Epidemiology
- History: first described in 1932 (as Farmer’s Lung)
- Age: most cases occur in adults (cases in children, especially associated with pigeons, may occur)
- Tobacco Use: protective effect against HP (although >90% of patients are non-smokers at time of diagnosis)
Etiology
General Comments
- Over 300 Different Etiologic Agents Have Been Associated with HP
- However, Bird Fancier’s Lung Accounts for Approximately 66% of All HP Cases
Animal Products
- Bird Fancier’s Lung (Feathers and Bird Droppings)
- Avian Proteins (Intestinal Mucin, IgA, and IgG): these proteins are contained in both bird droppings and bloom (the waxy keratinous powder which waterproofs the feathers)
- Associated with Multiple Types of Birds
- Columbiformes: pigeons, doves
- Psitacciformes: budgerigars, cockatoos, cockatiels, lovebirds, parrots
- Passeriformes: canaries
- Anseriformes: geese, ducks
- Galliformes: turkeys, chickens, pheasants, partridges
- Laboratory Worker’s Hypersensitivity Pneumonitis (Rat Fur)
- Male Rat Urine
- Pituitary Snuff Taker’s Disease (Pituitary Powder)
- Bovine and Porcine Proteins
Insect Products
- Miller’s Lung (Wheat Weevils)
- Sitphilus Granarius
Vegetable Products
- Bagassosis (Moldy Sugar Cane)
- Thermophilic Actinomycetes
- Cheesewasher’s Disease (Cheese Casings)
- Penicillium (see Penicillium, [[Penicillium]])
- Familial/Domestic Hypersensitivity Pneumonitis (Contaminated Wood Dust)
- Bacillus Subtilis (see Bacillus Subtilis, [[Bacillus Subtilis]])
- Farmer’s Lung (Moldy Hay)
- Thermophilic Actinomycetes: ubiquitous bacteria that grow in decaying matter and resemble fungi (exposure may be <750,000 spores per min)
- Micropolyspora
- Hot Tub Lung (Contaminated Hot Tub)
- General Comments
- Occurs mostly in immunocompetent patients
- Pathology consists of well-formed granulomas (in contrast to loosely-formed granulomas in other types of HP)
- Increased BAL CD4/CD8 lymphocyte ratios are common
- Mycobacterium Avium Complex (see Mycobacterium Avium Complex, [[Mycobacterium Avium Complex]])
- Cladosporium
- Pullaria
- Epicocucum Nigrum
- General Comments
- Humidifier Lung (Contaminated Humidifiers/Dehumidifiers/Air-Conditioning Units)
- Thermophilic Actinomycetes
- Penicillium (see Penicillium, [[Penicillium]])
- Cephalosporium
- Amebae
- Malt Worker’s Lung (Contaminated Barley)
- Aspergillus Clavatus (see Aspergillus, [[Aspergillus]])
- Maple Bark Disease (Contaminated Maple Logs)
- Cryptostroma Corticale
- Mushroom Worker’s Disease (Moldy Compost)
- Thermophilic Actinomycetes
- Micropolyspora
- Paprika Splitter’s Lung (Paprika Dust)
- Rhizopus (Mucor) Stolonifer (see Rhizopus Stolonifer, [[Rhizopus Stolonifer]])
- Sequoiosis (Contaminated Wood)
- Graphium
- Pullularia
- Suberosis (Moldy Cork)
- Penicillium (see Penicillium, [[Penicillium]])
- Swimming Pool Lung (Mist from Pool Water, Sprays, and Fountains)
- Mycobacterium Avium Complex (see Mycobacterium Avium Complex, [[Mycobacterium Avium Complex]])
- Wood Trimmer’s Lung (Contaminated Wood Trimmings)
Reactive Simple Chemicals
- Diphenylmethane Diisocyanate HP (see Diphenylmethane Diisocyanate, [[Diphenylmethane Diisocyanate]])
- Altered Proteins
- Epoxy Resin Lung
- Heated Epoxy Resin: Phthalic Anhydride
- Toluene Diisocyanate HP (see Toluene Diisocyanate, [[Toluene Diisocyanate]])
- Altered Proteins and Others
- Trimellitic Anhydride HP (see Trimellitic Anhydride, [[Trimellitic Anhydride]])
- Altered Proteins
- Cobalt (see Cobalt, [[Cobalt]])
- “Hard Metal”: Tungsten Carbide + Cobalt
- Pyrethrum Pneumonitis
- Pyrethrum Insecticide (see Pyrethrum, [[Pyrethrum]])
- Pauli’s Reagent Alveolitis
- Sodium Diazobenzene Sulfate: lab reagent
- Water-Based Metal Working Fluid HP: pure petroleum oils, emulsion of petroleum in a water base (semi-synthetic fluids), or emulsion of synthetic oils in water (synthetic fluids) -> used in many industries (auto machinists, etc) to decrease heat from machine tools and the object in production
- Unknown Antigen: although biocides are added to metal working fluids, resistant microorganisms survive, leading to selection of organisms such as Mycobacterium Immunogenum
- Unlike hot tub lung, mycobacteria are not cultured from BAL fluid (measurement of M immunogenum-specific cell-mediated immunity using detection of specific antibodies against recombinant M immunogenum antigens by ELISA may be helpful)
- Unknown Antigen: although biocides are added to metal working fluids, resistant microorganisms survive, leading to selection of organisms such as Mycobacterium Immunogenum
Drugs
- Intravesical Bacillus Calmette-Guerin (BCG) (see Bacillus Calmette-Guerin, [[Bacillus Calmette-Guerin]])
- Flavocoxid (Limbrel) (see Flavocoxid, [[Flavocoxid]])
- Gold (see Gold, [[Gold]])
- Leflunomide (Arava) (see Leflunomide, [[Leflunomide]])
- Minocycline (see Minocycline, [[Minocycline]])
- Methotrexate (see Methotrexate, [[Methotrexate]])
- Sulfapyridine (see Sulfonamides, [[Sulfonamides]])
Physiology
- Organic dust exposure with deposition in distal lung (injury mainly involves type 3, type 4 hypersensitivity)
- Organic dusts as immunologic adjuvants (induce humoral and cell-mediated immunity):
- Micropolyspora Faeni antigens induces IL-1 and TNF-α from macrophages (anti-TNF-α infihibits pulmonary inflammation)
- Thermophilic Actinomycetes antigens activate alveolar macrophages and alternative complement (promoting PMN chemotaxis to lung)
- Ag’s contain enzymatic substances, endotoxins, histamine releasers, and inducers of non-specific precipitins
- Increased mast cells in BAL in normal farmers and in Farmer’s Lung (correlated with disease activity/ but no evidence for IgE-mediated type 1 mechanisms exists)
- Micropolyspora Faeni Ag, complement, mononuclear cells, and Ig present in bronchial wall of Farmer’s Lung (possible type II cytotoxic component)
- Sensitized lymphocyctes occur in both blood and lung
- Animal models of HP show that repeated exposure may lead to improvement (possibly due to antigen-specific T-suppressor cells)
- Type 3 immune-complex injury plays a major role in HP: immune complexex can induce IL-1 and TNF-alpha release from BAL cells, in-duce pulmonary granuloma formation, activate alveolar macrophages
- Precipitating Ab are present to specific Ag (but these are related to environmental exposure, not necessarily to disease)
- However, serum complement does not decrease with Ag exposure and histologic vasculitis is absent in lung tissue
- Type 4 delayed hypersensitivity injury plays a major role:
- Inhibitors of type 4 reaction (cortisone, CSA, antimacrophage sera, etc.) inhibit animal model granuloma formation
- Host Factors
- Less than 10% of exposed people develop HP
- No association between HLA types and susceptibility
- No higher incidence of HP in atopic patients
Pathologic Patterns
- Acute HP Pattern
- Usually resolves without sequelae
- Lymphocytes, plasma cells, activated alveolar macrophages/foamy macrophages/giant cells/obstructive bronchiolitis/absence of vasculitis
- Subacute HP Pattern
- Absence of vasculitis
- Granulomas: bronchocentric distribution/with giant cells
- Cellular bronchiolitis: chronic inflammation around airways with or without BO
- Interstitial pneumonitis: infiltrated with macrophages, plasma cells, and lymphocytes/may have UIP-like features in some cases
Diagnosis
Diagnostic Challenges
- Natural challenge: avoidance x 72 hrs with return to suspected site, monitor clinical and PFT’s x 24 hrs
- Leads to recurence of symptoms (may not be positive in chronic cases with only brief exposure)
- Does not reveal specific agent
- Lab challenge (although antigens are not usually available): nebulized challenge in PFT lab, monitor clinical and PFT’s x 24 hrs
- Bronchospasm may precede expected response 4-6 hrs later
- Caution: endotoxin, etc. in challenge material may cause febrile reactions in some people (mimicking HP)
Complete Blood Count (CBC) (see Complete Blood Count, [[Complete Blood Count]])
- Leukocytosis (see Leukocytosis, [[Leukocytosis]]): with increased neutrophils/mild lymphopenia
- Peripheral Eosinophilia (see Peripheral Eosinophilia, [[Peripheral Eosinophilia]]): typically absent
C-Reactive Protein (CRP) (see C-Reactive Protein, [[C-Reactive Protein]])
- May Be Elevated
Erythrocyte Sedimentation Rate (ESR) (see Erythrocyte Sedimentation Rate, [[Erythrocyte Sedimentation Rate]])
- Normal
Precipitating Antigen-Specific Antibodies
- Technique: ELISA is usually the preferred method to detect precipitins or total IgG antibodies (however, even the ELISA method lacks standardization)
- Other Methods: immunodiffusion, immunoelectrophoresis, electrosyneresis
- HP Cannot Be Ruled In Based Solely Upon Positive Antibodies or Ruled Out Based on Negative Antibodies [MEDLINE]
- Example: asymtomatic pigeon breeders (40% of cases) and farmers (105% of cases) may have significant antibody levels
- Example: specific antibody reactivity is lacking in Many Patients with HP
- Data from the HP Study Group: Significant Predictors of Hypersensitivity Pneumonitis [MEDLINE]
- Positive Precipitating Antibodies: Odds Ratio 5.3 (95% CI: 2.7-10.4)
Serum Immunoglobulin E (IgE) (see Serum Immunoglobulin E, [[Serum Immunoglobulin E]])
- Normal
Pigeon Ag Skin Test
- Wheel and flare seen in most Pigeon Breeder’s Lung (10% of these have bronchospasm on Ag challenge, possibly due to IgG4-mediated type 1 reaction)
- Skin tests: non-specific (not used)
Angiotensin Converting Enzyme (ACE) Level
- May be elevated (also seen in organic dust-exposed normals)
Arterial Blood Gas (ABG) (see Arterial Blood Gas, [[Arterial Blood Gas]])
- Acute HP: hypoxemia with hypocapnia
- Subacute HP:
- Chronic HP:
Clinical
General Comments
- Clinical Pattern is Determined by Intensity and Frequency of Antigen Exposure
- The Traditional 3-Group Classification System Below is Controversial: since the subacute group is difficult to define, some authors suggest that the clinical data better fits a 2-group classification system (Chest, 2012) [MEDLINE]
Hypersensitivity Pneumonitis Study Group: Significant Predictors of Hypersensitivity Pneumonitis (Am J Respir Crit Care Med, 2003) [MEDLINE]
- Exposure to Known Offending Antigen: Odds Ratio 38.8 (95% CI: 11.6-129.6)
- Symptoms 4-8 hrs After Exposure: Odds Ratio 7.2 (95% CI: 1.8-28.6)
- Positive Precipitating Antibodies: Odds Ratio 5.3 (95% CI: 2.7-10.4)
- Inspiratory Crackles: Odds Ratio 4.5 (95% CI: 1.8-11.7)
- Recurrent Episodes of Symptoms: Odds Ratio 3.3 (95% CI: 1.5-7.5)
- Weight Loss: Odds Ratio 2.0 (95% CI: 1.8-28.6)
Acute Hypersensitivity Pneumonitis
Characteristics
- Exposure: intermittent short duration exposure
- Symptom Onset: occur 4-6 hrs after challenge, last for 18-24 hrs after exposure ceases
- Presents like Acute Bacterial or Viral Pneumonia, But May Persist if Exposure Persists
- Course: reversible
Diagnosis
- Chest X-Ray (see Chest X-Ray, [[Chest X-Ray]]): acute pulmonary edema pattern
- Chest CT (see Chest Computed Tomography, [[Chest Computed Tomography]]): ground-glass infiltrates
- High-Resolution Chest CT (HRCT) (see High-Resolution Chest Computed Tomography, [[High-Resolution Chest Computed Tomography]]): due to characteristic clinical manifestations and rapid resolution in acute HP, HRCT is not usually performed in this subset of HP patients
- There are Case Reports of Normal HRCT in Biopsy-Proven HRCT: this may be related to the time interval between removal from the offending antigen and the performance of the HRCT
- HP Study Group [MEDLINE]: only 4% of patients had a normal HRCT
- Patchy or Diffuse Bilateral Ground-Glass Opacities: may be asymmetric in some cases
- Ground-glass opacities in acute HP may be similar to those seen in desquamative interstitial pneumonia (see Desquamative Interstitial Pneumonia, [[Desquamative Interstitial Pneumonia]])
- Small Poorly-Defined Ground-Glass Centrilobular Nodules (see Bronchiolar Disorders, [[Bronchiolar Disorders]]): characteristic feature
- Lobular Areas of Decreased Attenuation and Vascularity: inspiratory HRCT
- Focal Airspace Consolidation: may occur in some cases, due to organizing pneumonia or less commonly, diffuse alveolar damage
- Areas of Decreased Attenuation and Vascularity Indicating Air Trapping (Represent Bronchiolar Obstruction): expiratory HRCT
- Hilar/Mediastinal Lymphadenopathy (see Mediastinal Mass, [[Mediastinal Mass]]): occasionally seen
- Typical Absence of Effusions/Solitary Nodules/Cavitation/Calcification/Atelectasis
- There are Case Reports of Normal HRCT in Biopsy-Proven HRCT: this may be related to the time interval between removal from the offending antigen and the performance of the HRCT
- Pulmonary Function Tests (PFT’s) (see Pulmonary Function Tests, [[Pulmonary Function Tests]]): PFT’s have no discriminative ability to distinguish HP from other interstitial lung diseases
- General Comments: may be normal if done after acute symptoms resolve
- Restrictive Pattern with Decreased DLCO: typical pattern
- However, Data from the HP Study Group Demonstrate that the DLCO is Normal in 22% of Cases (Chest, 2012) [MEDLINE]
- Normal Raw
- Induced Sputum: contains increased total cells and lymphocytes (cell count differential suggest that induced sputum and BAL reflected different compartments of inflammation)
- The Clinical Utility of Induced Sputum in the Diagnosis of Acute HP is Unclear
- Bronchoscopy with Bronchoalveolar Lavage (BAL) (see Bronchoscopy, [[Bronchoscopy]]): BAL technique is not standardized
- BAL Lymphocytosis (>30% for Non-Smokers/Ex-Smokers, >20% for Current Smokers) is Mandatory for the Diagnosis of HP: a normal number of BAL lymphocytes rules out all but residual disease
- However, BAL Lymphocytosis Can Also Be Seen in Exposed Asymptomatic Subjects
- CD4/CD8 Ratio <1
- Open Lung Biopsy: not usually required for diagnosis
- Neutrophilic Infiltration of the Respiratory Bronchioles and Alveoli
- Diffuse Alveolar Damage and Temporally Uniform, Nonspecific, Chronic Interstitial Pneumonitis May Be Seen in Some Cases
Clinical Features
- Fever/Chills(see Fever, [[Fever]]): fever may be up to 104°
- Dyspnea (see Dyspnea, [[Dyspnea]])
- Cough (see Cough, [[Cough]])
- Common: due to bronchocentric involvement
- Usually Dry, But May Produce Sputum
- Diffuse Crackles
- Constitutional Symptoms
- Clinical Features Which May Differentiate HP from Sarcoidosis [MEDLINE]
- Inspiratory Crackles: HP more commonly presented with inspiratory crackles than sarcoidosis (87% vs 15%)
- Hilar/Mediastinal Lymphadenopathy: hilar and/or mediastinal lymphadenopathy was more commonly observed in sarcoidosis than in HP (46% vs 2%)
Subacute Hypersensitivity Pneumonitis
Characteristics
- Exposure: continuous but relatively short duration exposure
- Symptom Onset: insidious onset of above symptoms with progression over days-weeks
Diagnosis
- High-Resolution Chest CT (HRCT) (see High-Resolution Chest Computed Tomography, [[High-Resolution Chest Computed Tomography]])
- There are Case Reports of Normal HRCT in Biopsy-Proven HRCT: this may be related to the time interval between removal from the offending antigen and the performance of the HRCT
- HP Study Group [MEDLINE]: only 4% of patients had a normal HRCT
- Patchy or Diffuse Bilateral Ground-Glass Opacities: may be asymmetric in some cases
- Small Poorly-Defined Ground-Glass Centrilobular Nodules (see Bronchiolar Disorders, [[Bronchiolar Disorders]]): may be only finding in some subacute HP cases
- Irregular nodules >10 mm are unusual (they usually represent areas of focal organizing pneumonia)
- Lobular Areas of Decreased Attenuation and Vascularity: inspiratory HRCT
- Focal Airspace Consolidation: may occur in some cases, due to organizing pneumonia or less commonly, diffuse alveolar damage
- Areas of Decreased Attenuation and Vascularity Indicating Air Trapping (Represent Bronchiolar Obstruction): expiratory HRCT
- Seen in up to 90% of cases
- Cysts (3-25 mm) (see Cystic-Cavitary Lung Lesions, [[Cystic-Cavitary Lung Lesions]]): occur in 13% of patients with subacute HP
- Usually Associated with Ground-Glass Opacities
- Cysts Resemble Those of Lymphoid Interstitial Pneumonia: like the cysts of lymphoid interstitial pneumonia, they are presumably caused by partial bronchiolar obstruction by the peribronchiolar lymphocytic infiltrates
- Hilar/Mediastinal Lymphadenopathy (see Mediastinal Mass, [[Mediastinal Mass]]): occasionally seen
- Typical Absence of Effusions/Solitary Nodules/Cavitation/Calcification/Atelectasis
- Patchy Interstitial Infiltrates: less common pattern
- “Hilar Haze” Pattern: may mimic acute pulmonary edema
- There are Case Reports of Normal HRCT in Biopsy-Proven HRCT: this may be related to the time interval between removal from the offending antigen and the performance of the HRCT
- Pulmonary Function Tests (PFT’s) (see Pulmonary Function Tests, [[Pulmonary Function Tests]]): PFT’s have no discriminative ability to distinguish HP from other interstitial lung diseases
- Restrictive (and Sometimes Obstructive) Pattern
- Obstructive Pattern is Especially Common in Farmer’s Lung
- Methacholine Challenge: may be positive
- Decreased DLCO
- However, Data from the HP Study Group Demonstrate that the DLCO is Normal in 22% of Cases (Chest, 2012) [MEDLINE]
- Restrictive (and Sometimes Obstructive) Pattern
- Bronchoscopy with Bronchoalveolar Lavage (BAL) (see Bronchoscopy, [[Bronchoscopy]]): BAL technique is not standardized
- BAL Lymphocytosis (>30% for Non-Smokers/Ex-Smokers, >20% for Current Smokers) is Mandatory for the Diagnosis of HP: a normal number of BAL lymphocytes rules out all but residual disease
- However, BAL Lymphocytosis Can Also Be Seen in Exposed Asymptomatic Subjects
- CD4/CD8 Ratio <1
- Open Lung Biopsy
- Cellular Bronchiolitis, Non-Caseating Granulomas, and Bronchiolocentric Interstitial Pneumonitis with a Predominance of Lymphocytes
- Areas of Organizing Pneumonia May Be Seen
Clinical Features
- Fever/Chills(see Fever, [[Fever]]): fever may be up to 104°
- Dyspnea (see Dyspnea, [[Dyspnea]])
- Cough (see Cough, [[Cough]])
- Common: due to bronchocentric involvement
- Usually Dry But May Produce Sputum
- Diffuse Crackles
- Weight Loss (see Weight Loss, [[Weight Loss]])
- Constitutional Symptoms
- Clinical Features Which May Differentiate HP from Sarcoidosis [MEDLINE]
- Inspiratory Crackles: HP more commonly presented with inspiratory crackles than sarcoidosis (87% vs 15%)
- Hilar/Mediastinal Lymphadenopathy: hilar and/or mediastinal lymphadenopathy was more commonly observed in sarcoidosis than in HP (46% vs 2%)
Chronic Hypersensitivity Pneumonitis
Characteristics
- Exposure: long duration exposure
Diagnosis
- High-Resolution Chest CT (HRCT) (see High-Resolution Chest Computed Tomography, [[High-Resolution Chest Computed Tomography]]): radiographic changes in chronic HP may not allow accurate differentiation from idiopathic pulmonary fibrosis (with usual interstitial pneumonia pathology)
- Reticulation and Traction Bronchiectasis and Bronchiolectasis Due to Fibrosis Superimposed on Findings of Acute/Subacute HP
- Reticulation Be Patchy or Random
- Reticulation May Have a Predominantly Subpleural/Peri-Bronchovascular Distribution
- Reticulation Typically Spares the Lung Bases
- Subpleural Honeycombing: occurs in a minority of chronic HP cases
- Hilar/Mediastinal Lymphadenopathy (see Mediastinal Mass, [[Mediastinal Mass]]): occasionally seen
- Emphysematous Changes: for unclear reasons, emphysematous changes are more common than interstitial fibrosis in chronic HP associated with farmer’s lung (without a smoking history) [MEDLINE]
- Radiographic Features Which Best Differentiate Chronic HP from Idiopathic Pulmonary Fibrosis (IPF) and Non-Specific Interstitial Pneumonia (NSIP) [MEDLINE]
- Lobular Areas with Decreased Attenuation and Vascularity
- Centrilobular Nodules (see Bronchiolar Disorders, [[Bronchiolar Disorders]])
- Absence of Lower-Zone Predominance of Abnormalities
- Reticulation and Traction Bronchiectasis and Bronchiolectasis Due to Fibrosis Superimposed on Findings of Acute/Subacute HP
- Pulmonary Function Tests (PFT’s) (see Pulmonary Function Tests, [[Pulmonary Function Tests]]): PFT’s have no discriminative ability to distinguish HP from other interstitial lung diseases
- Restrictive (and Sometimes Obstructive) Pattern
- Obstructive Pattern is Especially Common in Farmer’s Lung
- Decreased DLCO
- However, Data from the HP Study Group Demonstrate that the DLCO is Normal in 22% of Cases (Chest, 2012) [MEDLINE]
- Restrictive (and Sometimes Obstructive) Pattern
- Bronchoscopy with Bronchoalveolar Lavage (BAL) (see Bronchoscopy, [[Bronchoscopy]]): BAL technique is not standardized
- BAL Lymphocytosis (>30% for Non-Smokers/Ex-Smokers, >20% for Current Smokers) is Mandatory for the Diagnosis of HP: a normal number of BAL lymphocytes rules out all but residual disease
- However, BAL Lymphocytosis Can Also Be Seen in Exposed Asymptomatic Subjects
- CD4/CD8 Ratio <1
- Open Lung Biopsy: may be required
Clinical Features
- Fever/Chills (see Fever, [[Fever]]): fever may be up to 104°
- Dyspnea (see Dyspnea, [[Dyspnea]])
- Cough (see Cough, [[Cough]])
- Common: due to bronchocentric involvement
- Usually Dry But May Produce Sputum
- Diffuse Crackles
- Weight Loss (see Weight Loss, [[Weight Loss]])
- Constitutional Symptoms
- Pulmonary Hypertension/Cor Pulmonale (see Pulmonary Hypertension, [[Pulmonary Hypertension]]): due to advanced interstitial lung disease
- Absence of Clubbing: usually
Treatment
Avoidance of Antigen/Exposure
- Cessation of exposure is usually adequate for milder, acute cases
Corticosteroids (see Corticosteroids, [[Corticosteroids]])
- Corticosteroids are usually used for more severe cases
- Prednisone 60 mg/day usually x 2-3 weeks, then taper over 3-6 weeks
- Typically result in rapid clinical response (over days)
- Subacute/Chronic HP: may require >8 week course
- Farmer’s Lung: steroids hasten acute recovery but do not have long-term clinical benefit
- Hot Tub Lung: treatment with steroids OR treatment aimed at MAI appear to be equally effective -> dual therapy is currently recommended
Treatment of Bronchospasm
- Albuterol and cromolyn are useful to treat obstructive component in some studies
Inhaled Corticosteroids (see Corticosteroids, [[Corticosteroids]])
- Have not been shown to be useful (but high dose inhaled steroids have not been studied)
Avoidance of Exposure/Respiratory Protection
- Symptoms usually resolve
- Masks probably do limit exposure adequately though
Immunotherapy
- Contraindicated (risk of causing immune-complex vasculitis)
- Possible future role of Ag-specific inhalational or IV desensitization
Prognosis
- Morbidity: 5-year morbidity is 30% (due to pulmonary fibrosis)
- Overall, there is an increased mortality in patients with HP compared with the general population (hazard ratio, 2.98), even though these individuals are less likely to smoke [MEDLINE]
References
- Difference in the phenotypes of bronchoalveolar lavage lymphocytes in patients with summer-type hypersensitivity pneumonitis, farmer’s lung, ventilation pneumonitis, and bird fancier’s lung: report of a nationwide epidemiologic study in Japan. J Allergy Clin Immunol. 1991;87(5):1002-1009 [MEDLINE]
- Lung and blood T-cell receptor repertoire in extrinsic allergic alveolitis. Eur Respir J. 1997;10(4):772-779 [MEDLINE]
- Hypersensitivity pneumonitis. AJR Am J Roentgenol. 2000;174(4):1061-1066 [MEDLINE]
- High-resolution computed tomographic characteristics in acute farmer’s lung and in its follow-up. Eur Respir J 2000; 16:56–60 [MEDLINE]
- Hypersensitivity pneumonitis: spectrum of high-resolution CT and pathologic findings. AJR Am J Roentgenol. 2007;188(2):334-344 [MEDLINE]
- Extrinsic allergic alveolitis: incidence and mortality in the general population. QJM. 2007;100(4):233-237 [MEDLINE]
- HP Study Group. Clinical diagnosis of hypersensitivity pneumonitis. Am J Respir Crit Care Med. 2003;168(8):952-958 [MEDLINE]
- Chronic hypersensitivity pneumonitis: differentiation from idiopathic pulmonary fibrosis and nonspecific interstitial pneumonia by using thin-section CT. Radiology. 2008;246(1):288-297 [MEDLINE]
- Recent advances in hypersensitivity pneumonitis. Chest 2012;142:208-217 [MEDLINE]
- Bird fancier’s lung: a state-of-the-art review. Clin Rev Allergy Immunol. 2012 Aug;43(1-2):69-83. doi: 10.1007/s12016-011-8282-y [MEDLINE]