
sented by CDAI of 150–220. All patients included were offered eradication treatment with sequential
were treated with stable medication doses and on therapy consisted of 5 days of esomeprazole (40 mg)
corticosteroid-free remission for 3–24 months. Pa- and amoxicillin (1000 mg) twice daily, followed by
tients maintained on constant treatment throughout 5 days of esomeprazole (40 mg), clarithromycin
study duration. (500 mg) and Tinidazole (500 mg) twice daily [27].
Patients that were unable to provide informed consent Notably, sequential therapy is the standard of care for
were excluded from the study. Patients with severe co- patients infected with HP in our institution. Prior to
morbidities or with any condition that will prevent them eradication treatment patients received detailed explan-
from swallowing VCE (difficulty in swallowing, history ation regarding HP infection implications and the import-
of aspirations or dysphagia, known or suspected intes- ance of compliance and adherence to treatment. HP
tinal obstruction or severe bowel stricturing) or under- eradication was confirmed using urease breath test and
going MRE (claustrophobia or implanted metal objects stool antigen detection kit 4 weeks following eradication
or cardiac pacemaker) were excluded as well. treatment completion.
The impact of HP eradication on disease activity and
Imaging studies degree of proximal small bowel inflammation was
All patients underwent an MRE upon enrollment. assessed using the disease activity measures specified
MR image acquisition was performed using a above, 8 weeks after eradication conformation.
Lahat et al. BMC Gastroenterology (2017) 17:27 Page 3 of 6

Statistical analysis measures before and 12 weeks following HP eradica-

Descriptive statistics were presented as means ± standard tion in all patients treated was compared, and are
deviations for continuous variables and percentages for shown in Table 2. A separate analysis was performed
categorical variables. Categorical variables were ana- only for patients who had gastro-duodenitis per VCE
lyzed by Chi Square/Fisher’s exact test and continuous before HP eradication. Results are shown in Table 3.
variables-by T-test/Mann Whitney test, as appropriate. As shown in Tables 2 and 3, all disease activity measures
P < 0.05 was considered significant. All computations as well as anatomical disease distribution (measured by
were performed with the MedCalc Software (Marieke, VCE Lewis inflammatory score) were unchanged fol-
Belgium). lowing HP eradication. Hence, HP eradication had no
influence on disease activity.
Results Figures 2a, b and 3a, b show active CD in the proximal
Fifty six patients were included in the study. Patients’ digestive system demonstrated by mucosal erosions in
demographic data and disease characteristics are shown stomach and duodenum - unchanged before and after
in Table 1. None of the patients was tested for HP prior eradication treatment, respectively.
to this study. A schematic graph of study design is
shown in Fig. 1. Discussion
Out of all patients included, only six patients (10.7%) HP infection is one of the most prevalent infectious
were infected with HP. Of them, five patients had diseases worldwide. However, in CD patients its preva-
gastro- duodenitis per VCE and one had no proximal lence was shown to be lower than in general population
disease and no upper GI symptoms. All HP positive [10–18]. The reason for that remains to be determined,
patients were offered eradication treatment with se- as is the mutual impact of CD and HP infection on pa-
quential therapy detailed above. All infected patients tients’ symptoms, severity of the disease and on disease
agreed to receive eradication treatment, and all treated distribution. In the current study, we initially assessed
patients underwent successful eradication, as was the prevalence of HP infection in a homogenous group
confirmed by a negative urease test and negative stool of CD patients with quiescent disease, and then tried to
antigen test. Thus, a 100% eradication rate was assess prospectively the impact of HP eradication on
achieved. disease activity measures and on anatomical inflamma-
Notably, 23 (50%) of patients had proximal disease per tory distribution.
VCE, most of them (78%) were HP negative. In agreement with data in the literature [10–18], HP
Four weeks after a verified eradication, a repeated infection rate was low among our patients’ group, with
evaluation of disease activity was performed. Physical only 11% of patients tested positive to HP. The current
examination, CBC, CRP was performed and CDAI prevalence of HP infection in Israel is unknown, yet data
was calculated. Capsule endoscopy was ingested as from 2002 [28] suggest a 60% prevalence among the
well 12 weeks following eradication. Disease activity general population in Israel. Thus, even if we assume a
possible reduction in HP infection in the general popula-
tion during the last decade, HP infection among CD pa-
Table 1 Patients’ demographic data and disease characteristics tients is still significantly low. Notably, none of our
Number Percent patients was tested for the presence of HP before enter-
Male/female 30/26 53.6/46.4 ing the study, and consequently none was ever treated
Age at diagnosis (years) 26 ± 11 for HP eradication. Therefore, we believe that our data
Disease duration (years) 6±5 reflects the true prevalence of HP infection in CD
Clinical remission 52 92.3 patients.
All the patients who tested positive for HP were of-
Smoking status current 11 19.6
fered eradication treatment, though one of them was a-
never smoked 36 64.3
symptomatic. Since HP is a well known carcinogen with
past smoking 9 16.1 a strong proven relation to gastric malignancy [2, 3],
Previous surgery 9 16.1 we decided to offer eradication treatment to all infected
Perianal disease 13 23.2 patients.
Current medical Thiopurine 25 44.6 In order to achieve maximal eradication rates pa-
treatment tients were treated with a 10 day sequential therapy,
Anti-TNF 21 37.5
which was shown to have eradication success of up
Combined anti-TNF 7 12.5
+ thiopurine
to 94% [29].
In addition, at treatment initiation patients received
No medical treatment 11 19.6
individual consultation with emphasis on the importance
Lahat et al. BMC Gastroenterology (2017) 17:27 Page 4 of 6

Fig. 1 Study design

of compliance and adherence to the offered treatment. Eight weeks following eradication verification, patients
Eradication was verified both with urease breath test and underwent repeated disease evaluation, including VCE.
with stool antigen detection kit. Using this meticulous Data in literature support repeated endoscopy for peptic
treatment option, we managed to reach a 100% eradica- disease 4 weeks following HP eradication treatment [31].
tion rate. Therefore, we postulated that 8 weeks following eradi-
Obviously, since our treatment group consisted of 6 cation verification and 12 weeks following end of
patients only, the results are underpowered to assess eradication treatment is appropriate for reevaluation,
treatments’ efficacy. However, we believe that the assuming that all mucosal damage caused by HP would
combination of a high- efficacy eradication protocol be healed.
and highly motivated patients with high compliance Our results show no improvement in proximal disease
rates probably lead to this unusually high eradication or in disease measures following HP eradication. Hence,
rate. CDAI, CRP and fecal calprotectin levels did not differ
Eradication was verified using breath test and stool significantly after HP eradication, implicating disease ac-
antigen kit 4 weeks following treatment completion [30]. tivity was unchanged following eradication. Moreover,

Table 2 Disease activity measures in all HP positive patients Table 3 Disease activity measures in HP positive patients with
before and after eradication (n = 6) gastroduodenitis on VCE before and after eradication (n = 5)
Disease measures Before eradication After eradication p Disease measures Before eradication After eradication p
CDAI 27.5 ± 21.25 22.83 ± 28.25 NS CDAI 23.18 ± 25.6 30.91 ± 25.2 NS
CRP 1.17 ± 0.82 2.97 ± 4.7 NS CRP 1.218 ± 0.9 5.12 ± 3.398 NS
Fecal calprotectin 75 ± 79.37 112.17 ± 123.2 NS Fecal calprotectin 85 ± 85.25 74.6 ± 71.57 NS
Lewis Score 425 ± 334.29 564.83 ± 529.46 NS Lewis Score 357.33 ± 465 587.995 ± 589.8 NS
NS non-significant NS non-significant
Lahat et al. BMC Gastroenterology (2017) 17:27 Page 5 of 6

Fig. 2 Stomach inflammatory changes by VCE. a Gastric erosions (circled) prior to HP eradication. b Gastric erosions (circled) post HP eradication

the VCE Lewis inflammatory score, as a measure of small number of patients included might affect the ap-
disease activity and distribution was showed no statisti- plicability of our results.
cally significant improvement following HP eradication Another theoretical drawback of our study is a selec-
as well. These results were unchanged after separate tion bias- only patients with quiescent disease were in-
sub analysis of patients with gastro-duodenitis per cluded, thus patients with active CD might have had
VCE. different results.
These data implicates that the proximal disease as However, we feel that our data supports the
well as disease activity was unrelated to HP. To the best evidence showing high incidence of gastroduodenitis
of our knowledge, up to date, no study addressed dis- in patients with quiescent CD, unrelated to HP
ease activity measures pre versus post HP eradication infection.
in CD patients.
In our study, 50% of patients had gastro-duodenitis
per VCE. These results are in agreement with previous Conclusions
studies that showed an increased prevalence of gastro- HP infection in patients with quiescent CD is lower
duodenitis disease in CD patients with no association to than in the general population, and reaches 11%.
HP infection [20–22]. Eradication of the bacteria did not change significantly
Our study has several limitations. First, our cohort neither disease measures nor the presence of gastro- duo-
of patients was relatively small. Therefore, due to the denitis per VCE, suggesting it might be part of proximal
low prevalence of HP infection in CD patients, the CD. The influence of HP on CD activity merits further
number of HP infected patients was very low. The investigation.

Fig. 3 Duodenum inflammatory changes by VCE0. a Erosion of proximal duodenum (circled) Prior to HP eradication. b Erosions in proximal
duodenum (circled) Post HP eradication
Lahat et al. BMC Gastroenterology (2017) 17:27 Page 6 of 6

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Author details
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