clinical clerk rhinitis and asthma
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8/3/2019 Clinical Clerk Rhinitis and Asthma
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Allergic Rhinitis and Asthma
Clinical Clerk Teaching Sessions
London, OntarioDr. DW Moote & Dr. JA Mazza
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Objectives to describe the diagnosis and treatment
of allergic rhinitis and asthma
to identify asthma medications and thecircumstances in which to use them
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Bring your own case
Anything on the ward to discuss with respectto Clinical Immunology & Allergy? There will
be time for at least one other topic for discussion
Adverse Drug Reactions
Anaphylaxis
Insect Venom Allergy
Urticaria
Food Allergy
Etc.
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Prevalence of Allergic Rhinitis
10±20% population
all ages, onset usually before 30 yrs
most common chronic illness in personsunder 30 yrs
not life threatening, but threatens quality of
life costs about $200 million/yr in Canada
50% individuals don¶t seek medical attention
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Diagnosis rhinorrhea,
obstruction
itching, sneezing,ocular symptoms
other allergysymptoms, familyhistory
?pain, headache,toothache
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Allergic salute nasal crease
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Skin testing
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Rhinitis
treatment Environmental
control measures
Medications Immunotherapy
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Dust mite avoidance
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Pollen avoidance
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Animal dander avoidance
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Pine B
irchGrass
Pollen
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Medication options Antihistamines
Decongestants
oral
topical
Intranasal glucocorticoid sprays
Immunotherapy
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Antihistamine problems
Sedation/Driving behaviour
Cost-benefit of newer products
Use in pregnancy and breast feeding Drug interactions±contraceptives
Dosing interval / half-life
Tachyphylaxis / subsensitivity Use in asthma
Cardiac risk?
Cancer?
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Antihistamines are common allergic rhinitis present in 15% of
population
antihistamines are profitable
none are perfect
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Gallup poll
801 adults²Sept 89 Productivity
74% say symptoms make them less productive
impairment due to side effects 14/240 work-days
Driving 67% aware medications may impair driving
61% drive anyway
53% are very or fairly concerned about others driving while
using antihistamines
Machine operation 30% operate machinery (includes household power tools)
when taking allergy medications
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Drowsiness attributed to blockade of central histaminergic
receptors
antagonism of serotonin and acetylcholine, andalpha-adrenergic stimulation may be involved
second generation antihistamines lipophobic: poor penetration into CNS
bind preferentially to peripheral receptors
relatively free of anti-serotonin, anticholinergic, and alpha-blocking effects
incidence of sedation is not zero, and may increasewith larger doses
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Cost/B
enefit chlorpheniramine
12¢/day
non-sedating agents$1.00/day
generic loratadine,cetirizine 11±80¢/day
most drug plans won¶tcover OTC meds. TryRx only hydroxyzine(sedating) or half acetirizine 20 mg.
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Antihistamine kinetics Older antihistamines
recommended dosing intervals date to
1940
no systematic studies until 1980¶s,because of difficulty measuring low blood
levels chlorpheniramine, brompheniramine,
hydroxyzine all have half-lives longer than20 hrs
Why QID dosing?
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Half-life Wheal suppression
Cetirizine 10 hours 24 hoursLoratadine 11 hours 12-24 hours
Terfenadine 17 hours 12-24 hours
Astemizole 9.5 days weeks
Antihistamine kinetics Duration of action longer than
expected from half-life
most can be dosed once daily
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Simons K, J Clin Pharm 1990
Half LivesElderly: 13.5 4.2 h Adults: 9.2 2.5 hChildren: 5.4 1.8 h
Diphenhydramine kinetics
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Children Adults Elderly Reference
Diphenhydramine 5.4 s1.8 9.2 s2.5 13.5 s 4.2Simons, J ClinPharm 2000
Chlorpheniramine 13.1 s 6.3 21±27 22.6 s 11.0Simons 82, 90
Rumore
Loratadine 15 (28 for
metabolites)
Desloratadine 27
Cetirizine 10.6 11.8 Simons 1988
Fexofenadine 11±16
Antihistamine Kinetics
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Subsensitivity / tachyphylaxis
Long-term administration of firstgeneration antihistamines associatedwith apparent loss of efficacy
Compliance a problem
No change in half-life with long termdosing
No loss in efficacy at suppressingsymptoms or skin tests for 12 weeks withrigorous monitoring of compliance, up toone year in dog studies
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Rhinitis andP
regnancy Ideally, no medication in first trimester, but consider
impact of disease itself
Antihistamines: chlorpheniramine (alsodiphenhydramine, hydroxyzine), OK data, loratadineand cetirizine now Category B
pseudoephedrine, topical decongestants²?no
intranasal steroids²see asthma data
immunotherapy²continue, but don¶t start. Usuallyreduce dose to minimize risk of anaphylaxis.
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Interaction with contraceptives CPS states increased incidence of
contraceptive failure when combined with
antihistamines Based on 16 case reports, self reported²De
Sano 1982
ampicillin plus ³cold tablet´ (four patients)
penicillin plus ³cold tablet´
penicillin, caffeine, chlorpheniramine, ASA,phenylephrine for ³cold´
antihistamines for ³hay fever, but some of these
³antihistamines´ were really decongestants
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Interactions with contraceptives Other databases do
not support any
associationwhatsoever!²Szoka 1988
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Antihistamines & thyroid CPS cautions against use of some
antihistamines in patients with ³thyroid
disease´ this is extrapolated from problems inhyperthyroid patients given stimulants, e.g.pseudoephedrine, and the fact that someantihistamines are found in combinations
not relevant to antihistamines alone, or topatients with treated thyroid disease
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Antihistamines & Cardiac Risk
Mainly in predisposed individuals (torsades de
pointes), with daily dosing and either metabolicidiosyncrasy or drug interaction
Newer preparations are safer, not without risk of QT prolongation
Risk in older (sedating) antihistamines isidentical, but associated mainly with overdose
Is it just that non-sedating preparations get totoxic levels without awareness of side effects?
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Antihistamines & Cancer
Rat study included rats givenintraperitoneal injections of
anthihistamine after being injectedwith tumor cells
» Brandes, L. J Natl Cancer Inst
Despite controversy, human datadoesn¶t support concerns raised byrat study
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Antihistamines & Asthma
CPS sometimes lists asthma ascontraindication, presumably because of
anticholinergic ³drying´ effect In fact, modest bronchodilator effect
chlorpheniramine, hydroxyzine, clemastine,terfenadine, cetirizine
Prevent challenge with histamine,antigen, hyperventilation, exercise, butnot methacholine
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Oral decongestants
pseudoephedrine
available alone, and incombination
phenylpropanolamine
available until October 2000,only in combination
also found in dietary³supplements´
phenylephrine
replaces pseudoephedrine inmost combinations
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Phenyl-propanolamine
Conclusions. The results suggest thatphenylpropanolamine in appetite
suppressants (odds ratio 15.92), andpossibly in cough and cold remedies(odds ratio 1.49), is an independent riskfactor for hemorrhagic stroke in women.
(N Engl J Med 2000;343:1826-32.) P aracelsus 16th century: ³the right dose
differentiates a poison from a remedy´
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Intranasal steroids
much moreeffective than oral
medications,especially for congestion
add if p.r.n.antihistamine useexceeds threetimes a week for any significant time
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Ben Johnson²Seoul 1988
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Steroids & growth suppression
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Allen DB, J Allergy Clin Immunol 2000
Metabolism
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Oral Intranasal Inhaled
Mometasone <0.1% <0.1% <1%
Fluticasone <1% 1.8% 12±26%
Triamcinolone 23% NA 22%
Budesonide 10% 33% Aq 30% turb
Beclomethasone 15±25% NA 15±25%
Bioavailability nasal steroids
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Bioavailability
Risk comparisons
between products
are few assays used in
different studies arenot directly
comparable longer half-life
drugs would requirelonger monitoring
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Kevin T Kavanagh,
Nasal septal perforation
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Septal perforation
Anecdotes of association with topicalnasal steroid use
Not seen in prospective studies of nasalsteroids
Retrospective anecdotes unreliable,since most physicians don¶t look at
septum before prescribing dose US recommends regular follow-up
observation in patients on chronic nasalsteroids
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Wilson et al, J Allergy Clin Immunol 1998
Plasma half-life
B
eclomethasone 0.5 hours
Budesonide 2.3 hours
Triamcinolone 3.6 hours
Mometasone 5.8 hours
Fluticasone 14.4 hours
Steroid half-life
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Systemic activity
Wilson AM et.al., J Allergy Clin Immunol 1998;102:598-604.
placebo
budesonide
mometasone furoate
triamcinoloneacetate
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Normal nasal mucosa
(even after years of daily use)
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Short stature 14 year old boy, 4
foot 8 inches, with
a history of asthmarequiring oralcorticosteroids
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Pederson, S. et.al., J Allergy Clin Immunol 1999
Growth rate
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Growth suppression mainly data from asthma studies
less common with once daily preparations
probably not sustained
short term studies can be flawed bydifferences in maturity of cohorts
worst case scenario²probably about 1cm if lifetime use, but consider prednisone!
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Immunotherapy
for rhinitis or asthma
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Treatment for rhinitis
make sure you know what it is
try avoidance first
try p.r.n. oral medications add an intranasal steroid if
antihistamines needed > 3x/wk
fine tuning consider immunotherapy if
avoidance and medications fail
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Asthma
C di A th C
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Canadian Asthma Consensus:2003, updated to December
2004CMAJ 2005; 173 (6suppl): S1±S56
LP Boulet et al.CMAJ 1999;161(11Suppl)
LP Boulet et al.C an Respir J 2001;8(Suppl A):5A-27A
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Canadian Asthma Consensus Report, 1999
Approach to Asthma
Confirm diagnosis objective measure of lung function
Assess severity
Achieve control rapidly
Assess environment and other contributing factors
Educate patients
Determine minimum medication needed to maintainoptimal control
Action plan for exacerbations
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Canadian Asthma Consensus Report,1999
Asthma management:
6 Components Educate patients
Assess asthma severity and control
Avoid or control asthma triggers
Medication plan: chronic management
Management plan: acute exacerbations
Regular follow-up care
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Canadian Asthma Consensus Report, 1999
Parameter Frequency or Value
Daytime symptoms < 4 days/wk
Night-time symptoms < 1 night/wk
Need for short-acting B2-agonist < 4 doses/wk
Physical activity Normal
Exacerbations Mild, infrequent
Absence form work or school None
FEV1 or PEFR 85-90% of personal best
PEF diurnal variation < 15% diurnal variation
Asthma Control
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Medication for Chronic Asthma Management
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Canadian Asthma Consensus
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Canadian Asthma Consensus Report, 2005
Medication for Chronic
Management Inhaled Corticosteroids
initial anti-inflammatory therapy [level I]
400-1000 µg/d (or higher) starting dose[level III]
early use better functional outcome
[level III] Insufficient data for short courses of
steroids in children with mild, intermittentasthma [Level II]
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Canadian Asthma Consensus Report, 2005
ProductDose, ug/d
Low Medium High
BDP pMDI and spacer 500 501 ± 1000 >1000
BUD Turbuhaler 400 401 ± 800 >800
FP pMDI and spacer 250 251 ± 500 >500
FP Diskus 250 251 ± 500 >500
BDP pMDI (HFA) 250 251 ± 500 >500
BUD wet nebulization 1000 1001 ± 2000 >2000
Dose Equivalencies for
Inhaled Corticosteroids
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Canadian Asthma Consensus Report, 2005
Long-Acting Beta-Agonists:
Salmeterol and Formoterol not recommended as maintenance
monotherapy [level I]
consider as an alternative to increased dosesof inhaled steroids; should be an adjuncttherapy to moderate or higher doses of inhaled steroids [level I]
formoterol is rapid acting and may be usedfor rescue therapy, but at greater cost [2001revision]
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F-agonists and corticosteroids
combination
Barnes PJ. Br J C lin P harmacol 199
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Canadian Asthma Consensus Report, 2005
Leukotriene-Receptor Antagonists
Monteleukast and Zafirlukast consider as an alternative to increased doses
of inhaled steroids; may be an adjunct
therapy to moderate or higher doses of inhaled steroids [level II]
insufficient evidence as first-line anti-inflammatory therapy; but primary treatment
of choice for patients who cannot or will notuse inhaled steroids [level IV]
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Canadian Asthma Consensus Report, 2005
Asthma Therapy
5 Most Important Aspects Achieve acceptable disease control
Control the environment
Asthma education: guided self-managementand use of an action plan
Inhaled steroids are the first line anti-inflammatory therapy
Additional therapy can be added to moderatedoses of steroid if acceptable control is notobtained
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Approach to a Patient with
Poor Asthma Control Confirm diagnosis of asthma
Objective assessment of airflow rates s MeCh
Assess device technique Assess adherence and barriers
Assess environment/triggers
Co-morbidities (eg.P
ost-nasal drip, GER,OSA)
Action Plan for exacerbations
Escalate therapy
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New therapies & concepts
New therapy
Xolair (omalizumab)
Alvesco (ciclesonide)
New concepts
Symbicort maintenance and reliever
therapy $100 each
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Sampson, J Allergy Clin Immunol
New therapies: Omalizumab
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Ciclesonide
Not very active asparent molecule,
less oropharyngealside effects
Activated in lungby esterases,
becomesbudesonide, thenexcreted
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Ciclesonide
Approved for asthma, dosing issuggested at 100µg = 200µg
budesonide, (but may be lower) Now approved for nasal spray also,
but not launched as of March 2008
Main difference is reducedoropharyngeal candidiasis (nothoarseness)
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Symbicort SMART
Oxeze (formoterol) fast enough onsetto use as reliever (c.f. salmeterol)
Budesonide/formoterol combinationnow approved for relief as well asmaintenance
Some advantages with respect toconvenience, symptom control
Total Asthma Exacerbations Requiring
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Total Asthma Exacerbations RequiringMedical Intervention
0
Bud/Form + SABA 330
events
280
200
120
40
3 6 9 12 15 19 23 27 31 35 39 43 47 51 55
4 x BUD + SABA294
events
Weeks since randomisation
0
280
200
120
40
3 6 9 12 15 19 23 27 31 35 39 43 47 51 55
Bud/Form SMART
16 0 events
0 3 6 9 12 15 19 23 27 31 35 39 43 47 51 55
280
200
120
40
# rate reduction 46 to 53% vs bothgroups; p<0.001
O¶Byrne PM et al. Am J RespirCrit Care Med 2005; 171:129-136
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Resources for rhinitis & asthma
J Allergy Clin Immunol. The Diagnosis andManagement of Rhinitis: An Updated PracticeP
arameter. 2008 Supp, Vol. 122, No 2S CMAJ. Canadian Asthma Consensus
Guidelines September 2005 Volume 173,Supp
Asthma, Cecil Medicine, Chapter 87
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Other resources for reference
Drug allergy, Greenberger P, J Allergy ClinImmunol. 2006, Vol. 117, Issue 2, Pages
S464-S470 Anaphylaxis, Simons FER, J Allergy Clin
Immunol, Feb 2008 Vol. 121, Issue 2, PagesS402-S407
Mini-Primer on Allergic and ImmunologicDiseases, J Allergy Clin Immunol, February2006 & February 2008
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