1. ศ.น.พ. อรรถ นานา คณะแพทยศาสตร์ศิริราชพยาบาล มหาวิทยาลัยมหิดล
Extrinsic allergic alveolitis Hypersensitvity pneumonitis ปอดอักเสบภูมิไวเกิน
ศ.น.พ. อรรถ นานา
คณะแพทยศาสตร์ศิริราชพยาบาล
มหาวิทยาลัยมหิดล

2. 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

3. HP: Introduction dusts derived from not atopic disease
dairy & grain products
animal dander & proteins
wood bark
water reservoir vaporizers
not atopic disease
not associated with increase IgE or eosinophils

4. 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
ปอดเครื่องทำความชื้น
ปอดอักเสบการระบาย
อากาศ
Source
หญ้าแห้งที่ขึ้นรา
ชานอ้อยที่ขึ้นรา
มูลนก, ขน
(พิราบ,นกแก้ว)
ปุ๋ยที่ขึ้นรา,หญ้าแห้ง
เครื่องทำความชื้น
ท่อเครื่องปรับอากาศ
Antigen
Micropolyspora faeni
Thermoactinomyces sacchari
Avian proteins
Thermoactinomyces vulgaris
Thermoactinomyces
vulgaris

5. 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.
4370
540
cases/100,000 / “
persons at “
risk “

6. Bagassosis : A Report of 8 Cases
จดหมายเหตุทางแพทย์ 2517:57;
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.******
Bagassosis is classified as an extrinsic allergic
pneumonia. It is considered to be the result of
allergic reaction to moldy sugar cane inhalation(1) .
Case Report
All of the patients worked at a paper produc-
tion factory in Karnchanaburi province and were

7. HP : Pathogenesis precipitating Ab against specific Ag
immune - complex mediated process
precipitating Ab against specific Ag
50% of asymptomatic persons exposed also have Ab

8. 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

9. 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

10. 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

11. 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

12. HP : Diagnostic criteria
Minor criteria
1. Basilar crackles
2. Decreased diffusion capacity
3. Arterial hypoxemia, at rest or with exercise

13. HP : Diagnostic criteria
Four major criteria
Two minor criteria
Other diseases have been excluded
Adapted from Schuyler + Cormier Chest 1997; 111:

14. HP : Diagnosis often unrecognized & misdiagnosed
respiratory symptoms with Hx. of
environmental
occupational exposure
respiratory symptoms with episodic radiographic infiltrates “Recurrent pneumonia”

15. 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)

16. HP : Radiographic findings
Subacute HP
fine linear shadows, small nodules = reticulonodular appearance
Chronic HP
volume loss
reticulonodular infiltrates
honeycombing
predominantly upper & mid lung zones

17. 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)

18. HP : BAL fluid intense lymphocytosis
predominantly CD 8+ T-suppressor cells
~ timing of the last antigen exposure, stage of disease

19. HP: key features Acute Subacute Chronic Time frame 4-48 hr
weeks to 4 M.
4 M. to years
Clinical features
fever, chills, cough
hypoxemia, aches
dyspnea , cough,
episodic flares
dyspnea, cough,
fatigue, weight loss
HRCT
ground glass
infiltrates
micronodules,
air trapping
fibrosis, honey
combing,
emphysema
Immunopathology
alveolitis, immune
complex
granulomas,
bronchiolitis
lymphocytic
infiltration,
fibrosis,air space
destruction
Prognosis
good

22. HP : Differential diagnosis
Acute stage
pneumonia
acute tracheobronchitis
organic dust toxic syndrome
BOOP

23. HP : Differential diagnosis
Subacute stage
recurrent pneumonia
granulomatous lung diseases
pneumoconiosis
Wegener’s granulomatosis

24. HP : Differential diagnosis
Chronic stage
IPF
bronchiectasis
COPD with pulmonary fibrosis
MAC

25. 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

26. HP: key features Acute Subacute Chronic Time frame 4-48 hr
weeks to 4 M.
4 M. to years
Clinical features
fever, chills, cough
hypoxemia, aches
dyspnea , cough,
episodic flares
dyspnea, cough,
fatigue, weight loss
HRCT
ground glass
infiltrates
micronodules,
air trapping
fibrosis, honey
combing,
emphysema
Immunopathology
alveolitis, immune
complex
granulomas,
bronchiolitis
lymphocytic
infiltration,
fibrosis,air space
destruction
Prognosis
good

27. Subacute HP, a 60-year-old dairy farmer had a 8-year history of intermittent dyspnea. CXR shows bilateral reticulonodular interstitial infiltration.

28. Chronic pigeon breeder’s disease
Chronic pigeon breeder’s disease. This patient has extensive pulmonary fibrosis & cor pulmonale.

29. Chronic HP, Pigeon breeder’s disease
Chronic HP, Pigeon breeder’s disease. Bilateral reticulonodular densities are present.

30. Acute HP, ground glass opacification

31. HRCT of a patient with Chronic HP demonstrating centrilobular
nodules not associated with bronchovascular bundles.

32. Chronic HP, centrilobular nodules.

33. Chronic HP, honeycombing in right upper lung & traction
bronchiectasis

34. Acute HP, mononuclear infiltration & noncaseating granulomas.

35. Chronic HP, mostly lymphocytic cellular infiltrate with epithelioid cells & numerous and clearly defined granuloma. (Wright-Giemsa)

36. Giant cells are characteristic feature of HP.

37. Chronic HP shows interstitial inflammation associated
with fibrosis.