for PG

1. Allergic and vasomotor
rhinitis
By Dr. Raju Kafle
2nd year resident
ORL HNS dept , NMCTH
1

2. Allergic rhinitis : Introduction
(Hay Fever)
• Allergic rhinitis (AR) is a common condition.
• Chronic allergen specific , IgE mediated hypersensitivity disorder affecting the mucus
membrane of nasal airway
• Characterized by nasal congestion, watery rhinorrhoea, sneezing, nasal itchiness
and or post nasal drip
• The lining of mucus membrane is continuous with PNS, hence they may be
involved.
• Global prevalence is from 37.9% - 50.6%
• Estimates of its prevalence 20 to 30% of adults and up to 40% of children are
affected
• Significant negative impact on the patients’ quality of life, often interfere with sleep
and contribute to poor performance at work and school
• Associated allergic conjunctivitis and Bronchial asthma may occur
2

3. Type I hypersensitivity reaction
3
These inflammatory mediators cause the classic
symptoms of allergic rhinitis: nerve irritation causing sneezing and
itching, loss of mucosal integrity causing rhinorrhoea and vascular
engorgement causing block. Histamine drives the majority of acute
nasal symptoms such as sneezing and itching with leukotrienes and
prostaglandins being involved in longer term symptoms such as block

4. Etiology
Atopy
• Atopy : represents a predisposition to develop allergic disease ,
refers to the tendency to develop an exaggerated IgE antibody
response
• common allergic disorders include rhinitis, asthma and eczema
• Cookson and Hopkin, 1988, defined atopy in terms of either
• an elevated total IgE or
• a positive skin prick test (greater or equal to 2 mm greater
than a negative control prick test) or
• elevated allergen specific IgE concentrations
• Genetically Inherited from autosomal recessive, autosomal
dominant, mixed and multifactorial genetic influences
• affecting up to one-third of the general population.
4

5. Allergens
Pernennial and seasonal :
 Perennial allergens: usually Indoor allergens
• Worldwide the commonest cause : house dust mite i.e, D. pteronysinnus*
D. farinae and Euroglyphus maynei
• Dominant allergens (m/c mite faeces as large pellets (20/nn) are present in
house dust, more abundant in humid homes, number increases in late
summer months.
• Optimal conditions for growth are approx.@5-20°C with relative humidity
60-70%.
• Bedroom is the preferential breeding ground, particular matress where
their food (human skin scales ) is present,
• Mites also flourish in the pillow, bed clothes, carpets, curtains and soft
furnishings.
• Although mite faecal particles become airborne when room air is
disturbed, faecal particles rapidly settle within 20 minute
5

6. • Other major perennial allergens include domestic pets (cats, dogs, rabbits, guinea
pigs, gerbils, hamsters and horses.
• Cat allergens are well characterized.
• The major cat allergen Fel dl, is a salivary secretoglobulin protein which is
preened on to its fur while cleaning by its beak , where it dries and becomes
airborne on minute particles (less than 5 /mi).
• Fel dl may remain airborne on the surface of respirable small particles for
prolonged periods and may provoke immediate symptoms of allergic rhinitis or
asthma many hours later.
• Cockroach( dead or alive, body parts , saliva or wastes) is a recently identified
cause of rhinitis.
6

7. Seasonal rhinitis
• Specific season, outdoor allergens
• May to July : grass pollen (m/c)
• February to June : tree pollens
• June to September : Weed
• The commonest grass in UK are perennial rye (Lolium perenne),
the large leafed Timothy-grass (Phleum pratense) and cocksfoot
(Dactylis glomerata).
• Majority of grasses flowers in early morning
At this time , pollen grains become airborne,
rise on hot air currents,
only to fall in evening and night when
pollen counts at ground level are at their
highest,
Corresponding to exacerbation of
hayfever symptoms 7

8. • Pollen counts are increased by warm, dry clear
conditions and fall during unseasonal cold or wet
periods.
• Pollen counts above 50 /m3 are considered the level at
which most, but not all, hayfever sufferers may
develop symptoms.
• Patients with high sensitivity may suffer for 10-12
weeks during the summer.
• Owing to 'priming' of the nasal mucosa, exposure to
even low counts late in the season may provoke
symptoms.
• Seasonal allergic rhinitis occurring during the spring
time may occur following exposure to tree pollens
including birch, hazel, plane tree, ash and pine.
Birch tree (सउर)
Hazel
Pine
Ash tree
8

9. • Weed pollens, including nettle, dock and mug-wort
flower in late summer.
• Fungi spore in late summer and autumn.
• Common species include Cladosporium, Alternaria,
Aspergillus and Basidio-spores.
• The number of outdoor air spores averages on a daily basis
10,000- 20,000 /m3 with peak concentrations up to 200,000
or higher for short periods.
• Paradoxically, rain fall : may provoke an initial increase in
spore numbers ( due to thunderstorm rather than rain itself)
Nettle (ससस्नु)
Mugwort (तििे पािी )
9

10. In Nepal (J Nepal Med Assoc 2020;58(231):866-70)
• Among 170 patients, altogether 103 (60.6%) patients yielded positive responses on the skin prick test. The most prevalent aeroallergens were
Lepidoglyphus 86 (50.60%), Dermatophagoides pteronyssinus 85 (50%), Dermatophagoides farina 82 (48.20%), Thyrophagus 50 (29.40%), Blomia 46
(27.10%), Acarus 43 (25.30%), cat dander 26 (15.30%), dog dander 24 (14.10%), cow and buffalo dander 20 (11.8%), ragweed 20 (11.8%), grass
pollen 18 (10.60%) and mugwort 17 (10%)
10

11. • As a consequence of exposure to allergens inhaled in the workplace
• Occupational rhinitis, occupational asthma, or may coexist frequently.
• Essential clue to diagnosis -The presence of symptoms during
working hours, with improvement during periods away from work.
• Common biological causes are :
• Animal wastes : farmers , veternarians , lab workers
• Flours and grain dusts : bakers , millers , food processors
• Moulds : Bakers , farmers , sawmill workers
• Wood-dusts : Sawmill workers and carpenters
• Solder flux : Electronic workers
• Latex : Gloves used by Surgeons, nurses, other health workers and patients
with indwelling latex urinary catheters.
• Chemical : painters (di-isocyanates, acid anhydrides and polyamines
• Other chemical causes : Platinum salts (in platinum refiners) and drugs
(antibiotics, in pharmaceutical workers and nurses).
Occupational allergens
11

12. Food induced rhinitis
• Food may occasionally provoke IgE-mediated allergic rhinitis,
Food-induced allergic rhinitis is more common in children
• Typically patients with rhinitis due to food allergy are atopic with
sensitivity to common aeroallergens.
• In addition to IgE-mediated mechanisms, food-induced rhinitis may
be due to sensitivity to preservatives such as sulphites, benzoates
and tartrazine.
• Histamine-containing foods such as cheese, poorly kept fish and
certain wines may also provoke 'pseudo-allergic' reactions
including flushing, headache and rhinitis.
• Alcohol may provoke nasal congestion in anyone although this may
be exaggerated in allergic rhinitis sufferers.
• Particular triggers include milk, eggs and cheese.
• In adults nuts, fish, shellfish and citrus fruits may provoke
immediate symptoms in sensitive subjects.
12

13. The mechanism of drug-induced rhinitis is largely unknown.
• Aspirin sensitivity is an important cause of rhinitis which may be severe and prolonged.
• Frequently associated with nasal polyposis and late onset asthma.
• Aspirin sensitivity is frequently, not always a/w sensitivity to other nonsteroidal
antiinflammatory drugs.
• The mechanism is unknown.
• Antihypertensive drugs (propranolol, other beta blockers, ACE inhibitors) may provoke
rhinitis with predominantly nasal congestion and rhinorrhoea.
• Rhinitis medicamentosa refers to rebound hyperaemia, nasal congestion and obstruction
with tachyphylaxis that occurs following prolonged and repeated use of topical
vasoconstrictors.
• In general patients should be advised not to use topical vasoconstrictors for more than 2
weeks at a time
Drug-induced rhinitis
13

14. Role of pollution
• Typical irritants include perfumes, tobacco smoke, traffic fumes,
domestic sprays and bleach
• Watery rhinorrhoea following changes in temperature is also
extremely common
• In urban pollution or very polluted cities , particularly from
motor exhaust fumes are responsible for increasing the
prevalence of hayfever.
• Exhaust fumes include nitrogen dioxide, ozone and (from diesel
engines) diesel particulates.
• In summary, the role of pollution in hayfever remains
controversial.
• Undoubtedly pollutants may irritate or exacerbate symptoms of
nasal hyperreactivity in hayfever sufferers
14

15. Clinical features
Rhinitis
• Rhinitis is defined clinically as having two or more symptoms of anterior or posterior
rhinorrhoea, sneezing, nasal blockage and/or itching of the nose during two or more
consecutive days for more than one hour on most days.
• Allergic rhinitis is diagnosed when these symptoms are caused by allergen exposure
leading to an IgE mediated reaction.
• Allergic rhinitis is subdivided into intermittent (IAR) or persistent (PER) disease and
the severity into mild or moderate/severe.
15

16. Classification
16

17. Seasonal rhinitis
• The first symptom of the hay fever season is usually sneezing.
• In severe cases paroxysms of sneezing occur at frequent intervals throughout the
day due to histamine release acting through reflexes.
• Excessive fluid and mucus secretion (rhinorrhoea) is believed to be the response of
sero-mucus glands to mast cell/basophil derived mediators.
• Nasal obstruction or blockage is the result of vascular engorgement, with resulting
vasodilatation and oedema formation.
• Itchiness of the nose, eyes and palate are common features resulting from histamine
and/or neural reflexes.
• Tearing, itching and redness of the eyes together with some degree of periorbital
oedema is usual.
• Other symptoms may include a burning or raw sensation in the throat and
development of asthma symptoms such as wheezing and chest tightness
17

18. Perennial rhinitis
• The symptoms of perennial rhinitis differ from seasonal rhinitis largely as a result
of long-standing nasal mucosal inflammation.
• Rhinorrhoea may be more viscous or purulent depending on the degree of cellular
recruitment.
• Conjunctivitis is far less frequent in perennial rhinitis.
• Perennial rhinitis may be accompanied by secondary symptoms including loss of
smell, loss of taste and associated sinusitis or ET-dysfunction.
• In general, sneezing is less common.
• Prolonged continuous symptoms of nasal congestion and postnasal drip are more
common.
• A history of mucopurulent rhinorrhoea, facial pain and systemic symptoms of fever
and malaise may point to associated infective sinusitis.
18

19. Examination
• In patients with current symptoms the allergic nasal mucosa
appears pale or bluish, boggy with swelling and watery
discharge.
• When asymptomatic the nasal mucosa appears entirely normal.
• The presence of polyps, septal deflection or prominent nasal
turbinates should also be recorded.
• Further endoscopic otolaryngological examination,
examination of the chest and general examination may be
relevant if the diagnosis is not clear-cut
19

20. Signs
• Crease on top of nose with crusting ( darrier
sign)
• Periorbital puffiness
• Dark circle around the eyes ( allergic shiners)
• Creases in lower eyelids due to spasm of muller
muscle (dennis morgan lines)
• Conjuctival congestion
• Epiphora
• Allergic Salute
• Allergic Gape
• Other allergic signs : eczema (skin allergy) ,
wheeze ( asthma)
20

21. Laboratory tests
• In the diagnosis of allergic rhinitis, helpful supportive information for
the clinical history may simply be achieved with skin prick testing.
• Skin prick testing is inexpensive, accurate, rapid and can be undertaken
with a wide variety of allergens at a single skin prick testing session.
• Skin prick tests are preferred to scratch or intradermal tests which are
less reproducible, more dangerous and may give false-positive
responses.
• The method of skin prick testing involves the use of a small lancet to
introduce an allergen into the skin.
• If the patient is sensitized to the allergen then IgE sensitized mast cells
will degranulate and cause a wheal and flare reaction in the skin.
• Negative (saline) and positive (histamine) controls are also used to rule
out dermographism and non–reactivity respectively.
• If the negative control shows a reaction or the positive control shows no
reaction then blood IgE levels should be measured.
21

22. • If an oral antihistamine has been taken in the preceding 7–10 days then the positive
control may not react.
• A positive reaction is noted by a wheal size 2 mm or greater than the negative
control
• Skin prick tests should be performed with standardized commercially available
extracts.
• Extracts of foods are, in general, less reliable with a higher rate of both false-
positive and false-negative responses when compared to aero-allergens.
• Immediate sensitivity to raw fruit and vegetables and other fresh foods may simply
be tested directly using a 25 gauge orange needle applied repeatedly through the
surface of the fruit before skin prick testing
22

23. Treatment
• The prevention of allergic rhinitis
• Methods of reducing allergen exposure
• Pharmacological treatment of allergic rhinitis (see also Chapter 28)
• Immunotherapy for allergic rhinitis
• Surgical treatment
• Complementary therapies
23

24. Prevention of allergic rhinitis
• Recommendations have been made on the available evidence.
• It has been advised that children should breastfeed for at least the first
three months after birth
• that there is no benefit in having a reduced antigen diet for the mother
in pregnancy and during lactation
• 44 and that parents should not smoke in pregnancy or near children,
although no definite link with allergy has been found
• .45 There was also limited evidence of benefit in reducing exposure to
house dust mite but no benefit in not exposing children to furry pe
24

25. REDUCING ALLERGEN EXPOSURE
• As the clinical effects of allergic rhinitis are caused by allergens it would seem logical
that reduced exposure would benefit symptoms.
• The major indoors allergens are house dust mite, cat, dog and other furry animals,
cockroach and moulds and major outdoors allergens are airborne pollens that varies
during the year and on local conditions.
WHO recommendations :
• House dust mites
1. Wash bedding regularly (every 1–2 weeks) at 55–60 °C to kill mites (washing with cold water
removes 90% of mite allergens; washing at 55–60 °C kills mites)
2. Wash pillows and duvets in hot water (55–60 °C) and encase pillows and mattresses with protective
coverings that have a pore size of 6 µm or less
3. Sufficient ventilation of dwellings to decrease humidity; aim to reduce indoor relative humidity to
below 50% and avoid damp housing conditions
25

26. ADDITIONAL STRATEGIES
1. Use a good quality vacuum cleaner
2. Use a damp duster when dusting and cleaning surfaces
3. Replace wall to wall carpets with linoleum or wooden floors which can be wiped clean
4. Remove/reduce curtains and soft furnishings in the bedroom
5. Replace fabric-covered seating with leather or vinyl
6. Remove soft toys from the bedroom; wash them at 55–60 °C or freeze them
7. Exposure of mattresses, rugs and carpets to direct strong sunlight (for more than 3 hours) kills mites and can be used in appropriate
regions
26
Pollen avoidance
1. Pollen avoidance provides mechanical barriers to pollen contact.
2. Keep windows closed at peak pollen times
3. Wear glasses or sunglasses to help prevent pollens entering the eyes
4. Consider wearing a mask over nose and mouth to prevent inhalation of pollens at peak
time
5. Use air-conditioning where possible
6. Install car pollen filters where possible

27. Pet allergen avoidance
Reduces the amount of pet allergen indoors.
• If possible, find another home for the pet and do not introduce new animals into the home.
• If the pet is not removed from the home then;
• Exclude pets from bedrooms and if possible keep pets outdoors
• Vacuum regularly- carpets, mattresses and upholstery
• Change clothes before going to school or work if you have had contact with any animal (e.g. horse/ cat/dog)
Cockroach avoidance
Involves removing the cockroaches, eliminating the places and conditions in which they can live and removing
all allergens.
• Eradicate cockroaches with appropriate insecticidal bait
• Seal cracks in floors and ceilings
• Enclose all food
• Do not store waste in the home
• Scrub floors with water and detergent allergens.
27

28. Mould allergen avoidance
• Aims to prevent mould from growing and mould spores from becoming airborne during
mould removal.
• Use dehumidifiers in the home if relative humidity is consistently high (above 50%)
• Ensure heating, ventilation or air-conditioning systems are properly maintained
• Use 5% ammonia solution to remove mould from bathrooms and other contaminated
surfaces
• Replace carpets with hard flooring and replace wallpaper with paint
• Repair indoor water damage immediately
28

29. Pharmacotherapy :
ARIA guidelines
29

30. 30

31. ANTIHISTAMINICS
• All symptoms except nasal blockage respond well to antihistamines
• Older first-generation antihistamines are rarely used now due to sedative effects (except: ketotifen
still used due to additional effect as a mast cell stabilizer)
• Second generation oral antihistamines such as loratadine and cetirizine are non-sedating, safe for
long-term use and can be used for children. They have a rapid onset of action (usually less than an
hour) and will give symptom reduction on a once daily dosing.
• Antihistamines give better symptomatic control when used regularly rather than on an as required basis-
hence, accordingly advised.
• Topical antihistamines: Azelastine may be used intranasally to achieve rapid symptom control and can
be combined with a topical nasal steroid.
• Azelastine eyedrops may also be useful in reducing ocular symptoms.
• Antihistamines with topical nasal steroid : Most patients required combination therapy rather than
monotherapy.
31

32. 32
First generation antihistaminics
Highly sedatives
Diphenhydramine Oral, 25-50mg
Dimenhydrinate Oral , 25-50mg
Promethazine Oral ( 25-50mg)
I.m(1mg/kg)
Hydroxyzine 25-50mg oral, I.m
Moderately sedative
Pheniramine Oral, 25-50mg
Cinnarizine
Meclizine 25-50mg , oral
Cyproheptadine 4mg , oral
Mild sedatives
chlorphenaramine Oral, 25-50mg
Dexchlorphenaramine 2mg, oral
Clemastine 1-2mg ,oral
Second generation
anthihistaminics
fexofenadine Oral,120-180 mg
loratidine Oral,10mg
Desloratidine 5mg, oral
Cetrizine 10mg, oral
levocetrizine 5-10mg, oral
Azelastine 4mg,oral
0.28 mg intranasal (topical)
Ebastine
Mizolastine
Rupatadine
10mg ,oral

33. GLUCOCORTICOIDS
• Glucocorticosteroids are the most effective treatment for allergic
rhinoconjunctivitis.
• Anti-inflammatory and immunosuppressive actions: Most important
therapeutic properties of glucocorticoids, mechanism are
• lowers circulating lymphocytes and inhibit the ability of leukocytes and macrophages to
respond to mitogens and antigens.
• Decrease the production and release of proinflammatory cytokines.
• Inhibit phospholipase A2, which blocks the release of arachidonic acid.
• Lastly, they helps in stabilizing mast cell and basophil membranes thus decreasing histamine
release.
• Formulations : Oral, IV, IM, intraarticular , topical , inhalation or intranasal
33

34. • Topical use in the form of a spray or drops is preferred to oral use to reduce side
effects (only if blockage is high and loss of smell --oral CS is more useful)
• Intra-nasal application allows a high concentration of the active drug to be
delivered to the nasal mucosa with minimal systemic absorption.
• The drugs reduce all symptoms of allergic rhinitis and ocular symptoms and are
the firstline treatment of choice in patients who complain of nasal block.
• As steroids have an effect on the production of pro-inflammatory mediators
within the cell nucleus their effect is slow to occur and long lasting.
• As, most steroids will not have an appreciable effect on symptoms for several
hours or days and it can take two weeks for full benefit to be noticed.
• Accordingly patients should be advised , as some will give up on treatment if it
does not work rapidly
34

35. 35
If aqueous based sprays
• 50% deposited in nostrils and non-ciliated anterior part of nose.
• 50% will reach the ciliated mucus membrane
• Either absorbed or removed by mucociliary clearence within 30 min.
Highly lipophilic molecules : Large tissue distribution, long elimination time
Fluticasone furoate :Each spray 27.5mcg , OD dosing
• In > 12 years of age : 110mcg /day ( 2 sprays in each )
• In children (2 to 11 Years of Age ) : 55mcg /day ( 1 spray in each )
Mometasone furoate : Each spray 50mcg , OD dosing
• In > 12 years of age : 200mcg /day ( 2sprays in each)
• Once symptoms controlled , maintainence at 100 mcg/day ( 1sprays in each) , if
not increased upto 400 mcg/day ( 4 sprays in each nostrils)
• In children (2 to 11 Years of Age ): 100mcg/day ( 1 spray in each)
Intranasal corticosteroids

36. 36
Less lipophilic molecules: Less distribution locally, quickly absorbed into
circulation, shorter elimination time
Beclomethasone : Each spray : 50mcg, OD dosing
• Adults and Children (6 years and older): 400mcg/day ( 2 sprays each
nostrils)
• NOTE: Less than 6 years : safety not established
Budesonide : Each spray delivers : 100mcg, OD dosing
• Adults and Children (6 years and older) : Initially, 2 sprays (400mcg) in
each
then,
For maintenance : one spray in each nostril (200mcg)
• Polyps : One spray in each nostril, morning and evening, for up to 3
months,BD-dosing
(NOTE: Not recommended below 6 years of age)

37. Methods of administering topical nasal
preparations:
• Head down position : best for steroid drops
• Nasal sprays :
1. Blow the nose to cleanse the nostrils
2. Shake the bottle gently
3. Head down position
4. Close 1 nostrils with fingers, insert nozzle upto ½ inch
5. Spray to lateral wall : during spray no inhalation or
gentle breathing
6. Repeat 3-6 steps in other nose
• If 2 sprays are to be administered to each nostrils , one
should spray directing upwards and other to backwards
whilst the patient doesn’t breath.
37

38. SYSTEMIC GLUCOCORTICOSTEROIDS
• Oral steroids may occasionally be useful in patients
with severe symptoms
• To allow reduction of mucosal swelling and
subsequent use of topical medication or
• To cover a short period when symptom control is
particularly bad.
• Prednisolone 20–40 mg/day is normally sufficient
• Oral steroids may cause serious side effects so their
use should be considered carefully and length of
treatment be kept as short as possible.
• For this reason depot injectable steroids, while
effective at symptom control, are not recommended
as once injected their effects cannot be stopped
38
4 mg methylprednisolone = 5mg
prednisolone= 0.75mg beta and
dexamethasone = 20mg hydrocortisone

39. LEUKOTRIENE RECEPTOR ANTAGONISTS
(LTRAS)
• Cysteinyl leukotrienes, LTC4, LTD4 and LTE4 are produced in
leukocytes, mast cells, eosinophils, basophils and macrophages
by oxidation of arachidonic acid
• Their effects are bronchoconstriction, increase vascular
permeability and attract inflammatory cells in the processes
underlying asthma and allergic rhinitis.
• Montelukast is licensed for the treatment of allergic rhinitis
associated with asthma.
• In studies it was found to be as effective as loratadine in
reducing nasal symptoms but less effective than a topical nasal
steroid.
• Combined use of cetirizine and montelukast was shown not to
improve symptom control above each drug individually in one
study but to be more effective when combined in another.
39

40. SODIUM CROMOGLICATE
• Sodium cromoglicate nasal spray has modest effects on rhinitis symptoms but must
be used four times daily, which limits compliance.
• It has no side effects and can be used on young children.
• Cromoglicate eye drops can be effective against ocular itching
IPRATROPIUM
• Topical ipratropium bromide spray is effective at controlling watery rhinorrhoea and
can be a useful addition to a topical steroid if rhinorrhoea is not being well
controlled.
• Side effects are infrequent but include prostatic symptoms and worsening of
glaucoma.
40

41. DECONGESTANTS
Alpha adrenergic agonists causing vasoconstrictions in 2
receptors
• 1st in capacitance vessels in nasal mucosa and
• 2nd in arterioles that supply the mucosa.
Rationale:
• to improve sinus ventilation and drainage ,markedly
reduces the size of inferior and middle turbinate and
improves osteomeatal complex patency .
Side effects:
• Insomnia, tachycardia and tremor.
Caution
• HTN, hyperthyroidism, DM , closed angle glaucoma,
infants < 3 months
41
TOPICAL SYSTEMIC
More potent
and rapid onset
of action
Less potent , late
onset
oxymetazoline
zylometazoline,
ephedrine, 0.5-
1%, weakest
Phenylephrine (
10mg) ,
pseudoephedrine
(30mg)
avoid using
more than 7-10
days(8th edi,
SB)
3-5 days( much
articles)
Can be combined
with
corticosteroids in
allergic rhinitis
Avoid in : children below 6 years and
pregnant , saline irrigation is adequate
(AAFP, BMJ journal 2018 , and medscape)

42. NASAL DOUCHING
• Saline nasal douches may help with symptom control and
can physically remove an allergen from the nasal mucosa.
• If pollen levels are high regular douching may be of
benefit.
42

43. Immunotherapy
• Immunotherapy (sometimes called desensitization) is a method of inducing tolerance to an
allergen and therefore reducing unwanted symptoms.
• It can reduce the symptoms of allergic rhinitis, offer long-lasting reduction of symptoms (even
when treatment has stopped) and can prevent the progression of allergic disease.
• It involves repeated exposure of the patient to the allergen usually, but not always, with a gradual
increase in allergen dose.
• It can be given subcutaneously by injection (SCIT) or sublingually in drops or tablets (SLIT).
• Allergen immunotherapy (AIT) has been in use since more than one century
• Since then, AIT was administered only as subcutaneous injections (SCIT) until the sublingual
route (SLIT) was proposed in 1986.
• The use of SLIT was proposed following several surveys from the USA and UK that repeatedly
reported fatalities due to SCIT
• Studies have shown similar efficacy for SCIT and SLIT
• It is effective in reducing symptoms in adults and older children though the results are less clear
for children under five.
43

44. Indications of immunotherapy
• Evidence of IgE-mediated disease in which allergens are considered to be the major
triggers
• Inability to avoid allergens
• Inadequacy of drug therapy or intolerable side effects of such treatment
• Limited spectrum of allergen sensitivities (in general one, or at most, two allergens)
• Compliance Contraindications
• Non-availability of suitable allergen extracts.
• Significant medical or immunological disease
• Multiple allergies
• Concurrent treatment with drugs likely to impair possible treatment for
anaphylaxis (beta-blockers or other adrenergic blocking drugs)
(Adapted from WHO/IUIS Report (WHO/IUIS working group. Current status of allergen immunotherapy. Shortened version of WHO/IUIS working group report. Lancet, i, 259-261, 1989)
44

45. • There are several guidelines regarding the selection of patients and treatment
protocols
• Immunotherapy use in the UK is limited but it is widely used elsewhere.
• The diagnosis of an IgE mediated response should be confirmed by skin prick tests
or measurement of IgE levels before treatment and correlated with the patient’s
history to ensure the correct allergen is used.
• For this purpose, most common allergens i.e, house dust mite, grass pollen, cat, dog
and tree pollen extracts should be made available in standardized doses.
• Treatment is usually continued over a 3-5 year period to achieve a long lasting
tolerance after treatment has stopped
45

46. EFFICACY
• With good patient selection immunotherapy can be very effective.
• In a study of patients with grass pollen sensitivity treated with SCIT,
over the peak pollen season mean symptom and medication scores
were 32% and 41% lower respectively than those in a placebo group.
• Immunotherapy for older children with allergic rhinitis also reduces
the risk of developing allergic asthma later in life and of developing
new allergies
46

47. Subcutaneous immunotherapy (SCIT)
• In SCIT, injections of allergens are administered in a medically
controlled environment and followed by an observation period of a
minimum of 30 minutes.
• Injections are given to subcutaneously on the arm between the elbow
and shoulder
• Usually an updosing phase of b/w 2 and 4 months when the dose of
allergen is gradually increased to the maintenance dose.
• This maintenance dose is then injected every 4–6 weeks for a 3-year
period.
• These are usually transient redness and itching around an injection site,
or oral itching
• Can be reduced by pre-treatment with an oral antihistamine.
• Rare:Urticaria, bronchoconstriction or anaphylaxis and resuscitation
facilities with adrenaline must be available.
• Almost all reactions will occur within 30 minutes of treatment
therefore patients should be observed for an hour after injection.
47

48. Sublingual Immunotherapy ( SLIT)
• With SLIT :
• May be updosed or, the patient starts with the maximum dose
and continues with this daily for 3 years.
Vs SCIT
48
SLIT SCIT
Newer immunotherapy Older immunotherapy
Efficacy +++ Efficacy
Safety +++ Safety ++ ( may result in fatality)
Tolerability ++ Tolarability ++
Cost effectiveness +++ Cost effectiveness ++
Compliance +++ Compliance ++
Long term effects +++ Long term benefits ++
After first dose , can be safely taken at home Must attend hospital for weekly or monthly injections,
non compliance in deedle phobic patients

49. ANTI-IgE ANTIBODY (OMALIZUMAB)
• Is a recombinant humanized monoclonal antibody that binds to
circulating IgE preventing it from binding to mast cells and causing
degranulation.
Mode of administration :
• It is administered by twice weekly or monthly injection (75 mg
/0.5 mL, 150 mg/mL)
• Omalizumab improves allergic rhinitis symptoms in severe cases
from the first year of therapy and remaining stable over the long-
term period
• Omalizumab reduces all nasal symptoms and improves asthma
control but has the risk of causing anaphylaxis and is expensive.
• Currently it is recommended only for patients with severe allergic
asthma with or without rhinitis symptoms.
• Side effects :
• common: Blistering, crusting, irritation, anaphylaxis
• Rare : dizziness , tachycardia, tiredness and weakness , malignant tumors
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Reference : up to date 2018 ,drugs.com

50. Surgery
• Surgery cannot cure allergy but can give relief of nasal blockage if other methods fail.
• Reduction of submucosal fibrotic tissue on the inferior turbinates that has developed
due to long-standing inflammatory changes may improve the airway and allow access
for topical nasal steroids.
• Polypoidal mucosa may also be found in some patients with severe allergic rhinitis
and occasionally this needs to be removed.
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Complementary treatments
• Trials of homeopathy, acupuncture and herbal remedies have not shown any evidence
of beneficial effect in allergic rhinitis
• But, many patients use them and are satisfied with the results

51. Vasomotor rhinitis : Introduction
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52. • It is nonallergic rhinitis but clinically simulating nasal allergy with
symptoms of nasal obstruction, rhinorrhoea and sneezing.
• One or the other of these symptoms may predominate.
• The condition usually persists throughout the year and all the tests of
nasal allergy are negative
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53. PATHOGENESIS
• Nasal mucosa has rich blood supply.
• Its vasculature is similar to the erectile tissue in having venous sinusoids or
“lakes” which are surrounded by fibres of smooth muscle which act as sphincters
and control the filling or emptying of these sinusoids.
• Sympathetic stimulation causes vasoconstriction and shrinkage of mucosa, while
parasympathetic stimulation causes vasodilation and engorgement.
• Overactivity of parasympathetic system also causes excessive secretion from the
nasal glands.
• Autonomic nervous system is under the control of hypothalamus and therefore
emotions play a great role in vasomotor rhinitis.
• Autonomic system is unstable in cases of vasomotor rhinitis.
• Nasal mucosa is also hyper-reactive and responds to several nonspecific stimuli,
e.g. change in temperature, humidity, blasts of air, small amounts of dust or
smoke.
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54. • SYMPTOMS
• 1. Paroxysmal sneezing. Bouts of sneezing start just after getting out of the bed in the
morning.
• 2. Excessive rhinorrhoea. This accompanies sneezing or this may be the only
predominant symptom. It is profuse and watery and may even wet several handkerchiefs.
The nose may drip when the patient leans forward and this may need to be differentiated
from CSF rhinorrhoea (see p. 183).
• 3. Nasal obstruction. This alternates from side to side. Usually more marked at night. It
is the dependent side of nose which is often blocked when lying on one side.
• 4. Postnasal drip.
• SIGNS
• Nasal mucosa over the turbinates is generally congested and hypertrophic. In some, it
may be normal
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55. • COMPLICATIONS
• Long-standing cases or VMR develop nasal polypi, hypertrophic
rhinitis and sinusitis
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56. TREATMENT
• Medical
• 1. Avoidance of physical factors which provoke symptoms, e.g. sudden change in temperature,
humidity, blasts of air or dust.
• 2. Antihistaminics and oral nasal decongestants are helpful in relieving nasal obstruction,
sneezing and rhinorrhoea.
• 3. Topical steroids (e.g. beclomethasone dipropionate, budesonide or fluticasone), used as spray
or aerosol, are useful to control symptoms.
• 4. Systemic steroids can be given for a short time in very severe cases.
• 5. Psychological factors should be removed. Tranquillizers may be needed in some patients.
• Surgical 1. Nasal obstruction can be relieved by measures which reduce the size of nasal
turbinates (see hypertrophic rhinitis). Other associated causes of nasal obstruction, e.g. polyp,
deviated nasal septum, should also be corrected.
• 2. Excessive rhinorrhoea, not corrected by medical therapy and bothersome to the patient, can be
relieved by sectioning the parasympathetic secretomotor fibres to nose (vidian neurectomy
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