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Intranasal Helicobacter pylori infection in patients with chronic

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DOI: 10.1017/S0022215118001299

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Main Article
Habil. Dr N Siupsinskiene takes responsibility
for the integrity of the content of the paper
Cite this article: Siupsinskiene N, Katutiene I,
Jonikiene V, Janciauskas D, Vaitkus S.
Intranasal Helicobacter pylori infection in
patients with chronic rhinosinusitis with
polyposis. J Laryngol Otol 2018;1–6. https://
doi.org/10.1017/S0022215118001299
Accepted: 28 March 2018
Key words:
Helicobacter Pylori; Sinusitis; Nasal Polyps;
Laryngopharyngeal Reflux
Author for correspondence:
Habil. Dr Nora Siupsinskiene,
Department of Otolaryngology,
Academy of Medicine,
Lithuanian University of Health Sciences,
Eiveniu 2, Kaunas LT-50009, Lithuania
E-mail: norai_s@yahoo.com
Fax: +370 37 326862
© JLO (1984) Limited, 2018
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Intranasal Helicobacter pylori infection in
patients with chronic rhinosinusitis
with polyposis
N Siupsinskiene1,2, I Katutiene3, V Jonikiene3, D Janciauskas4 and S Vaitkus2
1
Faculty of Health Sciences, Klaipeda University, 2Department of Otolaryngology, Academy of Medicine,
Lithuanian University of Health Sciences, Kaunas, 3Department of ENT, Klaipeda Republic Hospital and
4
Department of Pathologic Anatomy, Academy of Medicine, Lithuanian University of Health Sciences,
Kaunas, Lithuania
Abstract
Objective. To determine the prevalence of Helicobacter pylori infection in nasal biopsy speci-
mens from patients with chronic rhinosinusitis with polyposis versus control patients, and to
assess the correlations between H pylori infection identified in the nasal tissue and patients’
sociodemographic data and reflux-related symptoms and signs.
Methods. Nasal biopsy samples were taken from 75 adult patients who underwent nasal sur-
gery for chronic rhinosinusitis with polyposis (clinical group, n = 45) and a deviated septum
(control group, n = 30). H pylori infection was identified using histochemical and rapid urease
tests.
Results. The prevalence of intranasal H pylori infection was significantly higher in the clinical
group (28.9 per cent) compared to the control group (3.3 per cent) ( p = 0.005). A significant
yet weak association was found between positive H pylori status and laryngopharyngeal reflux
related hypertrophy of the posterior commissure of the larynx. No other correlations reached
statistical significance.
Conclusion. H pylori infection is potentially related to chronic rhinosinusitis with polyposis.
Further research is needed to clarify the role of H pylori as a risk factor for the development of
sinonasal diseases and to examine its link with laryngopharyngeal reflux.
Introduction
Helicobacter pylori is a microaerophilic, Gram-negative bacterium, composed of spiral-
shaped rods. It is associated with gastric ulcer, cancer and gastritis.1 It is one of the
most common human bacterial infections in the world, affecting more than half of the
entire population.2 Although the main localisation of this bacterium is the stomach, recent
studies have analysed an association between H pylori and upper airway diseases.2–6
It has been determined that the bacterium releases two key virulence factors: CagA
(cytotoxin-associated gene A), which results in the accumulation of genetic changes in
the cell, and VacA (vacuolating cytotoxin A), which causes immunosuppression and
blocks T-cell proliferation.2,7 H pylori affects the epithelium, causes an immune response,
increases cytokines, triggers chronic inflammation and eventually increases the risk of
gastric cancer.7 Some authors argue that similar changes may develop in the upper airway
as in the gastrointestinal tract.8
The role of H pylori infection in chronic rhinosinusitis is not yet completely under-
stood, but it is known that this infection can be detected in nasal and sinus mucosa.1–4
There are three theories explaining the bacterium’s appearance in the nasal mucosa:
(1) the nasal and sinus mucosa act as a reservoir for H pylori bacterium; (2) the oral cavity
is a reservoir for this bacterium, and H pylori enters the nasal cavity through oropharyn-
geal reflux; and (3) H pylori enters the nasal cavity through gastroesophageal reflux.1–4,9
Because nasal polyposis is a local mucosal reaction to inflammation, it usually forms at
the ostiomeatal complexes. Under the effect of inflammation-causing agents, the mucous
membrane of the sinuses becomes hyperplastic and intersected, which causes mucociliary
clearance dysfunction, increases oedema of the nasal mucosa and promotes
hyperplasia.10,11
Recently, H pylori bacterium itself has been proposed as a possible cause of chronic
rhinosinusitis.1–3 There are speculations that H pylori can damage the nasal mucosa,
which becomes more sensitive to other chronic rhinosinusitis causing agents. However,
chronic inflammation of the sinus and nasal mucosa may be a beneficial medium for
this bacterium, and in this case H pylori can be a result rather than a cause of chronic
rhinosinusitis.1,10
Although recent research has investigated the possibility of H pylori as an aetiological
factor in different nasal diseases, the numbers of studies and investigated patients in this
area are not sufficient to support this claim. There is also no clear link between H pylori in
the upper airway and gastroesophageal reflux or laryngopharyngeal reflux. Therefore, the
 2 N Siupsinskiene, I Katutiene, V Jonikiene et al.
primary aim of this study was to determine the prevalence of
H pylori infection in nasal biopsy specimens from patients
with chronic rhinosinusitis with polyposis versus that in con-
trol patients. The secondary aim was to assess the correlations
between H pylori infection identified in nasal tissue and
patients’ sociodemographic data and reflux-related symptoms
and signs.
Materials and methods
The study was performed at the Hospital of Lithuanian
University of Health Sciences, Kaunas, from January 2011 to
July 2012. A total of 45 adult patients (16 females and 29
males), aged 18–85 years (with an average age (± standard
deviation (SD)) of 51.8±14.9 years), who underwent endo-
scopic sinus surgery for chronic rhinosinusitis with nasal
polyposis, and agreed to participate in the study, were selected
for inclusion in the clinical group. Patients were excluded from
the study if: they were on antibiotics or proton pump inhibi-
tors (PPIs) four weeks prior to surgery; or they had antrochoa-
nal polyps, Samter’s triad, an immunological disorder, or
unilateral, allergic or fungal sinusitis.
All patients had received local steroid therapy for three
months, with no regression of the polyps. A diagnosis of
chronic rhinosinusitis with nasal polyposis was made on the
basis of clinical examination (nasal symptoms and nasal
endoscopy) and sinus computed tomography findings. Nasal
biopsy samples were obtained during endoscopic sinus surgery
under general anaesthesia.
The control group consisted of 30 patients (6 females and
24 males), aged 19–78 years (average age (± SD) 41.6 ± 17.6
years), who were admitted to the hospital because of nasal sep-
tum deviation. The absence of nasal polyps was confirmed by
nasal endoscopy. Nasal biopsy samples were collected from the
lateral nasal wall below the middle turbinate during septo-
plasty. Only patients whose histological examinations of the
removed nasal mucosa revealed normal tissue were selected
for inclusion in the control group.
The study was conducted after receiving permission from
the Kaunas Regional Biomedical Research Ethics Committee
(number P1-86/2011). Informed consent was obtained from
all the patients investigated.
Patient evaluation questionnaire
Prior to surgery, all patients were required to complete a spe-
cially designed questionnaire. This assessed demographics,
unhealthy habits, and reflux-associated information including
their history of gastroesophageal reflux disease (regular use of
PPIs reported in the anamnesis and/or reflux-related findings
on upper gastrointestinal endoscopy).
Reflux-related symptoms
These were assessed with a standardised, validated question-
naire and the reflux symptom index. The reflux symptom
index examines nine symptoms common in laryngopharyn-
geal reflux: hoarseness; throat clearing; excess throat mucus;
difficulty in food swallowing; coughing after eating or after
lying down; choking episodes; troublesome cough; lump in
the throat; and heartburn, chest pain, indigestion or regurgita-
tion.12 The symptoms were self-rated on a six-point scale from
0 (not a problem) to 5 (a severe problem). A reflux symptom
index of 13 points or more was considered abnormal.12
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Video rhinolaryngoscopy
Clinical examination of the condition of the patient’s ear, nose,
throat and larynx was carried out using a specially designed
form. For all patients, diagnostic rhinolaryngoscopy was per-
formed in the out-patient department with a flexible 3.2 mm
endoscope (RLS; Kay Elemetrics, Lincoln Park, New Jersey,
USA), according to standard protocol. The same examiner
used the same sterilised equipment for each patient.
A validated reflux finding score scale was used to determine
the presence of subglottic oedema, ventricular obliteration,
erythema, vocal fold oedema, diffuse laryngeal oedema, pos-
terior commissure hypertrophy, granuloma and thick endolar-
yngeal mucus.13 A reflux finding score of more than 7 was
considered abnormal.13
The video recordings were rated by an observer, who was
unaware of the patient’s identity. The intra-rater correlation
for the video recordings (calculated over a 1-month time inter-
val, using 10 patient video recordings randomly selected from
the list) was 0.86.
H pylori identification methods
H pylori infection was identified via a histochemical examin-
ation and a rapid urease test. The samples were collected
from nasal polyps for the clinical group patients and from
nasal lateral wall mucosa for the control group patients,
using sterile instruments. A rapid urease test was performed
at the beginning of nasal surgery according to the manufac-
turer’s instructions. The biopsy samples were kept in paraffin
blocks until needed for the histological and histochemical
examinations.
Regarding the histochemical examination, the biopsy
material from the nasal tissues was subjected to Giemsa stain-
ing. Specifically, two 4-μm thick, paraffin-embedded sections
were prepared and stained using the modified methodology
(H pylori acquires a dark blue colour) (Figure 1).14
Regarding the rapid urease test, at the beginning of surgery,
the sterile bioptate (minimum 2 × 2 mm pieces) was placed
into a medium with urea and a pH indicator. When the
material contained H pylori, the urease enzyme changed
the endogenous urea into ammonia and carbon dioxide.
Moreover, the pH was changed by the released ammonia, and
the indicator colour shifted from yellow to orange, red or purple.
The campylobacter-like organism test (Kimberly-Clark, New
Milford, Connecticut, USA) was used. The changes in colour
were evaluated after 20 minutes, and after 1 and 3 hours, as
recommended.15 If the results of the two tests were positive,
H pylori was considered present in the biopsy material of the
nasal tissues.
Statistical analysis
Statistical analysis was performed using SPSS software, version
17 for Windows (SPSS, Chicago, Illinois, USA). The differ-
ences in qualitative parameters were calculated using the chi-
square or Fisher’s exact tests. The unpaired student’s t-test
(two-tailed) was used to compare the differences between
the quantitative data of the two groups. Analysis examining
the correlations between H pylori infection identified in the
nasal tissue and different variables, such as demographics
(age, gender, body mass index), unhealthy habits (alcohol
consumption, smoking), a history of gastroesophageal reflux
disease, reflux-related symptoms (assessed by the reflux
 The Journal of Laryngology & Otology
Fig. 1. Histopathological image of a biopsy specimen taken from nasal polyps (arrow
indicates H pylori on the submucosal gland epithelium). (Modified Giemsa stain;
×400)
symptom index) and reflux-related signs (assessed by the
reflux finding score), was performed using the Pearson’s or
Spearman’s correlation co-efficient (r). An α level of 0.05
was considered statistically significant. The Spearman’s correl-
ation co-efficient was used for an assessment of intra-rater
reliability.
Results
Our study showed a significantly higher positive H pylori rate
in the chronic rhinosinusitis with nasal polyposis group as
compared to the control group. H pylori infection in the
biopsy material from the nasal polyps was found in 28.9 per
cent (13 of 45) of the patients from the clinical group. These
results differ significantly from those of the control group,
where H pylori infection in the biopsy material from the non-
inflammatory nasal mucosa was found in only 3.3 per cent
(1 of 30) of patients ( p = 0.005) (Figure 2).
A data comparison of patients in whom H pylori was
detected in the biopsy specimens from the nasal tissues (13
patients with chronic rhinosinusitis with polyposis and 1 con-
trol patient) and the patients in whom H pylori was not
detected (32 patients with chronic rhinosinusitis with polyp-
osis and 29 control patients) showed no statistically significant
differences with regard to patients’ gender, age, body mass
index, smoking habits, alcohol consumption, history of gas-
troesophageal reflux disease, and summaries of reflux symp-
tom index and reflux finding score ( p > 0.05) (Table 1).
Interestingly, we found that a reasonably high number of
both H pylori positive and H pylori negative patients had a
pathological reflux symptom index score (57.1 per cent and
41.0 per cent, p = 0.27) and pathological reflux finding score
(64.3 per cent and 54.1 per cent, p = 0.48), respectively.
The analysis of correlations between H pylori infection
identified in the nasal tissue and different variables, which
included separate reflux symptom index symptoms and reflux
finding score signs, similarly showed no statistically significant
relationships between intranasal H pylori infection and:
patients’ demographic data (r = 0.05–0.21, p > 0.05), unhealthy
habits (r = 0.006–0.02, p > 0.05) or laryngopharyngeal reflux
related symptoms (r = −0.07–0.15, p > 0.05). However, there
was a significant yet weak positive relationship between H pyl-
ori positivity and posterior commissure hypertrophy of the
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3
Fig. 2. Distribution of H pylori positive results in the biopsy material of removed nasal
polyps or normal nasal mucosa (n = 75). There was a statistically significant difference
between the groups ( p < 0.05).
larynx (r = 0.24, p = 0.04). Thus, the presence of intranasal
H pylori was weakly related to the manifestation of a common
laryngopharyngeal reflux related sign. The data for the analysis
of correlations between intranasal H pylori infection and
patients’ laryngopharyngeal reflux related symptoms and
signs are presented in Table 2.
Discussion
Our findings show that H pylori is present in the sinonasal tis-
sue in nearly one-third of patients with chronic rhinosinusitis
with nasal polyposis, and is significantly more frequent than in
samples of control patients with healthy nasal mucosa. These
results are in agreement with previously published data.11,16 In
2008, Cvorovic et al. used the same diagnostic kit as in our
study, and found H pylori in 26.1 per cent of 23 patients
with chronic rhinosinusitis with nasal polyposis, and in 0
per cent of 15 control group patients.16 The most recent
study, published in 2016, by Bansal et al., presented similar
results: H pylori was found in 22.8 per cent of 35 patients
with chronic rhinosinusitis with nasal polyposis, and in only
2.9 per cent of the 35 control group patients.11
Recent studies that used the most sensitive H pylori diag-
nostic method, polymerase chain reaction, did not demon-
strate uniform results. However, the majority of these studies
detected H pylori and the most virulent CagA gene in nasal
polyps specimens.17–20
Some authors have investigated patients with chronic rhi-
nosinusitis without nasal polyposis, and these studies have
revealed similar results: the prevalence of H pylori was higher
in those patients than in the patients without chronic
rhinosinusitis.1,10,21
A significantly higher rate of H pylori in inflammatory sino-
nasal mucosa than in normal mucosa may suggest a positive
role of H pylori in chronic rhinosinusitis and nasal polyposis.
Moreover, a recent study assessing functional endoscopic sinus
surgery results showed greater improvement in patients with
chronic rhinosinusitis and H pylori sinonasal colonisation.22
There are several possible explanations for more frequent
detection of intranasal H pylori in patients with chronic rhino-
sinusitis. Chronic inflammation of the sinus and nasal mucosa
may create a more suitable environment for this bacterium to
survive than normal nasal mucosa. Nevertheless, the presence
of H pylori alone in the nasal tissues cannot prove a causal
relationship between chronic rhinosinusitis and polyposis. It
is known that H pylori, and species with the CagA gene in par-
ticular, could modify the normal gastric mucosa surface;23
therefore, we could speculate that H pylori infection may
 4 N Siupsinskiene, I Katutiene, V Jonikiene et al.

Table 1. Characteristics of H pylori positive and negative patients Table 2. Correlations between H pylori infection in nasal tissue and patients’
laryngopharyngeal reflux related data*
H pylori H pylori
Variable positive* negative† p Correlation
Variable co-efficient (r)† p
Males/females (%) 50.0/50.0 75.4/24.6 0.06
Laryngopharyngeal reflux related
Average age (years) 49.5 47.4 0.66 symptoms
Average BMI (kg/m2) 29.0 27.3 0.60 – Hoarseness 0.02 0.83
Smokers (%) 35.7 26.2 0.44 – Throat clearing 0.03 0.78
Drinkers (%) 35.7 45.9 0.29 – Excess throat mucus 0.06 0.61
History of GERD (%) 35.7 23.0 0.32 – Difficulty in food swallowing −0.07 0.55
Patients with pathological 57.1 41.0 0.27 – Coughing after eating or after 0.005 0.96
reflux symptom index (%) lying down
Patients with pathological 64.3 54.1 0.48 – Choking episodes 0.07 0.54
reflux finding score (%)
– Troublesome cough 0.15 0.18
*Patients with identified nasal H pylori (n = 14); †patients with unidentified nasal H pylori
(n = 61). BMI = body mass index; GERD = gastroesophageal reflux disease – Lump in throat 0.08 0.45
– Heartburn, chest pain, indigestion 0.07 0.54
or regurgitation

modify the mucosa of the nose and maxillary sinus as well. Laryngopharyngeal reflux related
signs
Such modifications may not only facilitate colonisation by H
pylori, but could also provide a target for an antibody – Subglottic oedema −0.11 0.34
response.10,23 – Ventricular obliteration −0.12 0.28
In 2003, Morinaka et al. established that H pylori may play – Erythema −0.10 0.38
a role as an antigen in patients who have chronic sinusitis with
infiltration of eosinophils and neutrophils.10 Similar data are – Vocal fold oedema −0.005 0.96

also available in the recent Bansal et al. study.11 The authors – Diffuse laryngeal oedema 0.02 0.82
examined samples from 35 nasal polyposis patients and 35 – Posterior commissure hypertrophy 0.24 0.04‡
controls with normal nasal mucosa, and assessed the morpho-
– Granuloma −0.08 0.49
logical changes. They found that inflammatory symptoms –
lymphocyte infiltration forming lymphocyte aggregates and – Thick endolaryngeal mucus −0.11 0.35
epithelial hyperplasia – were significantly more frequent in †
*n = 75. Pearson’s correlation co-efficient was used for parametric data and Spearman’s for
H pylori positive samples from nasal polyps than in samples non-parametric data. ‡Statistically significant ( p < 0.05)

from nasal polyps in which H pylori was not detected.11

Thus, we can hypothesise that H pylori itself may cause or
contribute to the chronic inflammation. The prevalence of
H pylori and the virulent CagA gene might also depend on
demographics – a high incidence of infection with CagA-
positive H pylori has been observed in Western Asia and
Eastern Europe.20,24
However, there are contradictory results regarding the role
of H pylori in chronic rhinosinusitis and nasal polyps, based
on the fact that H pylori and even the CagA gene can also
be found in normal nasal mucosa, and similarly in nasal
polyps.20,24 Researchers have argued that the nose could
serve as a reservoir for H pylori, which may be transmitted dir-
ectly into the nasal cavity from saliva and dental plaque, or
from any extragastric location, including the adenoids or ton-
sils.2,5,25 Any of the extragastric sites, including the nose, could
serve as a reservoir for gastric re-infection rather than being a
cause of chronic rhinosinusitis and polyps, as recurrence after
antimicrobial therapy is not uncommon.25
The presence of H pylori in patients with chronic rhinosi-
nusitis with polyposis could be linked to pathological reflux
of the upper airway. It has been suggested that gastroesopha-
geal reflux might play a role in the pathogenesis of chronic
rhinosinusitis.25,26 Our study shows a high prevalence of lar-
yngopharyngeal reflux related symptoms and signs among
H pylori positive patients (mainly patients with chronic rhino-
sinusitis with polyposis) and H pylori negative patients (equal
numbers of patients with chronic rhinosinusitis with polyposis
and controls). However, we found a significant yet weak posi-
tive relationship between intranasal H pylori infection and the
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most common laryngopharyngeal reflux related sign, posterior
commissure hypertrophy of the larynx.
It is not surprising that we found a significant relationship
between intranasal H pylori and the most common laryngo-
pharyngeal reflux related sign, despite similar results for
pathological reflux symptoms and signs in H pylori positive
and H pylori negative patients. A possible explanation is that
not all episodes of extra-oesophageal reflux could reach the
nasopharynx and nasal cavity, which has been proven by diag-
nostic tests with 24-hour nasopharyngeal pH-metry using a
four-channel pH probe.27 Additionally, perhaps not all
patients had intragastric H pylori that could be transmitted
to the upper airway.28 Furthermore, nasopharyngeal reflux is
more commonly severely refractory to treatment in chronic
rhinosinusitis patients.26,29 Unfortunately, in our study we
did not use objective 24-hour pH-metry or multichannel
impedancometry to prove the laryngopharyngeal reflux diag-
nosis or to estimate the character of reflux episodes in the
upper airway. The reflux symptom index and reflux finding
scores that were developed for quantification of the laryngo-
pharyngeal reflux symptoms and signs are more concerned
with the larynx than how the reflux enters the nasal cavity.12,13
However, our study shows that patients with hypertrophy of
the posterior commissure of the larynx – one of the primary
signs of laryngopharyngeal reflux – have a greater probability
for positive H pylori in the nasal cavity. This fact could suggest
the importance of reflux as the transmitter of H pylori to the
upper airway.
 The Journal of Laryngology & Otology
The scientific literature linking H pylori infection identified
in the nasal cavity to reflux is limited. Although pepsin and
pepsinogen 1 has been detected in sinonasal samples,25 and
some authors found that intranasal H pylori in patients with
chronic rhinosinusitis was related to classical gastroesophageal
reflux disease symptoms,1,11 others did not find a significant
relationship between H pylori in nasal polyps and chronic rhi-
nosinusitis in patients without classical gastroesophageal reflux
disease symptoms or signs.30
These findings could suggest that gastric juice infected with
H pylori, and not H pylori itself, is involved in the development
of chronic rhinosinusitis with or without nasal polyposis.2
However, the scientific literature reveals several hypotheses
concerning the possible influence of gastroesophageal reflux
and H pylori on the pathogenesis of chronic rhinosinusitis
and nasal polyposis. Numerous researchers have reported
that gastroesophageal reflux and H pylori infection may be
an interrelated phenomenon.1,24,28 It is possible that, as previ-
ously mentioned, chronic inflammation in the nasal cavity
caused by reflux may constitute a hypoxic and acidic environ-
ment for H pylori colonisation.1,17 In addition, the H pylori
bacterium itself could act as an inflammatory co-factor, similar
to gastroesophageal reflux, by promoting inflammation,
increasing production of interleukin-1 β, altering the sinonasal
mucosa and contributing to the reactive hyperplasia of the epi-
thelium.1,9,17,25 Recent analytical studies summarising the data
on the role of H pylori in the upper airway also indicated that
gastric juices infected with H pylori, and systemic immune
responses to gastric H pylori infection, might play a causative
role in upper respiratory diseases.2,3,4,28
No relationship between H pylori and other factors such as
patients’ age, gender or unhealthy habits was established in
this study or in previously reported data on patients with
laryngeal and tonsillar diseases.5,6 Dinis and Subtil also
found that none of the variables examined, such as age, gen-
der, nasal side, disease site, disease extension or the
co-presence of allergy, were related to bacterial colonisation.25
Summarising the results of our study and the literature
data, we argue that H pylori infection, regardless of the route
of transmission, is potentially related to chronic rhinosinusitis
with polyposis. However, the effect of this bacterium on the
chronic inflammatory process in the nasal and sinus mucosa,
and its relationship with laryngopharyngeal reflux, are not yet
clear and need further investigation. The data presented in the
literature are quite controversial. The findings are difficult to
compare because of the different methods of H pylori identifi-
cation used and other factors, including small sample sizes,
various patient selection criteria and demographic conditions.
Further well-designed, large-scale, multicentre studies are
needed to determine the role of H pylori in the aetiology of dif-
ferent nasal and sinus diseases.
• This study investigated the incidence of intranasal
Helicobacter pylori infection in patients with chronic
rhinosinusitis with polyposis
• Associations with patients’ sociodemographic and
laryngopharyngeal reflux related data were also examined
• H pylori was more prevalent in nasal tissue of chronic
rhinosinusitis with polyposis patients than in control patients
with a deviated septum
• Intranasal H pylori was associated with posterior commissure
hypertrophy of the larynx
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5
Conclusion
Our findings show that H pylori infection is potentially related
to chronic rhinosinusitis with polyposis. H pylori was identi-
fied in the biopsy material of nasal polyps in nearly one-third
of all patients who underwent endoscopic sinus surgery for
chronic rhinosinusitis with polyposis, and it was significantly
more frequent in these patients than in patients with normal
nasal mucosa. The presence of H pylori in the nasal tissues
was weakly associated with the manifestation of laryngophar-
yngeal reflux related posterior commissure hypertrophy of the
larynx.
Competing interests. None declared
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