Atopic Disease Bronchial Asthma

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Atopic Disease

S y a m s u

Division of Allergy and ImmunologyDepartment of Internal Medicine

Medical Faculty Hasanuddin University

Makassar


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Atopy is the propensity of an individual to produce IgE

in response to various environmental antigens and to

develop strong immediate hypersensitivity (allergic

!eople "ho have allergies to environmental antigenssuch as pollen or house dust# are said to $e atopic%

Allergic rhinitis and allergic asthma are the most common

manifestation% Atopic dermatitis is less common# andallergic gastroenteropathy is rare% &hese manifestation may

simultaneously coe'ist in the same patient or at different

time% Atopy can also $e asymptomatic


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&he etiology of atopy is unkno"n%&here is su$stantial evidence for

comple' of genes "ith varia$le degree

of e'pression encoding protein factors#some of "hich are

pathogenic and others protective%


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Disease Mechanism AntigenSource

esult

Allergy Immunologic Foreign Disease

Immunity Immunologic Foreign Prophylaxis

Autoimmu

nity

Immunologic Self Disease

Toxicity Toxic Foreign Disease

)*M!AIS*+ *F A,,E-. /I&H *&HE ES!*+SES


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Allergic Asthma


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Definition

Chronic inflammatory disorder of the airways

leading to episodes that are associated to

airflow obstruction which is often reversible

Increased bronchial hyperresponsiveness

!ultiple cells and cellular components

involved

"eversibility may be incomplete


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General consideration

A% E'trinsic Asthma (allergic# atopic# or immunologic -enerally develop early in life# usually in infancy or

childhood# often coe'ist "ith ec0ema or allergic rhinitis%

A family history of atopic disease is common%

Skin test sho" positive reaction to the causative allergen

&otal serum IgE elevated # $ut sometimes normal

1% Intrinsic Asthma (nonallergic or idiopathic

Appears first during adult life# usually after respiratory

infection# $ut sometimes develop during chidhood% Skin test are negative to the usual allergens#

&he serum IgE concentration is normal%

1lood and sputum eosinophilia is present%

!ersonal and family history for atopic disease usuallynegative


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!echanisms of the late phase allergic

reaction

!echanisms of the late phase allergic

reaction2 3 4 5 67 75 (h

RANTESEctaxin

IL-8GM-CSF

PAF

TNF-

IL-4IL-5IL-8GM-CSF

MIP-1MCP-3

TNF-

IL-

IL-3IL-4IL-5IL-8GM-CSF

IL-3IL-4IL-5IL-6IL-13RANTES

IL-4IL-13MIP-1

RANTESEotaxinIL-8GM-CSFPAF

RANTES

MCP-4Eotaxin

ICAM-1VCAM-1

E-selection

ista!in" PG$%"

LTs etc

M&P" ECP"

E$N" CLC etc

M&P" ECP"

E$N" CLC etc

Early phase Late phase Very late phase

A!)

I,87

Endothelium

Epithelium

Endothelium

9)AM83

&h6 1 cells

Ag

Mast cells

FceI

&h6

&h2

Eos Eos1aso

1aso

Eos

&h6

ista!in" LTC4


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Mediators and cytokines involved in chronic

allergic inflammation


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Nonspecific trigger

Infection : 9iral resp% infection!hysiological Factors: % E'ercise# Hyperventilation# Deep

$reathing# !sychologic factors

Atmospheric factors: S*6# +H6# )old air# *6# dest%"ater

Ingestants# !ropanolol# aspirin# +SAID# SulfitE'perimental inhalants: hypertonic solution# citric acid#

histamine# metacholine# !-F6

*ccupational inhalant: isocyanate# "ool# cotton# coffee#

fragrance etc


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Clinical Features

A%Symptoms

Attack of "hee0ing# dyspnea# cough and tightness of chest

Fever is a$sent $ut fatigue# malaise# irrita$ility# palpitations

and s"eating are occasional systemic complaints

1% Sign &achypnea# audi$le "hee0ing# e'piration ;;inspiration%

Use of the accessory muscles of respiration%

!ulsus parado'us indicate severe asthma

In severe attack "ith high grade o$struction $reath soundand "hee0ing may $oth a$sent


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)% ,a$oratory Findings

8 Increased total eosinophil count in peripheral $lood

in nasal secretion# sputum# )harcot ,eyden crystals and)urschman


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Immunologic Diagnosis

Diagnosis made $y history# physical e'amination and !F&

to sho" reversi$le $ronchial o$struction%

1lood and sputum eosinophilia is confirmatory%

)= is useful to e'clude other cardipulmonary diseases

Metacholin challenge test for instances "hich history and!F& is normal

Skin !rick test or AS& for trigger allergens


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)lassification of Asthma Severity

!ersistentIntermittentMild Moderate Severe

)omponents of

Severity

Impairment

+ormalFE93BF9)

583C yr 5@

628C yr 52

728@C yr @

42852 yr 2

isk

ecommended Step for

Initiating &reatment

Symptoms

+ighttime

A"akenings

SA1A use for s'control

Interference "ith

normal activity

,ung Function

Exacerbations

(considerfrequency

and severity)

In 6 84 "eeks# evaluate asthma control that is achieved and adust therapy

accordingly

Step 3 Step 6 Step Step 7 or @

elative annual risk of e'caer$ations may $e related to FE9

#$%&year ' % &year

FreGuency and severity may vary over time for patients in any category

6 daysB"eek >2 days/weeknot daily

Daily )ontinuous

6'Bmonth 3-4x/mont ;3'B"eek

not nightly

*ften nightly

none Minor limitation Some limitationExtremely limited

6 daysB"eek >2days/weeknot daily

Daily !everal times daily

)onsider short course of oral steroids

+ormal FE93$et"een

e'acer$ations

FE93; 52

FE93BF9)

normal

FE93;52

FE93BF9)

normal

FEV1'6()

*+t , 8()

FEV1FVC

.e/+ce/

"#

$E%&

'#

$E%&/$%*

reduced> "#

),ASSIF.I+- AS&HMA SE9EI&. A+D I+I&IA&I+- &EA&ME+& I+

.*U&HS ; 36 .EAS A+D ADU,&SE!8# p7# 77

%(

ASSESSI+- AS&HMA )*+&*, A+D ADUS&I+- &HEA!. I+

E! p


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)lassification of Asthma )ontrol

)omponents of )ontrol

ASSESSI+- AS&HMA )*+&*, A+D ADUS&I+- &HEA!. I+

.*U&HS ; 36 .EAS *F A-E A+D ADU,&S

IM!AIME+&

ISJ

ecommended Action

For &reatment

/ell )ontrolled +ot /ell)ontrolled

9ery !oorly)ontrolled

Symptoms

)ighttime awa*enings

Interference with

normal activitySA+A use

F,-(or pea* flow

-alidated .uestionnaires

ATA/&ACT

,xacerbations

Progressive loss of lung

function

"x$related adverse effects Consider in overall assessment of ris*

,valuation re.uires long$term follow up care

#$ ( per year % $ 0 per year ' 0 per year

none Some limitation ,xtremely limited

1 % days&wee* ' % days&wee* Throughout the

day

1 %&month ($0&wee* ' 2&wee*

1 % days&wee* ' % days&wee* Several times&day

' 3#4 predicted&

personal best

5#$3#4 predicted&

personal best

15#4 predicted&

personal best

#&' %# ($%&(5$(6 0$2&1 (7

Maintain current

step

)onsider step

do"n if "ellcontrolled at least

months

Step up 3 step

eevaluate in 6 8

4 "eeks

)onsider oral

steroids

Step up 386

"eeks and

reevaluate in 6

"eeks

E!8# p#

7@

%%


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SE9EI&. *F AS&HMA E=A)E1A&I*+

8I)A %##5 %0


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%2


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!harmacologic &reatment

eliever- apid acting inhaled K6

L agonist- Anticholinergic- &heophylline- Short8 acting oral K6 88 agonist

)ontroller- Inhaled glucocorticoid- *ral antileucotrienes- inhaled long8acting K68

agonist- )romones- ( &heophylline - *ral long8acting K68agonist- *ral anti8Ig%E- Systemic glucocorticoid- *ral antiallergic- Allergen specific immunotherapy

%7


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*ther drugs

8*ther anti inlammation : methotre'ate#gold salt# cyclosporine# anti &+F- Anti leukotrine : 0afirlukast# montelukast-

Anti IgE : omali0uma$

E!8 p87


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Intermittent

Asthma

!ersistent Asthma: Daily Medication

)onsult "ith asthma specialist if step 7 or higher care is reGuired)onsider consultation at step

!atient Education and Environmental )ontrol at Each Step

Step 3Preferred:

SA1A prn

Step 6Preferred:

,o"8dose I)S

Alternative:,&A

)romolyn

&heophylline

Step Preferred:

Medium8dose

I)S *,o"8dose I)S>

either ,A1A#,&A#

&heophylline

*r ileutin

Step 7

Preferred:

Medium8dose

I)S>,A1A

Alternative:

Medium8dose

I)S>either,&A#

&heophlline

*r ileutin

Step @Preferred:

High dose I)S> ,A1A

A+D

)onsider

*lami0uma$for

patients "ith

allergies

Step 4

Preferred:

High8dose I)S

> ,A1A > oral

)orticosteroid

A+D

)onsider

*lami0uma$

forpatients "ith

allergies

Assess

Control

S&E!/ISE A!!*A)H F* MA+A-I+- AS&HMA

I+ .*U&HS ; 36 .EAS A+D ADU,&S

Ste0 +0 i

nee/e/ 2cec

a/e.ence"

eni.on!ental

cont.ol an/

co!o.*i/ities

Step do"n if

possi$le

(asthma "ell

controlledfor

months

E!8# p87

E!8# p87

%9


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T er m a K a s h

Atopic Disease Bronchial Asthma

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