JOURNAL READING

Rhinosinutis and
Asthma in Children
LEADER :
Dr. Agus Sudarwi, Sp.THT-KL
Dr. Afif Zjauhari, Sp.THT-KL

BY :
Sushanti Nuraini (30101307085)
Adita Ayu Aprilia (30101407112)
Vita

KEPANITERAAN KLINIK ILMU THT

RSUD DR. LOEKMONO HADI KUDUS
UNIVERSITAS ISLAM SULTAN AGUNG
2018
Journal Identity
Tittle Journal
Rhinosinutis and Asthma in Children

Authors
Amelia Licari, Ilaria Brambilla, Riccardo
Castagnoli, Alessia Marseglia, Valeria
Paganelli, Thomas Foiadelli ID and
Gian Luigi Marseglia

Publication by
Pediatric Clinic, University of Pavia,
Fondazione IRCCS Policlinico San
Matteo, 27100 Pavia, Italy
ABSTRACT
 Rhinosinusitis and asthma are two comorbid condi
tions that affecting the respiratory tract. They are
INTRODUCTION connected by significant anatomical, epidemiologic
al, pathophysiological, and clinical evidence, and
also share therapeutic principles.

The aim of this review is to provide an updated ov

GOAL
erview of the existing link between rhinosinusitis
and asthma focusing on the pediatric age.
1. Introduction

Rhinosinusitis and asthma are

major public health problem

frequency and their impact on

quality of life, school perform
ance and economic burden
European Position Paper on Rhinosinusitis
and Nasal Polyps
pediatric rhinosinusitis = an inflammation of the nose and the paranasal sinuses characterized by
two or more symptoms

nasal blockage endoscopic signs of nasal polyps

(mucopurulent discharge primaril
nasal obstruction
y from the middle meatus and ed
nasal congestion ema, mucosal obstruction primari
nasal discharge (anterior/ ly in the middle meatus)
posterior nasal drip) Computed tomography (CT) 
± facial pain, facial pressure an mucosal changes within the ostio
d coughing meatal complex or sinuses
 ACUTE
RHINOSINUSITIS
(ARS)

<12 weeks
sudden onset of symptoms
Up to 90% viruses agents
might be aggravated by underlying allergic
conditions (i.e., allergic rhinitis)
CHRONIC
RHINOSINUSITIS (CRS)
≥ 12 weeks
Coughing is a much more significant symptom in
children
Other widespread conditions such as allergic rhinitis,
adenoid disease, and gastroesophageal reflux
Affects approximately 5–15% population in US and
Europe

CRS with nasal poly

Based on nasal posis (CRSwNP)
endoscopic and
CT findings
CRS sine nasal poly
posis (CRSsNP)
 a. Nasal Polyposis (NP)

More frequently seen in men than in women

Adolescents or elderly

Asthmatic subjects

It is less common in childhood

NP may be either isolated or associated with other medical conditions. Isolated NP

in children is a rare condition, representing an alert sign for other underlying systemic d
iseases (including cystic fibrosis, immunodeficiencies, and primary ciliary dyskinesia)
b. Pediatric severe chronic upper airway dis
ease (P-SCUAD)
Introduced to define difficult-to-treat cases, characterized by the persistence of

upper airway inflammation and symptoms despite correct diagnosis and

management.

These cases often show a negative impact on quality of life, social functioning,

and school or work performance

CHRONIC RHINOSINUSITIS (CRS)
Adenoid hypertrophy
allergic rhinitis (AR)
asthma
• Adenoids may act as
a bacterial reservoir,
Clinical Outcom as well as an active
immunological organ
es and disease
control in CRS • Adenoidectomy is eff
ective in controlling
patients
symptoms in children
with CRS

Correlation between allergies

and the severity of a sinus disea
se, have long been supported as
a possible causal relationship
between CRS and AR. AR is not
a trigger for CRS, but rather a co
morbidity
 Asthma

A heterogeneous condition, with the specifi

c hallmark of chronic airway inflammation.

Symptoms : coughing, wheezing, shortness of breath and chest tightness, which may change over time
and in intensity due to airflow limitation in respiratory airways.

Exercise, allergen expos Patients

ure, weather, or viral inf
ections, and represent
a major health problem
to patients Flare-ups (exa Life-threatening
cerbations)
Goal
To provide an updated
overview on the existing
link between rhinosinusitis
and asthma focusing on
pediatric age.
2. Rhinosinusitis and Astma in Children

Strong anatomical, epidemiological,

pathophysiological, clinical, and
Therapeutic evidence

Regarding the link between upper and

lower airways

“united airway disease (UAD)”

2.1. Anatomical Evidence
 Upper air conduction and gas
Respiratory Respiratory
apparatus tracts exchange
Lower

Macroscopic
Share similarities
Nose + lung
several Microscopic

Pseudostratified respiratory epithelium with

Histologically columnas ciliated cell

Basement membrane and ciliary The whole respiratory tree

epithelium with glands and goblet
cells The respiratory bronchioles with
the air cells
 Complex anatomical structure

Humidif Temp Supply the air Protecting the lo

Filter with nitrat oxid
y er wer respiratory t
e ract

Inhalation of cold and dry

air

Loss of nasal breathin

g
Rhinosinusitis

Trigger for bronchial disorder

 Inhaled foreign substance

Air conduction system Protecting the lower tract

Avoiding particles of 5-10 in diameter

Mouth breathing concentrations of inhaled aeroallergens

Bronchoconstriction in asthmatic subjects

Nose +
to be implemented via mechanisms
bronkus

Neural reflexes Systemic pathways

 2.2. Epidemiogical Evidence
Eosinophilic asthma phenotypes + CRSwNP

Epidemiological In adult
Asma + CRS
evidence

10-30%
severity of mild Regardless of smoking
Presence of NP asthma
70-90% status
severe
European Unbiased Ocomarkers for the Prediction of Respiratory
Disease Outcomes ( UBIOPRED )

High incidence of upper airway

NP 25% of adult subjects

 Comorbidities on asthma severity and control

Us Severe Asthma Research UU Dificult Asthma National

Program ( SARP ) Registry

27% of pediatric patient with Radiological evidence of

status asthmaticus rhinosinusitis

Evidence of rhinosinusitis upon

44% of 128 asthmatic children
endoscopic examination

An asymptomatic “occult” 7,5% of an uncontrolled asthmatic chi

sinusal involvement ldren sinus surgery / adenoidectomy

children with Worse surgical outcomes VS

Dejima et al
asthma non asthmatic children
 Impact of upper airway Pre-school children
pathology on asthma Untreated / un diagnosed upper
severity + control airways obstruction

Rhinosinusitis + adenoid hypertropy

Worsen the obstructive pathology of

the lower airways

Analysis of pediatric Increase Inicidence of comorbidities

SARP in cluster 3

Bronchial hyperresponsiveness
Main comorbidities
+ lower lung function

Phenotypes in children differ in adults Rapidly change over time

 2.3. Pathophysiological Mechanisms
heterogeneous disorders
Asthma + CRS +
complex pathophysiology

- Th2 cell induction

type 2 inflammatory
- Production IL-5 and IL-13
pattern
- Eosinophilic infiltration

Upper + Lower
inflammation observed in an adult population
 typical Th2 cytokine response

allergic asthmatic children wit

h rhinosinusitis

Riccio et al.

a Th2 to a Th1

allergic and non-allergic

after medical treatment of CRS

 Tosca et al. change in levels of IL-4 and interferon-ϒ
(IFN-ϒ)

children with asthma and CRS

 After a 14-day t
reatment of oral a decrease in IL-4 and a significant increase
ntibiotics and intra in IFN ϒ  allergic study participants
nasal steroids
 A 10-day treatm decrease in IL-4 and a non-significant incr
ent of oral steroid ease in IFN- ϒ  non-allergic study partici
s. pants after the treatment
 Anfuso et al.

children with CRS and asthma

• levels of TNF-α
• adenoid levels of epidermal growth factor
• Eotaxin
• fibroblast growth factor-2
• growth-related oncogene,
• and platelet-derived growth factor-AA

with CRS and without asthma

 “united airways disease”

inflammation may start at one site and extend t

o other sections eventually

 extension by contiguity
 complex interplay among several immunological m
echanisms (inside and outside) involving the bone m
arrow
 experimental murin
eosinophilic
e

after intranasal allergen exposure

Th2 lymphocytes circulate and migrate significantly to several sites

released from the storage

bronchial airways
pools in the bone marrow

triggering inflammation in the airways may stimulate the bone marrow

inflammatory cells and mediators

respiratory sites other than those affected initially

2.4. Clinical and Therapeutic Management

Upper airway disease

Risk of more severe

disease

Early identification

Nasal endoscopy
 Nasal mucosal and
Blood

Enterotoxin-specific IgE
Diagnostic Biomarker Prognostic Biomarker
of S. aureus

• IgE • Risk factor for co

• ECP • IgE morbid asthma
• IL-4 • ECP • Recurrence of NP
• IL-5 • IL-5 after surgery
• IL-13
 Primary goal of
Maintain and clinical control
CRS treatment

Treatment for • Corticosteroid

CRSwNP and • Nasal saline irrigation
CRSsNP

Treatment for CRSwNP

• Antibiotics
NOT PROVEN
• Antihistamine
• Leukotrien receptor antagonist
Failure of medical
therapy

 Recurrence
ESS 80%

Must be with medical

therapy
Previous study

Recurrent CRSwNP and

comorbid asthma Identified by a type 2 immune response
(IgE, eosinophils, IL-5, IL-4/IL-13)

Monoclonal antibodies against IgE,

IL-5, IL-4, IL-13 pathways
• Omalizumab
• Mepolizumab
• Dupilumab
 CONCLUSION

Chronic Rhinosinusitis Asthma

- Pathophysological mechanism
- Therapeutic principal

Undiagnosed and Untreated

• Contribute to worsen
Identify patients at risk of more severe
Asthma
disease. Even in the case of minimal
• Complicate diagnostic
or absent symptoms
and management
 Thank you
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