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Extrinsic allergic alveolitis
Hypersensitvity pneumonitis
ปอดอักเสบภูมไิ วเกิน
ศ.น.พ. อรรถ นานา
คณะแพทยศาสตร์ ศิริราชพยาบาล
มหาวิทยาลัยมหิดล
HP: Introduction
• immunologically induced lung disease
• diffuse inflammation of lung parenchyma
& airways in previously sensitized
patients
• sensitized to repeated inhalation of dusts
containing organic & low molecular
weight chemical antigens
HP: Introduction
• dusts derived from
– dairy & grain products
– animal dander & proteins
– wood bark
– water reservoir vaporizers
• not atopic disease
• not associated with increase IgE or
eosinophils
HP: Selected etiological agents
Disease
Farmer’s lung
ปอดชาวไร่
Bagassosis
โรคชานอ้อย
Bird-breeder’s lung
Bird-fancier’s lung
Pigeon-breeder’s lung
Mushroom-worker’s lung
คนเพาะเห็ด
Humidifier/air conditioner
lung
ปอดเครื่ องทาความชื้น
ปอดอักเสบการระบาย
อากาศ
Source
Antigen
หญ้าแห้งที่ข้ ึนรา
Micropolyspora faeni
ชานอ้อยที่ข้ ึนรา
Thermoactinomyces
sacchari
มูลนก, ขน
(พิราบ,นกแก้ว)
Avian proteins
ปุ๋ ยที่ข้ ึนรา,หญ้าแห้ง
Thermoactinomyces
vulgaris
เครื่ องทาความชื้น
ท่อเครื่ องปรับอากาศ
Micropolyspora faeni
Thermoactinomyces
vulgaris
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
420-3000
cases/100,000 /
persons at
France
4370
“
“
Finland
1400-1700
“
“
U.S.A.
540
“
“
risk
“
“
“
Bagassosis : A Report of 8 Cases
จดหมายเหตุทางแพทย์ 2517:57;468-74.
Pee
Kamtorn, M.D.*
Poonkasem Charoenpan, M.D.**
Yosvi
Sukumalchantra, M.D. , F.A.C.P. , F.R.C.P. (C) ,F.A.C.C.**
Vijitr
Boonpucknavig, M.D.***
Kalyanakit
Kitiyakara, M.B. , B.S. , M.R.C.S. , L.R.C.P.****
Chirotchana Suchato, M.D.*****
Chaivej
Nuchprayoon, M.D.******
Case Report
Bagassosis is classified as an extrinsic allergic
pneumonia. It is considered to be the result of
allergic reaction to moldy sugar cane inhalation(1) .
All of the patients worked at a
paper production factory in Karnchanaburi
province and were
HP : Pathogenesis
•
immune - complex mediated process
– precipitating Ab against specific Ag
– 50% of asymptomatic persons exposed also
have Ab
HP: Pathogenesis
• cell - mediated immunity more important
• response
– increase PMN in alveoli & small airways
– influx of mononuclear cells
– formation of granulomas
• cytokine from T- lymphocytes &
macrophages
HP : Histologic findings
• diffuse interstitial infiltrate : lymphocytes,
macrophages, mast cells, plasma cells
• scattered noncaseating granulomas
• cellular inflammation of bronchioles, +
bronchiolar obstruction
• absent generalized vasculitis, necrotizing
granulomata
~ duration or stage of disease, adequacy of biopsy
sample
HP : Diagnostic criteria
Major criteria
1. Symptoms c/w HP , appear or worsens within
hours after Ag exposure
2. Confirmation of exposure to the offending agent
by
- Hx
-investigation of the environment
-serum precipitin test
-BAL Ab
HP : Diagnostic criteria
3. Compatible CXR or HRCT
4. Lymphocytosis in BAL
5. Compatible histologic changes
6. Positive “natural challenge” or by
controlled inhalational challenge
HP : Diagnostic criteria
Minor criteria
1. Basilar crackles
2. Decreased diffusion capacity
3. Arterial hypoxemia, at rest or with exercise
HP : Diagnostic criteria
Four major criteria
Two minor criteria
Other diseases have been excluded
Adapted from Schuyler + Cormier Chest 1997; 111:
534-6.
HP : Diagnosis
• often unrecognized & misdiagnosed
• respiratory symptoms with Hx. of
– environmental
– occupational exposure
• respiratory symptoms with episodic radiographic
infiltrates “Recurrent pneumonia”
HP : Radiographic findings
• vary to the stage of disease
• acute HP
– bilateral micronodular (1-4 mm.) infiltrates
– patchy ground-glass opacities
– decreased attenuation (air trapping from
bronchiolitis) and mosaic pattern
(expiratory view)
HP : Radiographic findings
• Subacute HP
– fine linear shadows, small nodules = reticulonodular
appearance
• Chronic HP
–
–
–
–
volume loss
reticulonodular infiltrates
honeycombing
predominantly upper & mid lung zones
HP : Pulmonary function tests
•
restrictive changes
•
(superimposed obstruction in chronic HP)
•
decreased diffusing capacity
•
ABG: increased alveolar-arterial oxygen gradient
–
frank hypoxemia (severe cases)
–
oxygen desat. with exercise (clue in suspected case)
HP : BAL fluid
• intense lymphocytosis
– predominantly CD 8+ T-suppressor cells
~ timing of the last antigen exposure, stage of
disease
HP: key features
Time frame
4-48 hr
Clinical features
Acute
fever, chills, cough
hypoxemia, aches
Subacute weeks to 4 M. dyspnea , cough,
episodic flares
Chronic 4 M. to years dyspnea, cough,
fatigue, weight loss
Immunopathology Prognosis
HRCT
good
ground glass alveolitis, immune
infiltrates complex
good
micronodules, granulomas,
air trapping bronchiolitis
good
fibrosis, honey lymphocytic
infiltration,
combing,
emphysema fibrosis,air space
destruction
HP : Differential diagnosis
• Acute stage
–
–
–
–
pneumonia
acute tracheobronchitis
organic dust toxic syndrome
BOOP
HP : Differential diagnosis
• Subacute stage
–
–
–
–
recurrent pneumonia
granulomatous lung diseases
pneumoconiosis
Wegener’s granulomatosis
HP : Differential diagnosis
• Chronic stage
–
–
–
–
IPF
bronchiectasis
COPD with pulmonary fibrosis
MAC
HP: Management
•
•
•
•
•
early diagnosis
avoidance of further exposure
protective devices :- personal respirators
relocation to a new job
reducing microorganism contamination in the
environment
– altering handling & storage
– wetting compost
– using antibiotics to decrease fungal growth
– preventive maintenance on all A/C equipment
HP: key features
Time frame
4-48 hr
Clinical features
Acute
fever, chills, cough
hypoxemia, aches
Subacute weeks to 4 M. dyspnea , cough,
episodic flares
Chronic 4 M. to years dyspnea, cough,
fatigue, weight loss
Immunopathology Prognosis
HRCT
good
ground glass alveolitis, immune
infiltrates complex
good
micronodules, granulomas,
air trapping bronchiolitis
good
fibrosis, honey lymphocytic
infiltration,
combing,
emphysema fibrosis,air space
destruction
Subacute HP, a 60-year-old dairy farmer had a 8-year history of
intermittent dyspnea. CXR shows bilateral reticulonodular
interstitial infiltration.
Chronic HP, Pigeon breeder’s disease. Bilateral reticulonodular
densities are present.
Acute HP, ground glass opacification
HRCT of a patient with Chronic HP demonstrating centrilobular
nodules not associated with bronchovascular bundles.
Chronic HP, honeycombing in right upper lung & traction
bronchiectasis
Acute HP, mononuclear infiltration & noncaseating
granulomas.
Chronic HP, mostly lymphocytic cellular infiltrate with
epithelioid cells & numerous and clearly defined granuloma.
(Wright-Giemsa)
Giant cells are characteristic feature of HP.
Chronic HP shows interstitial inflammation associated
with fibrosis.