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Juvenile Nasopharyngeal Angiofibroma Background Juvenile angiofibroma (JNA) is a benign tumor that tends to bleed and occurs in the nasopharynx of prepubertal and adolescent males. History of the Procedure Hippocrates described the tumor in the 5th century BC, but Friedberg first used the term angiofibroma in 1940. Other titles (eg, nasopharyngeal fibroma, bleeding fibroma of adolescence, fibroangioma) have also been used. The image below depicts a coronal CT scan. 1

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Juvenile Nasopharyngeal Angiofibroma

Background

Juvenile angiofibroma (JNA) is a benign tumor that tends to bleed and occurs in the nasopharynx

of prepubertal and adolescent males.

History of the Procedure

Hippocrates described the tumor in the 5th century BC, but Friedberg first used the term

angiofibroma in 1940. Other titles (eg, nasopharyngeal fibroma, bleeding fibroma of

adolescence, fibroangioma) have also been used.

The image below depicts a coronal CT scan.

Coronal CT scan of the lesion filling the left nasal cavity and ethmoid sinuses, blocking the

maxillary sinus and deviating the nasal septum to the right side.

1

Epidemiology

Frequency

Juvenile nasopharyngeal angiofibroma (JNA) accounts for 0.05% of all head and neck tumors. A

frequency of 1:5,000-1:60,000 in otolaryngology patients has been reported.

Sex

Juvenile nasopharyngeal angiofibroma (JNA) occurs exclusively in males. Females with juvenile

nasopharyngeal angiofibroma (JNA) should undergo genetic testing.

Age

Onset is most commonly in the second decade; the range is 7-19 years. Juvenile nasopharyngeal

angiofibroma (JNA) is rare in patients older than 25 years.

Etiology

The lesion originates in close proximity to the posterior attachment of the middle turbinate, near

the superior border of the sphenopalatine foramen.

A hormonal theory has been suggested because of the lesion's occurrence in adolescent males.

Other theories include a desmoplastic response of the nasopharyngeal periosteum or the

embryonic fibrocartilage between the basiocciput and the basisphenoid.

Etiology from nonchromaffin paraganglionic cells of the terminal branches of the maxillary

artery has also been suggested. Comparative genomic hybridization analysis of these tumors

revealed deletions of chromosome 17, including regions for the tumor suppressor gene p53 as

well as the Her-2/neu oncogene.

2

Pathophysiology

The tumor starts adjacent to the sphenopalatine foramen. Large tumors are frequently bilobed or

dumbbell-shaped, with one portion of the tumor filling the nasopharynx and the other portion

extending to the pterygopalatine fossa.

Anterior growth occurs under the nasopharyngeal mucous membrane, displacing it anteriorly and

inferiorly toward the postnasal space. Eventually, the nasal cavity is filled on one side, and the

septum deviates to the other side. Superior growth is directed toward the sphenoid sinus, which

may also be eroded. The cavernous sinus may become invaded if the tumor advances further.

Lateral spread is directed toward the pterygopalatine fossa, bowing the posterior wall of the

maxillary sinus. Later, the infratemporal fossa is invaded. Occasionally, the greater wing of the

sphenoid may be eroded, exposing the middle fossa dura. Proptosis and optic nerve atrophy

result if orbital fissures are encroached upon by the tumor. Extranasopharyngeal angiofibroma is

extremely rare and tends to occur in older patients, predominately in females, but the tumor is

less vascular and less aggressive than juvenile nasopharyngeal angiofibroma (JNA).

Presentation

Symptoms

Nasal obstruction (80-90%) - Most frequent symptom, especially in initial stages

Epistaxis (45-60%) - Mostly unilateral and recurrent; usually severe epistaxis that

necessitates medical attention; diagnosis of angiofibroma in adolescent males to be ruled

out

Headache (25%) - Especially if paranasal sinuses are blocked

Facial swelling (10-18%)

Other symptoms - Unilateral rhinorrhea, anosmia, hyposmia, rhinolalia, deafness, otalgia,

swelling of the palate, deformity of the cheek

3

Signs

Nasal mass (80%)

Orbital mass (15%)

Proptosis (10-15%)

Other signs include serous otitis due to eustachian tube blockage, zygomatic swelling,

and trismus that denote spread of the tumor to the infratemporal fossa, decreasing vision

due to optic nerve tenting (rare)

Differentials

Other causes of nasal obstruction, (eg, nasal polyps, antrochoanal polyp, teratoma,

encephalocele, dermoids, inverting papilloma, rhabdomyosarcoma, squamous cell

carcinoma)

Other causes of epistaxis, systemic or local

4

Other causes of proptosis or orbital swellings

Nasal Endoscopy

Given the presenting symptoms, the patient should be examined by nasal endoscopy which

usually shows a large, lobulated mass behind the middle turbinate filling the choana with a

smooth surface and clear signs of hypervascularization.

Endoscopic appearance of JA showing a lobulated hypervascularized mass with a smooth surface

partially covered by fibrin growing into the left nasal fossa. NS: nasal septum; IT: inferior

turbinate; JA: juvenile angiofibroma.

Imaging Studies

Plain radiography views of the sinuses may demonstrate nasopharyngeal polyp. Bowing of the

posterior wall of the maxillary sinus and maxillary sinus opacification is very suggestive of

juvenile nasopharyngeal angiofibroma (JNA). Newer radiographic modalities have surpassed

plain films in usefulness.

5

CT scan images below demonstrate the extent of the tumor. Extension to the sphenoid sinus,

erosion of the greater sphenoidal wing, or invasion of the pterygomaxillary and infratemporal

fossae is usually visualized, as in the images below.

Coronal CT scan of the lesion filling the left nasal cavity and ethmoid sinuses, blocking the

maxillary sinus and deviating the nasal septum to the right side. Axial CT scan of lesion

involving the right nasal cavity and paranasal sinuses.

Magnetic resonance imaging (MRI) is indicated to delineate and define the extent of the tumor,

especially in cases of intracranial involvement. Coronal MRI scan showing extension of the

lesion to the cavernous sinus is seen in the image below.

6

Coronal MRI scan showing extension of the lesion to the cavernous sinus.

Angiography shows the branches of the external carotid system to be the primary feeders (94%).

The main supply comes from the internal maxillary artery, but ascending pharyngeal or vidian

arteries may contribute to the blood supply. Unnamed branches from the internal carotid artery

contribute to vascularity in rare instances. Bilateral vascular supply may be an underappreciated

factor in JNA, and thorough radiographic investigation via angiography of bilateral carotid

systems should be routinely performed preoperatively.[1] An angiofibroma before and after

embolization can be seen in the images below.

Angiogram depicting angiofibroma before embolization.

7

Angiogram depicting angiofibroma after embolization.

 

 Histologic Findings

On gross examination, the tumor is usually sessile, lobulated, rubbery, and red-pink to tan-gray

in appearance. In rare cases, the tumor is polypoid or pedunculated.

Nasopharyngeal angiofibroma is usually encapsulated and composed of vascular tissue and

fibrous stroma with coarse or fine collagen fibers. Vessels are thin-walled, lack elastic fibers,

have absent or incomplete smooth muscle, and vary in appearance from stellate or staghorn to

barely conspicuous because of stromal compression. Stromal cells have plump nuclei and tend to

radiate around the vessels. An abundance of mast cells in the stroma and a lack of other

inflammatory cells exist. Localized areas of myxomatous degeneration may be observed in the

stroma.

When examined under electron microscope, stromal cells are mostly fibroblasts and show

intensive immunostaining for vimentin. However, myofibroblasts may occur focally in

connection with fibrotic areas and are characterized by the coexpression of vimentin and smooth

muscle actin.

8

(a) (b)

Microscopic appearance of JA (hematoxylin-eosin staining (a) and immunohistochemistry for

factor VIII (b)). Vessel caliber is extremely variable, the muscular layer of vessels is frequently

absent, and stromal cells have usually a spindle-shaped appearance.

Angiofibroma; Staghorn-shaped blood vessels (arrows) with endothelial cells but no smooth muscle are

compressed by fibrous tissue

9

Staging

Different staging systems exist for nasopharyngeal angiofibroma. There are many classification

described although none is universally accepted. There are a variety of staging criteria developed

for evaluating JNAs which include those developed by Radkowski, Fisch, Andrews, Chandler,

Johns, Onerci and Sessions although none is universally accepted. In several staging systems that

of Andrews (1989) is the most robust and practical for exclusively endoscopic surgery for

JNAs17. Another staging system is Radkowski (1996) that is the most recently developed

staging system and appears most commonly in recent literature on JNAs.

Classification according to Sessions

o Stage IA - Tumor limited to posterior nares and/or nasopharyngeal vault

o Stage IB - Tumor involving posterior nares and/or nasopharyngeal vault with

involvement of at least 1 paranasal sinus

o Stage IIA - Minimal lateral extension into pterygomaxillary fossa

o Stage IIB - Full occupation of pterygomaxillary fossa with or without superior

erosion of orbital bones

o Stage IIIA - Erosion of skull base (ie, middle cranial fossa/pterygoid base);

minimal intracranial extension

o Stage IIIB - Extensive intracranial extension with or without extension into

cavernous sinus

Classification according to Fisch

o Stage I - Tumors limited to nasal cavity, nasopharynx with no bony destruction

o Stage II - Tumors invading pterygomaxillary fossa, paranasal sinuses with bony

destruction

o Stage III - Tumors invading infratemporal fossa, orbit and/or parasellar region

remaining lateral to cavernous sinus

o Stage IV - Tumors invading cavernous sinus, optic chiasmal region, and/or

pituitary fossa

10

Classification according to Andrews

Stage I - Limited to the nasopharynx and nasal cavity. Bone destruction negligible

or limited to the sphenopalatine foramen

Stage II - Invading the pterygopalatine fossa or the maxillary, ethmoid, or

sphenoid sinus with bone destruction

Stage III

(a) Invading the infratemporal fossa or orbital region without intracranial

involvement

(b) Invading the infratemporal fossa or orbit with intracranial extradural

(parasellar) involvement

Stage IV

(a) Intracranial intradural without infiltration of the cavernous sinus, pituitary

fossa or optic chiasm

(b) Intracranial intradural with infiltration of the cavernous sinus, pituitary fossa

or optic chiasm

Classification according to Radkowski

Stage I

(A) Limited to posterior nares and/or nasopharyngeal vault

(B) Involving the posterior nares and/or nasopharyngeal vault with involvement

of at least one paranasal sinus

Stage II

(A) Minimal lateral extension into the pterygopalatine fossa

(B) Full occupation of pterygopalatine fossa with or without superior erosion

orbital bones

(C) Extension into the infratemporal fossa or extension posterior to the pterygoid

plates

Stage III

(A) Erosion of skull base (middle cranial fossa/base of pterygoids)—minimal

intracranial extension

11

(B) Extensive intracranial extension with or without extension into the cavernous

sinus

Classification according to Önerci

o Stage I - Nose, nasopharyngeal vault, ethmoidal-sphenoidal sinuses, or minimal

extension to PMF

o Stage II - Maxillary sinus, full occupation of PMF, extension to the anterior

cranial fossa, and limited extension to the infratemporal fossa (ITF)

o Stage III - Deep extension into the cancellous bone at the base of the pterygoid or

the body and the greater wing of sphenoid, significant lateral extension to the ITF

or to the pterygoid plates posteriorly or orbital region, cavernous sinus

obliteration

o Stage IV - Intracranial extension between the pituitary gland and internal carotid

artery, tumor localization lateral to ICA, middle fossa extension, and extensive

intracranial extension

Classification according to Snyderman

o Stage I - No significant extension beyond the site of origin and remaining medial

to the midpoint of the pterygopalatine space

o Stage II - Extension to the paranasal sinuses and lateral to the midpoint of the

pterygopalatine space

o Stage III - Locally advanced with skull base erosion or extension to additional

extracranial spaces, including orbit and infratemporal fossa, no residual

vascularity following embolisation

o Stage IV - Skull base erosion, orbit, infratemporal fossa. Residual vascularity.

o Stage V - Intracranial extension, residual vascularity

M: medial extension

L: lateral extension

12

Medical Therapy

Hormonal therapy

The testosterone receptor blocker flutamide was reported to reduce stage I and II tumors to 44%.

Despite tumor reduction with hormones, this approach is not routinely used. Schuon et al

reported on the immunohistochemical analysis of growth mechanisms in juvenile

nasopharyngeal angiofibroma. They concluded that juvenile angiofibroma (JNA) growth and

vascularization are driven by factors released from stromal fibroblasts. Therefore, inhibition of

these factors might be beneficial for the therapy of inoperable juvenile nasopharyngeal

angiofibroma (JNA).

Radiotherapy

Some centers have reported 80% cure rates with radiation therapy. However, concerns regarding

potential effects of radiation make radiation therapy a nonuseful modality in most cases.

The use of radiotherapy for the primary treatment of angiofibroma has been advocated in recent

publications. External beam radiation is generally reserved for larger and/or unresectable tumors

and tumors that are life threatening due to their location. Studies by Briant et al. and Cummings

et al. both reported an 80% control rate with moderate dose primary radiotherapy (30 to 35 Gy

given in 15 fractions over a 3 week period). Additional other authors have reported good results

after radiotherapy for surgically inaccessible intracranial extension or for recurrences following a

primary procedure. Long-term severe complications of radiation therapy are encountered

including growth retardation, panhypopituitarism, temporal lobe necrosis, cataract, and radiation

keratopathy. Also others reported remote secondary malignancy of the head and neck such as

thyroid carcinoma and sarcomas of bone-soft tissue a serious adverse effect of radiation therapy

on JNA.

Stereotactic radiotherapy (ie, Gamma Knife) delivers a lower dose of radiation to surrounding

tissues. However, most authorities reserve radiotherapy for intracranial disease or recurrent

cases.

13

Conformal radiotherapy in extensive juvenile nasopharyngeal angiofibroma (JNA) or intracranial

extension provides a good alternative to conventional radiotherapy regarding disease control and

radiation morbidity, even with advanced disease.

Surgical Therapy

Liston(1841), performed the first successful resection of an angiofibroma on a 21-year-old man

from Gibraltar. The treatment of choice in the vast majority of patients is surgical resection.

Surgical techniques for JNAs include open surgical approach and endoscopic surgery or

combined those techniques depending on the stage of the tumor. Several factors are critical when

choosing the surgical technique for JNA; adequate exposure of the tumor, ability to control

bleeding, prevention of postoperative facial deformity and avoidance of interference with growth

of the face.

Open Surgical Approach

Open surgical approaches are transoral, transfacial, and combined craniofacial approaches (more

specifically transpalatal, transantral, transnasal, lateral rhinotomy, midfacial degloving, LeFort 1

osteotomy, and infratemporal fossa approach).

A lateral rhinotomy, transpalatal, transmaxillary, or sphenoethmoidal route is used for small

tumors (Fisch stage I or II). Lateral rhinotomy approach has the advantage of access to the nose,

maxillary antrum, ethmoids and nasopharynx, pterygopalatine fossa. However it leaves an

external scar and removal of nasal and facial bones in prepubertal boys could lead to facial

asymmetry. Persistent nasal crusting, facial paresthesia, lacrimal apparatus injuries are also seen

in this approach.

Transpalatine approach provides access to the nasopharynx, sphenoid, sphenopalatine foramen

and posterior nares. It avoid external scar and does not effect the facial growth but oronasal

fistula is a more common side effect. This approach was selected in the majority of patients with

advanced disease by Cansiz et al. Open approaches are favored by some surgeons and remain

indicated for larger JNAs. Additional all open approaches can be supplemented by the use of

endoscopes.

14

The infratemporal fossa approach is used when the tumor has a large lateral extension.

The midfacial degloving approach, with or without a LeFort osteotomy, improves posterior

access to the tumor. Midfacial degloving approach provides good exposure to the maxillary

antrum, nose, pterygopalatine fossa and infratemporal fossa. There will be no deforming scar on

face because of the use of a sub labial incision, but needs extensive removal of bones from the

anterior, posterior, medial and lateral walls of maxillary antrum

The facial translocation approach is combined with Weber-Ferguson incision and coronal

extension for a frontotemporal craniotomy with midface osteotomies for access.

An extended anterior subcranial approach facilitates en bloc tumor removal, optic nerve

decompression, and exposure of the cavernous sinus.

Endoscopic Surgery

Improvements in endonasal technique and knowledge of the intranasal anatomy enable the use of

nasal endoscopic surgery to remove some JNA tumors. The decision to perform JNA resection

endoscopically should be based on the experience and skill of the surgeon as well as the extent of

the tumor. Endoscopic sinonasal surgery and embolize these tumors preoperatively is to allow

atraumatic dissection, minimizing bleeding and more precise tumor resection, thus minimizing

the possibility of residual tumor. Patient selection for endoscopic resection is of paramount

importance for a successful outcome. It has been suggested that tumors involving the ethmoid,

maxillary, or sphenoid sinus, the sphenopalatine foramen, nasopharynx, pterygomaxillary fossa

and have limited extension into the infratemporal fossa are amenable to endoscopic resection.

Onerci et al. reported no recurrence for tumors extension into infratemporal fossa.

Some authors advocate the use of intranasal endoscopic surgery for lesions with limited

extension to the infratemporal fossa. Endoscopic surgery has a great advantage because it

preserves both the anatomy and physiology of the nose, requires less rehabilitation days after

surgery, requiring less days of hospitalization and is less subject to hospital infections. The

“push-pull” technique involves an incision of about 1 inch in the upper bucco-gingival sulcus,

one more step in the evolution of endoscopic surgery for JNA. It is now possible to excise

15

tumors with large lateral extensions in the infratemporal and parapharyngeal regions without

resorting to an open approach. Image-guided, endoscopic, laser-assisted removal has also

recently been used. Hackman et al (2009) reviewed 31 cases of JNA at the University of

Pittsburgh Medical Center from 1995 to 2006. Most tumors were completely excised using the

expanded endonasal approach (EEA) alone or in combination with minor sublabial incisions,

avoiding the morbidity associated with larger open approaches or postoperative radiation

therapy.

Radical removal of a large JNA may be difficult because of its extreme vascularity and extension

to the cavernous sinus, orbit, middle fossa, and anterior fossa. Nevertheless, most of JNAs with

intracranial extension can be resected in the first operation with minimal morbidity through a

facial degloving and further combination of expanded endoscopic endonasal approaches.

Preoperative Details

Preoperative embolization has typically been performed via a transarterial route using a variety

of embolic materials. It is accomplished using reabsorbable microparticulate substances (eg,

Gelfoam, polyvinyl alcohol, dextran microspheres) or nonabsorbable microparticulates (eg,

Ivalon, Terbal). Limiting blood loss during surgery is essential. Endoscopic assistance has been

used for direct transnasal tumor puncture and intratumoral embolization using the liquid embolic

agent Onyx.

Postoperative Surveillance

Based on the experience by Kania et al., Lund et al., and Nicolai et al., recommended

postoperative MR imaging after removal of the nasal packing and until 72 hours for early

identification of any suspicious residual disease. The reason for this is the presence of minor

inflammatory changes, typically observed 3-4 months after treatment, which frequently

challenge differentiation between residual JA and active scar tissue. Although this surveillance

policy has to be validated by longer follow-up periods, Nicolai et al., observed that patients with

no signs of persistence do not develop any lesion even at subsequent MR examination.

Endoscopic examination has limited value in the identification of residual/recurrence disease

16

because of the submucosal growing pattern of JA, which is detected with more precision by

enhanced MR or MSCT. Whatever technique is selected, the examination should be performed

every 6–8 months for at least 3 years after surgery. Moreover, depending on suspicious

enhancement, incomplete resection and age of onset, angio-MR imaging may be scheduled.

Closer radiologic survey may be required to better evaluate the growth and plan treatment for

persistent JA.

Complications

Preoperative angiography and embolization minimize intraoperative blood loss, and the current

shift in the treatment to endoscopic excision in selected cases reduces perioperative morbidity.

Low-grade consumption coagulopathy may complicate small juvenile nasopharyngeal

angiofibroma (JNA) and implies that preoperative coagulation screening may have a role in

perioperative hemostasis.

Malignant transformation has been reported in 6 cases; 5 of these patients were treated with

radiotherapy, according to a study by Makek et al.

Transient blindness has been reported as a result of embolization, but it is a rare occurrence.

Osteoradionecrosis and/or blindness due to optic nerve damage may occur with radiotherapy.

Fistula of the palate at the junction of the soft and hard palate may occur with the transpalatal

approach but is prevented by preservation of the greater palatine vessels during flap elevation.

Anesthesia of the cheek is a frequent occurrence with the Weber-Ferguson incision.

Outcome and Prognosis

The presence of tumor in the pterygoid fossa and basisphenoid, erosion of the clivus, intracranial

extension, feeders from the internal carotid artery, a young age, and a residual tumour were risk

factors associated with the recurrence of juvenile nasopharyngeal angiofibroma.

17

RESOURCES:

1. Ted L Tewfik, MD, FRCSC. 2011. Juvenile Nasopharyngeal Angiofibroma. Available at

http://emedicine.medscape.com/article/872580-overview.

2. Piero Nicolai, Alberto Schreiber, and Andrea Bolzoni Villaret. 2012. Juvenile

Angiofibroma: Evolution of Management. International Journal of Pediatricsn Volume

2012 (2012), Article ID 412545, 11 pages doi:10.1155/2012/412545. Department of

Otorhinolaryngology, University of Brescia, Piazza Spedali Civili 1, 25123 Brescia, Italy.

3. Mehmet Fatih Garça1, Sevil Ari Yuca2, Köksal Yuca. 2010. Juvenile Nasopharyngeal

Angiofibroma. European Journal of General Medicine.

18

Allergic Rhinitis

Allergic rhinitis is a symptomatic disorder of the mucous membrane of the nose induced after

allergen exposure due to an IgE-mediated infl ammation of the membranes lining the nose. It

was defi ned in 1929: “The three cardinal symptoms in nasal reactions occurring in allergy are

sneezing, nasal obstruction and mucous discharge”.

Allergic rhinitis is a global health problem that affects patients of all ages and ethnic groups.

It causes major illness and disability worldwide. Allergic rhinitis affects social life, sleep, and

performance at school and work, and its economic impact is substantial. However, rhinitis is still

underdiagnosed and undertreated. Over 600 million patients suffer from this disease, but there

are still differences between rural and urban areas, both in developed and developing countries,

possibly due to differences in immune reactions.

In 1999, during the ARIA (Allergic Rhinitis and its Impact on Asthma) World Health

Organization (WHO) workshop, an evidence-based document was produced using an extensive

review of the literature available up to December 1999. The statements of evidence for the

development of ARIA followed WHO rules and the recommendations of Shekelle et al. The

ARIA document presented the state-of-the-art for the specialist, general practitioner, and other

health care professionals. Its aims were as follows:

• To update knowledge of allergic rhinitis

• To highlight the impact of allergic rhinitis on asthma

• To provide an evidence-based documented review of diagnostic methods

• To provide an evidence-based review of the treatments available

• To propose a stepwise approach to the management of the disease

The ARIA update began in 2004 and was published earlier this year. Several chapters were

extensively reviewed using the Shekelle evidence-based model, and papers published in peer-

reviewed journals. These papers cover the area of tertiary prevention of allergy, complementary

and alternative medicine, pharmacotherapy and anti-IgE treatment, allergenspecific

immunotherapy, links between rhinitis and asthma, and mechanisms of rhinitis. The need arose

for a global document to highlight the interactions between the upper and the lower airways

19

including diagnosis, epidemiology, common risk factors, management, and prevention.

Moreover, attention was also given to allergy in developing countries.

The grading of evidence and the recommendation for an evidence-based management

system in the ARIA 2008 update did not follow the Grading of Recommendations Assessment,

Development and Evaluation (GRADE) approach. It is expected that some of the

recommendations offered by the 2008 ARIA update would differ if the GRADE approach had

been applied. A large list of treatments was considered in the ARIA 2008 update. Intranasal

corticosteroids are the first line therapy in patients with moderate to severe disease and are also

effective against ocular symptoms, H1-antihistamines are important treatments for all patients

and leukotriene receptor antagonists are particularly important for patients with rhinitis and

asthma. Tertiary prevention of allergy is still a matter of debate, since clinical trials do not

usually show any effi cacy of single allergen avoidance measures. Sublingual immunotherapy

has proven to be a safe and effective treatment, but clinical trials need to be standardized. An

algorithm of the management of allergic rhinitis is provided.

However, our progress in understanding the mechanisms of allergic rhinitis is continuous

and novel treatment approaches are constantly being published. Nonallergic rhinitis is still a

matter of discussion and may pose some treatment problems. Another important aspect of ARIA

was to consider comorbid conditions of allergic rhinitis, in particular, asthma. Epidemiologic

studies throughout the world have consistently shown that asthma and rhinitis often coexist in the

same patient. The vast majority of patients with asthma have rhinitis, but the prevalence of

asthma in rhinitis patients still needs to be assessed. The treatment of nasal symptoms has little

effect on the lower airways, but there have been some compelling data suggesting that new

studies with innovative methods need to be started. Specific immunotherapy in patients with

allergic rhinitis has a prolonged effect on the development of asthma when stopped. The

perception of patients and physicians regarding the links between asthma and rhinitis varies

between countries, but this perception appears to be stronger than expected.

However, knowledge is not directly translated into practice, since fewer physicians

coprescribe treatments for rhinitis and asthma. The recommendations of the ARIA workshop in

1999 are still valid, and patients with allergic rhinitis, in particular persistent allergic rhinitis,

should be evaluated for asthma. Patients with asthma should be evaluated for rhinitis, and an

20

efficacious and combined strategy should be adopted to treat diseases of the upper and lower

airway.

Aria Recommendations

1. Allergic rhinitis is a major chronic respiratory disease due to its:

- Prevalence

- Impact on quality-of-life

- Impact on work/school performance and productivity

- Economic burden

- Links with asthma

2. In addition, allergic rhinitis is associated with sinusitis and other co-morbidities such as

conjunctivitis.

3. Allergic rhinitis should be considered as a risk factor for asthma along with other known risk

factors.

4. A new subdivision of allergic rhinitis has been proposed:

- Intermittent (IAR)

- Persistent (PER)

5. The severity of allergic rhinitis has been classified as “mild” or “moderate/severe” depending

on the severity of symptoms and quality-of-life outcomes.

6. Depending on the subdivision and severity of allergic rhinitis, a stepwise therapeutic approach

has been proposed.

7. The treatment of allergic rhinitis combines:

- Allergen avoidance (when possible)

- Pharmacotherapy

- Immunotherapy

- Education

8. Patients with persistent allergic rhinitis should be evaluated for asthma by means of a medical

history, chest examination, and, if possible and when necessary, the assessment of airflow

obstruction before and after bronchodilator.

9. Patients with asthma should be appropriately evaluated (history and physical examination) for

rhinitis.

21

10. Ideally, a combined strategy should be used to treat the upper and lower airway diseases to

optimize efficacy and safety.

22

Aria Classification Of Rhinitis

Proper diagnosis and classification of patients with allergic rhinitis are essential to initiate

proper treatment. The symptoms of allergic rhinitis include rhinorrhea, nasal obstruction, nasal

itching, and sneezing, which are reversible spontaneously or with treatment.

23

24

25

26

RESOURCES:

1. ARIA At-A-Glance Pocket Reference. 2007. Based On The Allergic Rhinitis And Its

Impact On Asthma Workshop Report In Collaboration With The World Health

Organisation,Ga2len, And Allergen

2. Allergic Rhinitis and its Impact on Asthma Update (ARIA 2008) The Perspective From

Spain. 2008. J Investig Allergol Clin Immunol 2008; Vol. 18(5): 327-334.

3. Rhinitis. 2010. J Investig Allergol Clin Immunol 2010; Vol. 20, Suppl. 1: 37-42.

4. David M. Quillen, M.D., And David B. Feller, M.D. 2006. Diagnosing Rhinitis: Allergic

Vs. Nonallergic, American Family Physician.

27