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Allergic rhinitis (part1)
1. Allergic rhinitis
(Part I)
Pannipa Kittipongpattana, M.D.
2 November 2018
Division of Allergy and Immunology , Department of Pediatrics
King Chulalongkorn Memorial Hospital
2. Outline
Definition and classification
Epidemiology
Pathophysiology and mechanisms
Risk factors
Evaluation and diagnosis
Associated conditions
Management
3. Outline
Definition and classification
Epidemiology
Pathophysiology and mechanisms
Risk factors
Evaluation and diagnosis
Associated conditions
Management
4. First description of Hay fever
“ About the beginning or middle
of June in every year….
A sensation of heat and fullness is
experienced in the eyes….
…. To this succeeds irritation of
the nose producing sneezing….
….To the sneezing are added a
further sensation of tightness of the
chest, and a difficulty of breathing”
John Bostock, Med Chir Trans,1819; 10:161
5. Definition
Allergic rhinitis is an IgE-mediated inflammatory
nasal condition resulting from allergen introduction
in sensitized individual.
The classic cardinal symptoms:
Nasal congestion
Rhinorrhea (usually clear and watery)
Sneezing
Pruritus of nose, palate, throat or ears
6. ARIA Classification of Allergic rhinitis
(Old)
Seasonal AR
Outdoor allergens
Tree pollinate (spring)
Grasses (early
summer)
Weeds (late summer)
Perennial AR
Persistent
(year-round symptoms)
Indoor allergens
House dust mites
Animal dander
Molds
Cockroaches
Intermittent
(cyclical exacerbation)
7. ARIA Classification of Allergic rhinitis
(New)
Intermittent
symptoms
< 4days/week
OR
< 4 weeks at a time
Persistent
symptoms
≥ 4days/week
AND
≥4 weeks at a time
Mild
Normal sleep
Normal daily activities
Normal work and school
No troublesome symptoms
Moderate-to-severe
One or more items
Abnormal sleep
Impairment of daily activities
Abnormal school or work
Troublesome symptoms
9. Outline
Definition and classification
Epidemiology
Pathophysiology and mechanisms
Risk factors
Evaluation and diagnosis
Associated conditions
Management
10. Prevalence of allergic rhinitis in different regions of
the world, according to the Global Atlas of allergic
rhinitis
Adapted from Akdis et al. European Academy of Allergy and Clinical Immunology 2015.
20. Nasal Hyperresponsiveness
Specific hyperresponsiveness (Priming)
Dose of allergen required to evoke response
Non-specific hyperresponsiveness
Capacity to response to various non-specific
substances
21. Connell JT: Quantitative intranasal pollen challenge: III. The priming effect in allergic rhinitis. J Allergy 1969; 43:
Nasal Hyperresponsiveness
23. Mouth breathing &
Bronchoconstriction
Theory
Nose function as filter
& air-conditioning
Mouth breathing
bypass this filter and
result in
Cold & dry air
Unfiltered irritants &
allergens
J Appl Physiol (1985). 2000 Mar;88(3):1043-50.
24. Mouth breathing & Asthma
Allergy. 2016 Jul;71(7):1031-6
- N = 9,804
- 17% of the population had Mouth breathing
- OR for asthma morbidity was
- mouth breathing alone 1.85 (95% CI, 1.27-2.62)
- AR alone 2.20 (95% CI, 1.72-2.80)
- when coexisted 4.09 (95% CI, 3.01-5.52)
Allergy. 2016 Jul; 71(7):1031-6.
25. Aspiration of nasal content
Theory: Post-nasal drip aspirate coughing
However, nasal application of radioactive-
labeled allergen could not reach lower
respiratory tract
Stimulation of pharyngolaryngeal receptors is
more likely to be responsible for a postnasal
drip-related cough
J Allergy Clin Immunol. 1997 Jul;100(1):122-9
Proc Am Thorac Soc. 2009 Dec;6(8):652-4.
26. Nasobronchial reflex & Systemic
spill
Q: Is there a neural reflex between nasal &
airway
Am Rev Respir Dis. 1990
Metacholine nasal spray
Asthma + AR subjects
lidocain
e
phenylephrin
e
Bronchoconstriction
J Allergy Clin Immunol. 1992
Study in asthma + AR
subjects
nasal provocation with
allergen
bronchial responsiveness
to methacholine
at 30 minutes & 4.5 hours
28. Outline
Definition and classification
Epidemiology
Pathophysiology and mechanisms
Risk factors
Evaluation and diagnosis
Associated conditions
Management
29. Risk factors for allergic rhinitis
ISCAR: Allergic Rhinitis. Int Forum Allergy Rhinol. 2018 Feb;8(2):108-352.
30. Genetics
Twin study
Support role of genetics
GWAS
Screen for association
Candidate gene study
Prove & explain
ISCAR: Allergic Rhinitis.Int Forum Allergy Rhinol. 2018 Feb;8(2):108-352.
31. Genome-Wide Association Study (GWAS)
Genome-wide association and HLA fine-mapping studies identify risk loci and genetic pathways underlying allergic rhinitis. Nat Genet. 2018 Aug;50(8):1072-1080.
Known association
Novel loci in study
Not carried forward
~ 41 loci found to be associated with AR
Their function involve in
- Regulation of B cell & T cell
- Antigen recognition
> Most strong signal: HLA-DQB1
> Overlapped with asthma, eczema,
autoimmune diseases, and also non-
allergic rhinitis
33. Pollens: PRO
The Melbourne Atopy Cohort Study (MACS): 620 babies with atopy in family
Pollens exposure & AR development
OR (95%CI)
First 3 months 1.14 1.01-1.29
First 6 months 1.11 1.01-1.21
Clin Exp Allergy. 2013 Mar;43(3):337-43.
Adjusted for gender and family history of atopy
34. Pollens: only associated with Asthma and Sensitization
Unusually high birch pollen in 1993 → study in children with atopy in family
J Allergy Clin Immunol. 2002 Jul;110(1):78-84.
36. Fungal allergens
Most studies showed fungal allergens as a risk factor for AR development
But some studies found no association with AR
Animal dander
Results are very conflicting regarding pets and development of AR
Many variables: pet age, gender, and species; number of household pets;
home characteristics; atopic predisposition of the pet owners
ISCAR: Allergic Rhinitis. Int Forum Allergy Rhinol. 2018 Feb;8(2):108-352.
40. Food Allergens: in utero food exposure
Avoidance of milk, egg, peanut during
pregnancy, lactation, and infancy to
reduce allergy
NOT SIGNIFICANT
Lower milk and egg ingestion in 3rd
trimester to reduce allergy
NOT SIGNIFICANT
Avoidance of milk and egg after GA 28w to
reduce allergy
NOT SIGNIFICANT+LBW+Preterm
ISCAR: Allergic Rhinitis. Int Forum Allergy Rhinol. 2018 Feb;8(2):108-352.
Evidence for the effects of food allergen exposure on the development of AR
42. Pollution: Cohort studies showed no correlation
Study limitations
- Many confounders: socioeconomic status, background pollutant, type of pollutant
- Accuracy of pollution level measurement
- Geographic diversity
ISCAR: Allergic Rhinitis. Int Forum Allergy Rhinol. 2018 Feb;8(2):108-352.
45. Tobacco Smoke
PLoS Med. 2014 Mar 11;11(3):e1001611.
“Weak association between smoke
exposure and allergic disease in
adults but suggest that both active
and passive smoking are associated
with a modestly increased risk of
allergic diseases in children and
adolescents.”
46. Socioeconomic Status (SES)
The oldest and the most controversial risk factor
A proxy of
- Siblings number
- Breast feeding
- Diet
- Housing
- Overall hygiene
ISCAR: Allergic Rhinitis. Int Forum Allergy Rhinol. 2018 Feb;8(2):108-352.
47.
48. Risk factors for AR
ISCAR: Allergic Rhinitis. Int Forum Allergy Rhinol. 2018 Feb;8(2):108-352.
49. Protective factors against allergic
rhinitis
Breastfeeding
Childhood exposure to pets
Hygiene (biodiversity or microflora) hypothesis
Number of siblings
Farming
Bacterial endotoxin
Microbial diversity
ISCAR: Allergic Rhinitis. Int Forum Allergy Rhinol. 2018 Feb;8(2):108-352.
51. Does breastfeeding protect against allergic rhinitis during childhood?
A meta-analysis of prospective studies
The horizontal bars represent the 95% confidence intervals
(CI).
The vertical lines represent the OR for each study.
Mimouni Bloch et al. Acta Paediatr. 2002;91:275–
Protective effect close to statistical significance in the general population
but not in children with a family history of atopic disease
52. Breastfeeding and asthma and allergies:
a systematic review and meta-analysis
Lodge CJ, Tan DJ, Lau MX, et al. Acta Paediatr. 2015;104:38–53.
53. Childhood exposure to pets
The association of petkeeping in childhood
with the subsequent development of AR is
more controversial, and difficult to establish.
57. Association of symptoms and disease labels with total
and older siblings, before and after adjustment for
covariates
Clin Exp Allergy. 2015 Jan; 45(1): 126–
OR for Hay fever Unadjusted Adjusted
Total siblings 0.92 (0.92-0.95) 0.92 (0.92-0.95)
Older siblings 0.91 (0.89-0.93) 0.91
(0.88-0.94)
sex, region, language
national GNI per capita
59. Bacterial endotoxin
Exposure to bacterial endotoxin has been
studied as a possible protective factor.
Inverse association between exposure to
endotoxin in
infancy and childhood
the development of allergic sensitization has been
shown in rural and urban environments
the results have not been uniform between the
studies.
65. Potential protective effect on the development
of AR
ISCAR: Allergic Rhinitis. Int Forum Allergy Rhinol. 2018 Feb;8(2):108-352.
66. Outline
Definition and classification
Epidemiology
Pathophysiology and mechanisms
Risk factors
Evaluation and diagnosis
Associated conditions
Management
Notes de l'éditeur
10% - 40%, depending on geographic location
Highest incidence occurring in children
Allergic rhinitis affects up to 40% of the global population. It is
present in more than 20% of people in the United Kingdom, and
denotes a major cause of morbidity that affects the quality of life of
individuals. The prevalence of AR in Europe is highest in Belgium (29%) [6]. Rhinoconjunctivitis symptoms are higher in high vs low income nations [7] (Fig. 2). In England, 10% of children aged 6 and 7 years and 15e19% of 13 and 14 year olds have allergic rhinitis. The International Study of Asthma and Allergies in Childhood (ISAAC study) stated an average prevalence of allergic rhinitis in 8.5% (1.8e20.4%) of 6e7 year olds and 14.6% (1.4e33.3%) in children aged between 13 and 14 years [3]. The likelihood of receiving a diagnosis of AR progresses with age in younger individuals but declines in the mid-20s. Allergic rhinitis globally is on the rise in most areas with few exceptions. According to the World Allergy Organization, Australia, New Zealand and the United Kingdom are countries with a very high prevalence of AR. Conversely, countries with a very low prevalence include Albania, Indonesia, Georgia, Romania and Greece [8].
The atopic march. AD prevalence peaks early in infancy, opening the door for consequent development of the atopic march. Development of FA, asthma, and allergic rhinitis in the young toddler age group is common after cutaneous manifestations. (J Allergy Clin Immunol 2017;139:1723-34.
a meta-analysis of prospective studies evaluating the effects of exclusive breastfeeding for the first 3 months of life on the development of AR.
Six prospective studies met the inclusion criteria. In their pooled analysis, they found a protective effect of exclusive breastfeeding for the first 3 months of life that approached statistical significance in the general population (OR 0.74; 95% CI, 0.54 to 1.01).
Interestingly, the protective effect was not seen in childrenwith a family history of atopic disease (OR 0.87; 95% CI,0.48 to 1.58).
There is some evidence that breastfeeding is protective for asthma (5-18 years). There is weaker evidence for a protective effect for eczema ≤2 years and allergic rhinitis ≤5 years of age, with greater protection for asthma and eczema in low-income countries.
While the authors of
this meta-analysis argued for the benefit of breastfeeding in
the prevention of AR, they do acknowledge that the protective
effect of breastfeeding seen in patients less than 5 years
of age may have been confounded by known protective effects
of breast milk against viral respiratory infections. The
authors hypothesized that, given the difficulty of differentiating
between AR and viral rhinitis in young children, a reduction in viral respiratory infections have been possibly
interpreted as a reduction in rhinitis symptoms.
The impact of pet avoidance on AR development is best evaluated via longitudinal birth cohort studies.
A systematic review of 9 studies conducted solely in urban environments
evaluated perinatal pet exposure.642
Six studies found that exposure to dogs, or cats/dogs protected against allergic
disease.
Two studies found increased risk of allergy only in highly atopic families. Furthermore, in a cohort of 620 children with family history of allergic diseases, exposure to cats or dogs was protective only in children with nonallergic fathers.534
Of the 17 studies that reported a result on hay fever in relation to siblings, all found a significant negative relation (fig 3,
table 1). The odds ratios vary between 0.20 and 0.65 for three or more siblings versus no siblings.1 8 12–19 26 29 33 37–39 42 43
Lewis et al reported associations for four children and more.17 23 Taylor et al found a prevalence ratio of 6% for the oldest and of 3.4%
for children with older siblings (table 1), but did not provide the actual number of siblings.19 Some of the studies reported
the results separately for older and younger siblings.8 42
In this case, the effect of older siblings was stronger than the effect of
younger siblings (fig 3).
Of the 17 studies, eight had a cross sectional design, and nine a cohort design. Again, the weighted average was influenced by the large sample size of the Swedish study.
Therefore, the weighted odds ratio including this study was 0.56. The odds ratio without the Swedish sample was 0.44.
A large study based on questionnaire data for children aged 6 to 7 years from 31 countries and 13 to 14 years from 52 countries confirmed that the inverse association between the number of older siblings and prevalence of hay fever was strongest in more affluent countries.
In both age groups, inverse trends (P < 0.0001) were observed for reported ‘hay
fever ever’ and ‘eczema ever’ with increasing numbers of total siblings, and more specifically
older siblings. These inverse associations were significantly (P < 0.005) stronger in
more affluent countries.