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INTRODUCTION

Laryngophatyngeal Reflux (LPR) Gatroesophageal Reflux

- occurs when gastric contents pass (GERD)
the upper esophageal sphincter - develops when the reflux
- hoarseness, sore throat, coughing, causes symptoms like
excess throat mucus, and globus. heartburn and acid
- usually occurs during the daytime in regurgitation.
the upright position
- Helicobacter pylori (H. pylori) is
found in many sites including
laryngeal mucosa and
interarytenoid region

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 - half of otolaryngology
patients with laryngeal and
voice disorders have LPR
- common factors causing
inflammation in the upper
airways
- It may be caused by direct
exposure to acid, pepsin
and bile
- the presence of H. pylori
may be related to the
symptoms and findings
of LPR

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Belafsky et
al

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“

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“

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Belafsky et
al

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- ambulatory 24-h double
pH probe monitoring has
become the diagnostic
gold standard for LPR

- it is expensive and is not

widely available.

- high degree of specificity

and sensitivity.

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 Helicobacte
r pylory
- Gram-negative
bacterium
- Spiral-shaped with
four to six flagella
- obligate - susceptible to acid but
microaerophilic, protected by its motility
and urease, and its ability to convert
catalase and urea to ammonium by
oxidase positive urease

- routes of contamination
 fecal-oral, oral-oral,
gastro-oral, and
iatrogenic
Helicobacte
r pylory

- localized primarily in the

gastric mucosa

- Reported that the

microorganism may exist
in laryngeal mucosa and
interarytenoid region,
paranasal sinuses,
tonsils, adenoids
 diagnosis for H. pylori

- an empiric trial of PPI therapy over a

- Breath
prolonged period  proposed as a
test valid diagnostic test for LPR.
- Blood Biopsy
tests - The typical regime is twice daily PPI
- Stool test therapy for 1-6 mo.
TREATMENT

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 DISCUSSION
Regarding the relationship between LPR and
H. pylori, the literature is limited

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Oridate et al

compared H. pylori antibody positivity,

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laryngopha- ryngeal reflux symptoms,
objective laryngopharyngeal findings, and
rate of response to acid suppressive therapy
in 42 patients with GERD

 the laryngopharyngeal symptom

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relief induced by acid suppression was
significantly lower among H. pylori
antibody-negative than antibody-
positive cases
Rouev et al

compared 46 patients with GERD and LPR

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symptoms

found that there was an increasing

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tendency in GERD patients that
develop LPR symptoms

found 11 patients with H. pylori infection

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Cekin et al

found no association between H. pylori and

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LPR status

In addition, they analyzed two subgroups

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based on whether their lesions were
benign/malignant/premalignant  found a
significant relationship between LPR
positivity and the presence of malignant/
premalignant laryngeal lesions. But no
association between H. pylori status
Tezer et al

concluded that the expression of H. pylori

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positivity and degree of GERD correlated
with LPR in 45 patients. H. pylori positivity
and degree of GERD were more adverse in
patients with an RFS of ≥ 7
Ercan et al

32 LPR patients were investigated

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regarding the presence of H. pylori, degree
of gastritis and esophagitis, and also the
number of reflux episodes, acid exposure
(proximal probe readings)

They found that there was no relationship

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between the presence of H. pylori and LPR.
Islam et al

took biopsies from the vocal fold and

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interarytenoid region of 50 patients.

H. pylori was not found in the histological

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specimens of the vocal fold and
interarytenoid region

The presence of H. pylori in the gastric

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mucosa (by UBT) and H. pylori antibodies
does not have an effect on the RFS and
RSI.
Siupsinskiene et al
found H. pylori in the biopsy material from
01 the larynx in more than one-third of the
patients  suffering from benign laryngeal
disease and laryngeal cancer

Patients with chronic laryngitis and laryngeal

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cancer showed the highest rate of H. pylori
infection in the larynx.

However, the relationship was not clearly

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identified and they concluded that further
studies are needed
Youssef and Ahmed
H. pylori treatment and LPR symptom
01 resolution was investigated  H. pylori
stool antigen (HPSA) test was positive in
57%

Patients with negative HPSA were treated

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with esomeprazole  reported improvement
score of 96.6%

Patients with positive HPSA test results

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were divided into two groups: one received
only esomeprazole, with reported
improvement in 40%
Youssef and Ahmed
the second group was treated with
04 esomeprazole, plus amoxicillin sodium and
clarithromycin (triple therapy)  90%
incidence of symptom improvement.
The incidence of H. pylori infection in
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patients with LPR was 57%.

Concluded that H. pylori infection should be

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considered when treatment is prescribed to
patients with LPR the standard therapy for
GERD might be insufficient
 CONCLUSION

Most LPR patients

have only mild
symptoms. Unlike
GERD patients, they
seldom have
heartburn or Laryngoscopic examination
Detailed history
regurgitation. most commonly
taking and
demonstrates findings in
laryngoscopic
the posterior glottis & vocal
examination  the
folds  Laryngeal edema is
basis for diagnosis
an important indicator for
of LPR.
LPR ,that is most often
neglected.

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 CONCLUSION

Acid suppression with

PPI on a long-term basis
is the mainstay of
treatment  a trial of
PPIs may also be useful
as a diagnostic maneuver
but it should be at least 4
mo.
Laryngeal acid and
pepsin sensitivity is
greater in oropharyngeal
mucosa than
esophageal mucosa 
the main difference of
LPR and GERD
pathophysiology.

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 CONCLUSION

H. pylori is found in many sites,

including laryngeal mucosa and
interarytenoid region.

the importance of this

colonization and its effects on
disease progress and treatment
outcome is yet to be identified
with prospective clinical
studies

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