extrinsic allergic alveolitis hypersensitvity pneumonitis...
TRANSCRIPT
Extrinsic allergic Extrinsic allergicalveolitisalveolitis
Hypersensitvity p Hypersensitvity pneumonitisneumonitis
ปอดอ�กเสบภู�มิ ไวเก นปอดอ�กเสบภู�มิ ไวเก นศ.น.พ. อรรถ นานาคณะแพทยศาสตร�ศ ร ราชคณะแพทยศาสตร�ศ ร ราช
พยาบาลพยาบาลมิหาว ทยาล�ยมิห ดลมิหาว ทยาล�ยมิห ดล
HP: IntroductionHP: Introduction• immunologically induced lung disea immunologically induced lung diseasese
• diffuse inflammation of lung parenc diffuse inflammation of lung parenc hyma & airways in previously sensit hyma & airways in previously sensit
ized patients ized patients• sensitized to repeated inhalation of sensitized to repeated inhalation of
dusts containing organic dusts containing organic & low & low molecular weight chemical molecular weight chemical antigenantigenss
HP: IntroductionHP: Introduction• dusts derived from dusts derived from
– dairy & grain products dairy & grain products– animal dander & proteins animal dander & proteins– wood bark wood bark– water reservoir water reservoir
vaporizers vaporizers• not atopic disease not atopic disease• not associated with not associated with
increase IgE or eosinop increase IgE or eosinophilshils
HP: Selected etiological HP: Selected etiological agentsagents
Disease Farmer’s lung
ปอดชาวไร่Bagassosisโร่คชานอ�อยBird-breeder’s lungBird-fancier’s lungPigeon-breeder’s lung
-Mushroom worker’s lung
คนเพาะเห็�ดHumidifier/air conditionerlungปอดเคร่��องทำ�าความช��นปอดอ�กเสบการ่ร่ะบายอากาศ
Sourceห็ญ้�าแห็�งทำ$�ขึ้&�น
ร่า
ชานอ�อยทำ$�ขึ้&�นร่า
ม'ลนก , ขึ้น(พ)ร่าบ,นก
แก�ว)
ป*+ยทำ$�ขึ้&�นร่า,ห็ญ้�าแห็�ง
เคร่��องทำ�าความช��น
ทำอเคร่��องปร่�บอากาศ
Antigen Micropolyspora
faeni
Thermoactino myces
sacchari
Avian proteins
Thermoactino myces
vulgaris
Micropolyspora faeni
Thermoactino myces
vulgaris
HP: Epidemiology HP: Epidemiology• Varies• 0.5-5% of farmers (Farmer’s lung disease)• 8-30% of members of pigeon breeding clubs (pigeon breeder’s disease)• Prevalence Farmer’s lung
UK
France
Finland
U.S.A.
420-3000
4370
1400-1700
540
cases/100,000 /
“
“
“
persons at
“
“
“
risk
“
“
“
Bagassosis : A Report of 8 Bagassosis : A Report of 8 CasesCases
Pee Kamtorn, M.D.*Pee Kamtorn, M.D.*
Poonkasem Charoenpan, M.D.**Poonkasem Charoenpan, M.D.**
Yosvi Sukumalchantra, M.D. , F.A.C.P. , F.R.C.P. (C) ,F.A.C.C.**Yosvi Sukumalchantra, M.D. , F.A.C.P. , F.R.C.P. (C) ,F.A.C.C.**
Vijitr Boonpucknavig, M.D.***Vijitr Boonpucknavig, M.D.***
Kalyanakit Kitiyakara, M.B. , B.S. , M.R.C.S. , L.R.C.P.****Kalyanakit Kitiyakara, M.B. , B.S. , M.R.C.S. , L.R.C.P.****
Chirotchana Suchato, M.D.*****Chirotchana Suchato, M.D.*****
Chaivej Nuchprayoon, M.D.******Chaivej Nuchprayoon, M.D.******
Bagassosis is classified as an extrinsic allergicBagassosis is classified as an extrinsic allergic
pneumonia. It is considered to be the result ofpneumonia. It is considered to be the result of
allergic reaction to moldy sugar cane inhalationallergic reaction to moldy sugar cane inhalation(1)(1) . .
Case ReportCase Report
All of the patients worked at a All of the patients worked at a
paper produc-paper produc-
tion factory in Karnchanaburi tion factory in Karnchanaburi
province and wereprovince and were
จดหมิายเหต"ทางแพทย� 2517:57;468-74.
HP : PathogenesisHP : Pathogenesis
• - immune complex m - immune complex m ediated process ediated process
– precipitating Ab precipitating Ab against specific Ag against specific Ag
– 50% o 50% o f asymptomatic persons f asymptomatic persons
exposed also have Ab exposed also have Ab
HP: PathogenesisHP: Pathogenesis
• - cell mediated immunity m - cell mediated immunity m ore important ore important
•responseresponse– increase PMN in alveoli increase PMN in alveoli && sm sm
all airways all airways– influx of mononuclear cells influx of mononuclear cells– formation of granulomas formation of granulomas
• - cytokine from T - cytokine from T lymphocytes & macrophag lymphocytes & macrophag
eses
HP : Histologic HP : Histologicfindingsfindings
• diffuse interstitial infiltrate : lympho diffuse interstitial infiltrate : lympho cytes, cytes,
macrophages, mast cells, plasma cell macrophages, mast cells, plasma cell s s
• scattered noncaseating granulomas scattered noncaseating granulomas• cellular inflammation of bronchioles, cellular inflammation of bronchioles,
+ bronchiolar obstruction + bronchiolar obstruction• absentabsent generalized vasculitis, necrot generalized vasculitis, necrot
izing granulomata izing granulomata
~ duration or stage of disease, adequ ~ duration or stage of disease, adequ acy of biopsy acy of biopsy samplesample
HP : Diagnostic HP : Diagnostic criteriacriteria
Major criteriaMajor criteria1. Symptoms c/w HP , appear or 1. Symptoms c/w HP , appear or worsens within hours after Ag worsens within hours after Ag exposureexposure
2. Confirmation of exposure to the 2. Confirmation of exposure to the offending agent byoffending agent by
- Hx- Hx
-investigation of the environment-investigation of the environment
-serum precipitin test-serum precipitin test
-BAL Ab -BAL Ab
HP : Diagnostic HP : Diagnostic criteriacriteria
3. Compatible CXR or HRCT3. Compatible CXR or HRCT
4. Lymphocytosis in BAL4. Lymphocytosis in BAL
5. Compatible histologic changes 5. Compatible histologic changes
6. “ ”Positive natural challenge or b 6. “ ”Positive natural challenge or b y y
cccccccccc cccccccccccc ccccccccccccccc cccccccccccc ccccccccccccc
HP : Diagnostic HP : Diagnostic criteriacriteria
Minor criteria Minor criteria
1. Basilar crackles 1. Basilar crackles
2. Decreased diffusion cap 2. Decreased diffusion capaci tyaci ty
3 . ,Arterial hypoxemia at res 3 . ,Arterial hypoxemia at res t or wi thexerci se t or wi thexerci se
HP : Diagnostic HP : Diagnostic criteriacriteria
Four major criteria Four major criteria
Two minor criteria Two minor criteria
Other diseases have been ex Other diseases have been excludedcluded
Adapted from Schuyler + Cormier Adapted from Schuyler + Cormier -Chest 1997; 111: 534 6. -Chest 1997; 111: 534 6.
HP : DiagnosisHP : Diagnosis
• often unrecognized & misdiagnosed often unrecognized & misdiagnosed
• respiratory symptoms with Hx. of respiratory symptoms with Hx. of
– environmental environmental
– occupational exposure occupational exposure
• respiratory symptoms with episodic respiratory symptoms with episodic radiographic infiltrates radiographic infiltrates “Recurre“Recurre
nt pneumonia” nt pneumonia”
HP : Radiographic HP : Radiographic findingsfindings
•vary to the stage of diseasevary to the stage of disease•acute HPacute HP
– bilateral micronodular (1-4 bilateral micronodular (1-4 mm.) infiltratesmm.) infiltrates
– patchy ground-glass patchy ground-glass opacitiesopacities
– decreased attenuation (air decreased attenuation (air trapping from bronchiolitis) and trapping from bronchiolitis) and mosaic pattern (expiratory mosaic pattern (expiratory view)view)
HP : Radiographic HP : Radiographic findingsfindings
• Subacute HP Subacute HP– fine linear shadows, small nodules fine linear shadows, small nodules
= reticulonodular appearance = reticulonodular appearance
• Chroni c HP Chroni c HP– volume loss volume loss– reticulonodular infiltrates reticulonodular infiltrates– honeycombing honeycombing– predominantly upper & mid lung z predominantly upper & mid lung z
onesones
HP : Pulmonary HP : Pulmonary function testsfunction tests
• restrictive changesrestrictive changes
• (superimposed obstruction in chronic (superimposed obstruction in chronic HP)HP)
• decreased diffusing capacitydecreased diffusing capacity
• ABG: increased alveolar-arterial ABG: increased alveolar-arterial oxygen gradientoxygen gradient
– frank hypoxemia (severe cases)frank hypoxemia (severe cases)
– oxygen desat. with exercise (clue oxygen desat. with exercise (clue in suspected case)in suspected case)
HP : BAL fluidHP : BAL fluid
• i ntense l ymphocytosi s i ntense l ymphocytosi s–
8predominantly CD 8predominantly CD ++ c-ccc c-ccc pressor cells pressor cells
~ timingof the l ast anti genexpos ~ timingof the l ast anti genexpos ure, stage of disease ure, stage of disease
HP: key featuresHP: key featuresTime frame
4-48 hr
weeks to 4 M.
4 M. to years
Acute
Subacute
Chronic
Clinicalfeatures
fever, chills,cough
hypoxemi a, aches
dyspnea ,cough,
episodicflares
dyspnea,cough,
fatigue, weight los
s
HRCT
ground glass
infiltrates
microno dules,
airtrapping
fibrosis, honey
combin g,
emphysema
Immunopathology
alveolitis, immune
complex
granulom as,
bronchiolitis
lymphocytic
infiltration ,
fibrosis,air space
destruction
Prognosis
good
good
good
HP : Differential HP : Differential diagnosisdiagnosis
• Acute stage Acute stage– pneumoni apneumoni a– acute tracheobronchi ti s acute tracheobronchi ti s–
organic dust toxic syndrome organic dust toxic syndrome– BOOPBOOP
HP : Differential HP : Differential diagnosisdiagnosis
• Subacute stage Subacute stage– recurrent pneumoni a recurrent pneumoni a–
granulomatous lung diseases granulomatous lung diseases– pneumoconi osi spneumoconi osi s– Wegener’sgranul omatosi s Wegener’sgranul omatosi s
HP : Differential HP : Differential diagnosisdiagnosis
• Chronic stage Chronic stage– IPFIPF– bronchiectasisbronchiectasis– COPD with COPD with
pulmonary fibrosis pulmonary fibrosis– MACMAC
HP: ManagementHP: Management•early diagnosisearly diagnosis•avoidance of further exposure avoidance of further exposure •protective devices :- personal protective devices :- personal
respiratorsrespirators•relocation to a new jobrelocation to a new job•reducing microorganism reducing microorganism
contamination in the environmentcontamination in the environment– altering handling & storagealtering handling & storage– wetting compostwetting compost– using antibiotics to decrease fungal using antibiotics to decrease fungal growthgrowth
– preventive maintenance on all A/C preventive maintenance on all A/C equipmentequipment
HP: key featuresHP: key featuresTime frame
4-48 hr
weeks to 4 M.
4 M. to years
Acute
Subacute
Chronic
Clinicalfeatures
fever, chills, cough
hypoxemi a, aches
dyspnea ,cough,
episodicflares
dyspnea,cough,
fatigue, weight los
s
HRCT
ground glass
infiltrates
microno dules,
airtrapping
fibrosis, honey
combin g,
emphysema
Immunopathology
alveolitis, immune
complex
granulom as,
bronchiolitis
lymphocytic
infiltration ,
fibrosis,air space
destruction
Prognosis
good
good
good
Subacute HP Subacute HP - - 60, a year old dair ffff ff fff f f -ffff fffffff ff fff8
ffffffff fff fffff fffffffff ffffffffff. dulari nt er st i t i al i nfi l t r at i on.
Chronic HP Chronic HP fffffffff fffff, ’ fffffffff fffffffffffffff fffffffff fff .present.
Acute HP Acute HP , ground glass opacification
f fff ff f fffffff f fff Chronic HP Chronic HP fffffffffffff fffffffffffff fff ffffffffff f fff fffffffffffffff ffffffff.
Chronic HP Chronic HP , honeycombing in right upper lung & traction
ffffffffffffff
Acute HP Acute HP , mononuclear infilt ration & noncaseating granulo
mas.
Chronic HP Chronic HP , mostly lymphocytic c ellular infiltrate with epithelioid cell
f fff fffff fff fffffff fffffff & -. ( )
Giant cells are characteristic feature of HP.
Chronic HPChronic HP shows interstitial inflammation associated with fibrosis.