Dr Lorraine Masotja

ENT

April 2019

Allergic Rhinitis and asthma

Intro

Rhinitis= Inflammation of the membranes lining the nose

AR - IGE mediated immune response to specific allergens

Affects social life, school/ work performance

Epidemiology

Worldwide affects 10- 40% of population

20 – 40% in developing countries & incidence is rising ( C Rondon et al)

AR Affects 20-40 million in USA

Prevalence is increasing in relation to increase in all IGE mediated diseases

Currently its the most common atopic dz & one of the leading chronic conditions in children < 18yrsFemale =Male

Age- before age 20. Earlier in children with bilateral family history of AR or other Allergic conditions

Childhood history of food allergy or Eczema

Risk factors- Frequency increases with age.

+ SPT is a sig. Risk factor.

Higher socioeconomic classes

Polluted areas

+ family H/O allergy

Individual born during pollen season,

Firstborns

Early introduction of foods or formula

Heavy maternal cigarette smoking in 1st yr of life

Exposure to indoor allergens

High serum IGE( >100 before age of 6 yrs)

Recent studies – association between obesity, nutrition & atopy

Rhinitis

AR

AR

with systemic atopy

Seasonal

perennial

Local AR without systemic atopy

Intermittent

persistent

NAR

Infectious

Occupational (irritant)

Drug induced

Hormonal

Irritant

Food

Emotional

Atrophic

GER

Idiopathic (NARES included)

Etiological classification of rhinitis ( C Rondon et al)

Seasonal AR 10%.Perennial AR 10-20%

NARES

Perennial nasal symptoms with profound eosinophilia in nasal

secretions with no sign of allergy

Not IR- pts respond nasal corticosteroids

VS

IR

Its usually assoc. With nasal polyps, bronchial hyperreactivity, non allergic

asthma & sleep apnoea

Classification - based on duration of symptoms& impact on QOL

ARIA supported by WHO

In line with GINA classification of Asthma

Long pollen seasons in GP,LP,WC,EC & eastern FS, most pts with pollen induced rhinitis have persistent rhinitis

Management

AR in children often misdiagnosed – recurrent colds

When cough is present esp at night, misdiagnosed as “ cough

variant asthma”

Clinician should ask directed questions

Be aware of cormorbidities- asthma, sinusitis, OM, pursue

specific diagnostic tests, often administer therapeutic trials of

anti-inflammatory meds.

QOL may be worse than in Asthmatics

SYMPTOMS

Nasal Itching

Sneezing

Rhinorrhoea

Nasal blockage (90%)

PND

Repeated throat clearing

Hyposmia

Hyponasal speech

Epistaxis

Red ,itchy eyes, itchy throat and

ears. Cough

20% have symptoms of Asthma

“ Allergic salute”

“Allergic nasal crease”

“ Allergic shiners’

Dennie- Morgan lines

Grimacing; twitching & picking the nose-

Mouth breathing

Dental malocclusion,

Patients should be examined for other allergic diseases-

eczema, asthma

Clear nasal secretions,

Oedematous nasal mm.

Mucosa look pale &blue-gray

Swollen turbinates

Allergic Conjunctivitis-Conjuctival oedema, itching, tearing, hyperaemia

Diagnostic tests

SPT

children younger than 1yr may not display + rxn

Child with seasonal allergic dz may not have + test until two

seasons of exposure

Allergy testing should be guided by the history and prevalent

aeroallergens in the area

Inhalant allergy - dust mite, animal dander & weed, grass

tree pollen

Geographic distribution is NB

In vitro tests Total IGE NOT useful Lab. Confirmation of presence of IGE abs

Helpful to convince family

The ImmunoCAP is sensitive and specific blood test

Should be based on history & exposure

Phadiotop may be used for screening

Nasal secretions & sputum for eosinophil - non specific

The ultimate standard for diagnosis remains a combination of

1. positive history

2. presence of specific IGE antibodies

3.demonstration that symptoms are a result of IGE-

mediated inflammation

Management Patient education

• Environmental control

Intranasal steroids

Most potent anti-infla. Meds for management of AR

First line for pts with moderate-severe & persistent AR

Also have effect on ocular symptoms

MOA: vasoconstriction & reduction of edema, suppression of cytokine production & inhibition of inflammatory cell influx

Proper instruction is essential

Work best if taken regularly daily or prophylactically in anticipation of pollen season

Rapid onset of action – 12-24hrs, may be effective when used intermittently

Safe for long term use

Relieve symptoms of nasal pruritis, rhinorrhea, sneezing & congestion

Some pts experience nasal dryness and epistaxis

Systemic steroids

Should not be used as first line

For severe incapacitating AR after excluding other causes

Short periods- 5-10days

Study in SA- Short term adrenal suppression within 2 weeks

of 1mg betamethasone given daily, which was reversible on

discontinuing therapy

Long term use not recommended

Intraturbinate injections- not recommended

Oral steroids+ Sedating antihistamine are often

abused in treatment of AR

Antihistamines

2nd generation & new generation antihistamines available in SA

Preferential binding to peripheral H1 receptors with minimal

penetration to the CNS, minimal anticholinergic & -adrenergic

blocking activities.

New gen. Also have anti-inflammatory effects

They act to control the “wet” symptoms of AR- rhinorrhoea, sneezing,

itchy membranes

Less effective for nasal congestion

Decongestants Produce vasoconstriction

through adrenergic action -> relieve nasal congestion

Topical : if used > 5-7 days may cause rebound congestion after withdrawal of the drug

If used for prolonged periods-> Rhinitis Medicamentosa

ARIA – suggest that they not be used in preschool children

Saline.

Nasal irrigation- simple non expensive

Improves symptoms and QOL

Reduces medication requirements

Hypertonic & Isotonic saline are of modest benefit in reducing

symptoms & improving QOL. Improvement of mucocilliary

clearance, removal of allergen & inflammatory mediators &

protective effect on nasal mucosa

May improve effect of INCS

Leukotriene receptor antagonist May be considered in patients

with AR + Asthma- Add on .

Also patients unresponsive or noncompliant with intranasal steroids.

On its own its less effective than intranasal corticosteroids

Beneficial effects also due to anti-inflammatory effect on vascular permeability, eosinophils & mucus production

DOC for Samters triad

Samter's Triad is a chronic condition defined by asthma, sinus inflammation with recurring nasal polyps, and aspirin sensitivity. It's also called aspirin-exacerbated respiratory disease (AERD), or ASA triad.

Other meds

Mast cell stabilizers e.g. Cromolyn sodium

- May be useful in relieving symptoms, minimal affect on

congestion. Better if taken before allergen exposure. Short

duration of action therefore poor compliance

Anti- cholinergics (Ipratropium bromide.) Reduces volume of

watery secretions. May be used in AR when rhinorrhea is

refractory to other treatment or in blocking reflex mediated

rhinitis ( spicy foods, cold air exposure)

Omalizumab. Monoclonal antibody against IGE. Currently

approved for severe persistent allergic asthma refractory to other

meds. Studies show efficacy in AR But costly.

Allergen immunotherapy

Specific allergen immunotherapy (SIT) is the only therapy that can change

natural h/o AR, prevent progression of the disease & cure patients if they

are selected carefully

Should be considered in Pts who

-Do not respond to combination of environmental control measures and

medication

-Experience substantial side effects with medication

-Have symptoms for a sig. Portion of the year that require daily treatment

-Prefer long term modulation of their allergic symptoms

Two forms- SCIT, SLIT

Both highly effective for pts with HDM or grass pollen allergies

Contraindications for Immunotherapy

Polysensitisation to several unrelated allergen groups

Severe / poorly controlled Asthma

Over 60 yrs

Thyrotoxicosis

Coronary vascular dz

Mental disorders

Autoimmune dz

Hypertension

Algorithm for DX & MX of AR ( SAARWG)

Sinusitis / Rhinosinusitis

Adenoid hypertrophy

AR and ASTHMA

AR and Asthma frequently coexist

Asthma occur in 15-35% of pts with AR

Nasal symptoms resent in approx 75 % of pts with asthma

AR may aggravate asthma

United airway Upper & lower airways are

considered a unified

morphological and functional unit

The upper and lower respiratory

tracts form a continuum, allowing

passage of air into and out the

lung and sharing many anatomical

and histological properties

They share common structures

like ciliary epithelium, BM, lamina

propria, glands, goblet cells

forming the so called united

airway

Upper airway is the first target for allergens and for

physical and chemical environmental stimuli. Therefore

tend to be affected first by allergic airway dz.

If the intensity of the disease is low, the upper airway may

be the only part affected

Rhinitis and asthma are chronic inflammatory diseases of the upper and lower airways

Mx of rhinitis and asthma must be together leading to better control of both diseases

AR is risk factor in developing asthma

Over 80% of asthmatics have AR.

And 10-40% pts with AR have asthma

“one airway, one disease”

Pts with perennial AR have greater bronchial reactivity than those with seasonal rhinitis

Rx of rhinitis can be beneficial to lower airway

Reduces symptoms, emergency room visits and

hospitalization and severity of attacks

UNITED AIRWAY

asthmaAllergic rhinitis

with asthmaAR