Hypersensitivity pneumonitis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Hypersensitivity pneumonitis (HP), also called extrinsic allergic alveolitis (EAA), is not a single disease but is a complex syndrome of varying intensity, clinical presentation, and natural history.

The syndrome was first described in Iceland in 1874 and termed heykatarr. The syndrome is caused by sensitization to repeated inhalation of dusts containing one of 300 organic antigens. These organic dusts come from a wide variety of sources but most commonly include:

• Dairy and grain products
• Animal dander and protein
• Wood bark
• Water reservoir vaporizers

The two most common antigens are:

1. Thermophilic actinomycetes and
2. Avian proteins

As a rseult of exposure to thee antigens, the two most common causes (i.e. diseases) are:

1. Farmer’s lung and
2. Bird fancier’s lung

Pathologically, the HP syndrome is associated with diffuse inflammation of lung parenchyma and airways.

Based on the length and intensity of exposure and subsequent duration of illness, there are 3 clinical presentations of HP:

1. Acute
2. Subacute (intermittent)
3. Chronic progressive

Synonyms and related keywords: hypersensitivity pneumonitis, HP, bird fancier’s lung, extrinsic allergic alveolitis, farmer’s lung, Saccharopolyspora rectivirgula, S rectivirgula, Micropolyspora faeni, M faeni, Thermoactinomyces sacchari, T sacchari, Thermoactinomyces vulgaris, T vulgaris, Penicillium casei, P casei, Aspergillus clavatus, A clavatus, Mucor stolonifer, M stolonifer, Sitophilus granarius, S granarius, Cladosporium, heykatarr, bagassosis, grain handler’s lung, humidifier lung, air-conditioner lung, bird breeder’s lung, cheese worker’s lung, malt worker’s lung,paprika splitter’s lung, mollusk shell hypersensitivity, chemical worker’s lung, pulmonary disease, lung disease.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Sargun Singh Walia M.B.B.S.[2]

Hypersensitivity pneumonitis was first discovered more than a 100 years ago. It was called “bird fancier’s lung”.In 1960s, etiology and immune mechanism was described by Dr Jack Pepys. In 1977, Dr Peter C Warren described the pathogenesis of hypersensitivity pneumonitis in detail. Dr Hubert Reynolds from Hershey, Pennsylvania, USA described the relation between inflammatory lymphocytes in the lungs and hypersensitivity pneumonitis.In 1990, Dr Marc Lalancette, a medical student of Laval found that permanent lung damage occurs in farmers suffering from hypersensitivity pneumonitis due to emphysema.

• Hypersensitivity pneumonitis was first discovered more than a 100 years ago and was called bird fancier’s lung.^[1]
• In 1960s, etiology and immune mechanism was described by Dr Jack Pepys.^[2]
• In 1977, Dr Peter C Warren from University of Manitoba, Winnipeg, Manitoba described the pathogenesis of hypersensitivity pneumonitis in detail.^[3]
  • He was the first to report that cigarette smokers were exposed to a farmer lung antigen called Saccharopolyspora rectivirgula ( then called Micropolysporafaeni), had very low levels of antibodies against this bacteria in their serum.
• The association between increased number of inflammatory lymphocytes in the lungs and hypersensitivity pneumonitis was made by Dr Hubert Reynolds from Hershey, Pennsylvania, USA.
• In 1990, Dr Marc Lalancette, a medical student of Laval found that permanent lung damage occurs in farmers suffering from hypersensitivity pneumonitis due to emphysema. ^[4]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Sargun Singh Walia M.B.B.S.[2]

The clinical presentations of hypersensitivity pneumonitis depend on the frequency, length, exposure, and duration of illness. Due to a lot of variation in the the presentation hypersensitivity pneumonitis has been classified according to various schemes. Hypersensitivity pneumonitis may be classified into several subtypes based on various classifications methods such as classical classification, boyd classification, cormier classification, and selman classification.

• The clinical presentations of hypersensitivity pneumonitis depend on:
  • Frequency
  • Length
  • Exposure
  • Duration of illness
• Due to a lot of variation in the the presentation hypersensitivity pneumonitis has been classified according to various schemes.
• Hypersensitivity pneumonitis may be classified into several subtypes based on:
  • Classical classification:
    • Acute
      • Abrupt in onset.
      • Occurs after heavy exposure to antigen.
      • Symptoms can be confused with bacterial or viral infection.
      • On auscultation diffuse crackles and tachypnea are notable.
      • Histopathology reveals non-caseating interstitial granulomas with giant cells. 
    • Subacute
      • Gradual in onset.
      • Symptom like cough, fatigue, weightloss, and dyspnea may be seen.
      • Removal of exposure leads to complete resolution.
      • On auscultation diffuse crackles and tachypnea may be seen.
      • Histopathology reveals more well formed non-caseating interstitial granulomas and interstitial fibrosis.
    • Chronic
      • Insidious in onset with history of acute episodes.
      • Digital clubbing may be seen. ^[1]
      • Pulmonary fibrosis leads to disabling and irreversible respiratory symptoms.^[2]
  • Boyd classification:^[3]
    • Acute progressive
      • Severe symptoms occur after exposure to antigen.
      • Recurrent exposure leads to symptom progression.
      • Clinically patients are pyrexial with bilateral crackles on chest auscultation.
      • Patients may require hospitalization due to respiratory compromise.
    • Acute intermittent nonprogressive
      • Similar to acute progressive disease but less intense.
      • Patients feel well in between episodes.
      • Subsequent exposure leads to less severe symptoms.
      • Patients are clinically stable in the long run.
      • Pulmonary inflammatory response deteriorates with recurrent exposure to the antigen.^[4]
    • Chronic progressive disease
      • Occurs after recurrent acute episodes or insidiously.^[5]
      • Patients are diagnosed in the late stages.
      • Only clue for diagnosis is antigen exposure.
      • Patients often present with permanent disability in the form of pulmonary fibrosis or respiratory failure.
      • Disease is not reversed even after antigen exposure is avoided. ^[6]
    • Subclinical disease
      • Patients are immunological sensitized but are asymptomatic.
      • Patients with recurrent exposure to antigens may convert to chronic form.
  • Cormier classification:
    • Active
    • Residual
  • Selman classification:
    • Active non-progressive and intermittent
    • Acute progressive and intermittent
    • Chronic
      • Nonprogressive
      • Progressive

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Hypersensitivity pneumonitis involves inhalation of organic dusts which act as an antigen. This leads to an exaggerated immune response, which is called hypersensitivity reactions. In hypersensitivity pneumonitis, its either Type III hypersensitivity or type IV hypersensitivity.

There are noncaseating interstitial granulomas and mononuclear cell infiltration in a peribronchial distribution. Giant cells are prominent.

The noncaseating granulomas are more well formed. There is bronchiolitis with or without organizing pneumonia. Interstitial fibrosis is present.

There is chronic interstitial inflammation and alveolar destruction (honeycombing). There is dense fibrosis. The pathologic findings of chronic HP that are often associated with a poorer prognosis include the following 3 patterns of fibrosis:

• Predominantly peripheral fibrosis: in a patchy pattern with architectural distortion and fibroblast foci similar to usual interstitial pneumonia (UIP)

• Homogeneous linear fibrosis: similar to fibrotic nonspecific interstitial pneumonia (NSIP)

• Irregular predominantly peribronchiolar fibrosis

Exposure results in the development of circulating immunoglobulin G antibodies that are specific for the offending antigen. This antibody that forms is called the precipitating antibody, and it reacts with the specific putative antigen to form a precipitant. Initially the disease process was thought to be immunecomplex-mediated. However, subsequent studies have demonstrated that cell-mediated immunity is more important.

In the acute phase, there is a local increase in neutrophils in the alveoli and small airways. This is followed by an influx of mononuclear cells which release proteolytic enzymes, prostaglandins, and leukotrienes.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Sargun Singh Walia M.B.B.S.[2]

Hypersensitivity pneumonitis can be caused by exposure to organic antigens that can occur in different occupations. Hundreds of etiological causes can lead to hypersensitivity pneumonitis. Different types of occupations like farmers, poultry/bird handlers, veterinarians, construction workers and textile industry workers are exposed to different kinds of antigens that lead to hypersensitivity pneumonitis.

• Hypersensitivity pneumonitis can be caused by exposure to organic antigens that can occur in different occupations.
• Hundreds of etiological causes can lead to hypersensitivity pneumonitis.
• Etiology can be divided among various occupations:

Farmers^[1]

• Farmers lung is the most common form of hypersensitivity pneumonitis.
• It can further be divided based on the type of farming and antigen exposure.
  • Tobacco farmer: Most common antigen are aspergillus and scopulariopsis brevicaulis.
  • Paprika pods farmer: Most common antigen mucor stolonifer.
  • Wine makers: Most common antigen botrytis cincrea.
  • Mushroom cultivaters: Most common antigens are mushroom spores and thermophilic actinomycetes.
  • Potato farming: Most common antigens are thermophilic actinomycetes, T. vulgaris and F. rectivirgula.

Poultry/bird handling^[2]

• Excreta of birds and cattle may induce hypersensitivity pneumonitis.
• Proteinaceous material on droppings, feathers and serum proteins is dispersed through dust.
• It can further be divided based on the type of antigen exposure:
  • Poultry workers: Serum proteins from chicken products lead to feather plucker’s disease.
  • Turkey handlers: Most common antigens are serum proteins from turkey products.
  • Duck handlers: Most common antigens are serum proteins from duck feathers products.

Veterinarians

• Vererinarians are exposed to variety of organic antigens as they work in close proximity to animals.

Constructions workers^[3]

• Construction workers work with a variety of materials which can get infected with mold
• This can then disperse in fine dust particles carrying mold particles acting as antigens.
• It can further be divided based on the type of antigen exposure:
  • Wood dust: Most common antigens are Alternaria sp and Bacillus subtilis.
  • Maple bark: Most common antigen is cryptostroma corticale.
  • Composter: Most common antigens are T. vulgaris, and aspergillus.
  • Thatched-roof: Most common antigen is saccharomonospora viridis
  • Esparto dust: Most common antigens aspergillus fumigatus and T. actinomycetes.

Textile workers^[4]

• This exposure can lead to atypical type of hypersensitivity pneumonitis.
• Diffuse alveolar injury in the form of desquamative interstitial pneumonitis is most common.
• Exposure to antigens like cotton mill dust, aflatoxin-producing fungus and puffball spores leads to hypersensitivity pneumonitis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

The differential diagnosis of hypersensitivity pneumonitis is, primarily, a group of diseases known as idiopathic interstitial pneumonia. This group of diseases includes idiopathic pulmonary fibrosis (IPF) (which manifests histologically as usual interstitial pneumonia), idiopathic non-specific interstitial pneumonia (NSIP) and cryptogenic organizing pneumonia, among others. There are several important clinical syndromes that occur as a result of inhalation of organic agents but are not true forms of Hypersensitivity Pneumonitis.

• HP occurs due to inhalation of organic agents .
• Several diseases can occur due to this and mimic HP.
• These disorders are as follows:
  • Inhalation fever:
    • Patients present with fever, chills, headache, and myalgias.
    • There are no pulmonary findings (although mild dyspnea may occur).^[1]
    • Onset is 4-8 hours following exposure.
    • No long-term symptoms.
  • Organic dust toxic syndrome:
    • This syndrome occurs due to of exposure to bioaerosols contaminated with toxin-producing fungi (mycotoxins).^[2][3][4]
    • Patients present with fever, chills, and myalgias 4-6 hours after exposure. ^[5]
    • In contrast to inhalation fever, the chest X ray may show diffuse opacities.
    • Bronchiolitis or diffuse alveolar damage may be present on lung biopsy specimens.
    • This is not a true form of HP because no prior sensitization is required.
  • Chronic bronchitis:
    • This is a very severe form of pulmonary disease.
    • Most common respiratory disorder among agricultural workers.
    • The prevalence of chronic bronchitis is much higher at 10%, compared with 1.4% for HP.
  • Exposure to aerosolized Mycobacterium avium complex (MAC):
    • Occurs due to exposure to aerosolized mycobacterium avium complex (MAC).
    • Hot tub lung is a term used to describe these hypersensitivity pneumonitis-like cases because they have generally been associated with hot tub use.
    • The syndrome has been linked to the high levels of infectious aerosols containing MAC organisms found in the water. Whether this syndrome represents a true MAC infection or classic HP remains controversial (Marras, 2005).

By frequency of Interstitial Lung Diseases (Xaubet, 2004):

1. Idiopathic pulmonary fibrosis (38.6%)
2. Sarcoidosis (14.9%)
3. Cryptogenic organizing pneumonia (10.4%)
4. Interstitial lung disease associated with collagen vascular diseases (9.9%)
5. Hypersensitivity Pneumonitis (HP) (6.6%)
6. Unclassified (5.1%)

In alphabetical order:

• Air-conditioner lung
• Aspergillus clavatus
• Bagassosis
• Bird breeder’s lung
• Bird fancier’s lung
• Cheese worker’s lung
• Chemical worker’s lung
• Cladosporium
• Farmer’s lung
• Grain handler’s lung
• Humidifier lung
• Malt worker’s lung
• Micropolyspora faeni
• Mollusk shell hypersensitivity
• Mucor stolonifer
• Paprika splitter’s lung
• Penicillium casei
• Saccharopolyspora rectivirgula
• Sitophilus granarius
• Thermoactinomyces sacchari
• Thermoactinomyces vulgaris

Restrictive lung disease must be differentiated from other diseases that cause dyspnea, cough, hemoptysis, and fever such as ARDS, bronchitis, hypersensitivity pneumonitis, pneumoconiosis.

Pulmonary Function Test	Obstructive Lung Disease	Restrictive Lung Disease
TLC	↑	↓
RV	↑	↓
FVC	↓	↓
FEV1	↓↓	↓
FEV1/FVC	↓	N to ↑
MVV	↓	↓

Spirometry

Low FEV1/FVC ratio

Normal to high FEV1/FVC ratio

Obstructive Lung Disease

Restrictive Lung Disease

Bronchodilator therapy

DLCO

Increased FEV1

No change in FEV1

Normal DLCO

Decreased DLCO

Asthma

COPD

Chest wall disorders

Interstitial Lung Disease

Disease		Clinical manifestations											Diagnosis
		Symptoms				Physical exam							Lab findings	Imaging			Gold standard
		Cough	Dyspnea	Hemoptysis	Fever	History/Exposure	Cyanosis	Clubbing	JVD	Peripheral edema	Auscultation	Other prominent findings		CXR	CT	DLCco
Hypersensitivity Pneumonitis		+	+	–	+	History of allergen exposure	–	+	–	–	Diffuse fine bibasilar crackles	Constitutional symptoms Weight loss Anorexia Muscle weakness	Neutrophilia Elevated ESR Elevated CRP Elevated immunoglobulin No peripheral blood eosinophilia	Poorly defined micronodular or diffuse interstitial pattern In chronic form Fibrosis Loss of lung volume Coarse linear opacities	Ground-glass opacities or Diffusely increased radiodensities Diffuse micronodules Focal air trapping Mosaic perfusion Occasionaly thin-walled cysts Mild fibrotic changes	↓	Clinical diagnosis
Acute Respiratory Distress Syndrome (ARDS)		–	+	–	–	Trauma Sepsis Drug overdose Massive transfusion Acute pancreatitis Aspiration	+	–	–	–	Coarse breath sounds Rhonchi crackles Decreased breath sounds	Initially respiratory alkalosis transforming to respiratory acidosis	BNP level of less than 100 pg/mL PaO2 / FiO2 <300 Leukopenia Leukocytosis Thrombocytopenia	Bilateral pulmonary infiltrates Initially patchy peripheral Later diffuse bilateral Ground glass Frank alveolar infiltrate	Bronchial dilatation within areas of ground-glass opacification	↓	PaO2 / FiO2 <300
Bronchitis	Acute	+	–	+/-	+	–	–	–	–	–	Diffuse wheezes High-pitched continuous sounds The use of accessory muscles  Prolonged expiration Rhonchi Rales	Hoarseness	N/A	Normal	N/A	–	Clinical diagnosis
	Chronic	+	+	–	–	A positive history of chronic productive cough  Shortness of breath	+	–	+	+	Prolonged expiration; wheezing Diffusely decreased breath sound Coarse crackles with inspiration Coarse rhonchi	N/A	Chronic hypoxemia may lead to polycythemia  Increase in Neutrophils count Chronic respiratory acidosis.	Radiolucency Diaphragmatic flattening due to hyperinflation Increased retrosternal airspace on the lateral radiograph	N/A	↓	N/A
Pneumoconiosis[6]	SIlicosis[7][8]	+	+	+/-	–	Occupational history Sandblasting Bystanders Quartzite miller Tunnel workers Silica flour workers Workers in the scouring powder industry	+	+	+	–	Hyperresonant Fine crackles Rhonchi Bronchial breath sounds Expiratory wheezing Increased tactile fremitus. Loud P2	Increased susceptiblity to tuberculosis.	Respiratory acidosis Abnormal sputum Anemia Neutrophilia Elevated ESR Elevated CRP Elevated immunoglobulin	Small round opacities Symmetrically distributed Upper-zone predominance Diffuse interstitial pattern of fibrosis without the typical nodular opacities in chronic case	Nodular changes in lung parenchyma Progressive massive fibrosis Bullae, emphysema Pleural, mediastinal, and hilar changes	↓	Lung biopsy
	Asbestosis					Shipyard workers Pipe fitting Insulators						Lung cancer Mesothelioma		Predilection to lower lobes Fine and coarse linear, peripheral, reticular opacities	Subpleural linear opacities seen parallel to the pleura Basilar lung fibrosis Peribronchiolar, intralobular, and interlobular septal fibrosis; Honeycombing Pleural plaques.
	Berylliosis					Electronic manufactures						–		Hilar adenopathy Increased interstitial markings.	Ground glass opacification Parenchymal nodules Septal lines
	Byssinosis					Cotton wool workers						Increased susceptibility to Actinomyces and Aspergillus infection.		Diffuse air-space consolidation	Pulmonary fibrosis with honeycombing Peri bronchovascular distribution of nodules Ground-glass attenuations
Sarcoidosis		+	+	+	+	African Americans Autoimmune	–	–	–	–	Usually normal Occasional crackles	Dermatologic manifestations Ocular involvement Osseous involvement Heart failure from cardiomyopathy Lymphocytic meningitis Cranial nerve palsies	Hypercalcemia or hypercalciuria  Elevated 1, 25-dihydroxyvitamin D levels Elevated angiotensin-converting enzyme (ACE)	Bilateral hilar lymphadenopathy	High-resolution CT (HRCT) scanning of the chest may identify Active alveolitis Fibrosis	↓	Biopsy
Pleural Effusion		+	+	+/-	+/-	Transudate CHF Cirrhosis Exudate Parapneumonic causes  Malignancy	+/-	+/-	+/-	+/-	Decreased tactile fremitus  Diminished or inaudible breath sounds Pleural friction rub	Peripheral edema, distended neck veins, and S3 gallop suggest congestive heart failure. Edema may also be a manifestation of nephrotic syndrome, pericardial disease, or, when combined with yellow nailbeds, the yellow nail syndrome. Cutaneous changes and ascites suggest liver disease. Lymphadenopathy or a palpable mass suggests malignancy.	Thoracentesis  Exudate Transudate LDH, glucose, cytology Other specific labs of underlying etiology	Supine Blunting of the costophrenic angle Homogenous increase in density spread over the lower lung fields Lateral decubitus Free flowing effusion as layers	Thickened pleura Mild effusions can aslo be detected	↓	Thoracocentesis
Interstitial (Nonidiopathic) Pulmonary Fibrosis		+	++	+	–	Connective-tissue disorder Pneumoconiosis	+	+	+	+	Wheezing S3 P2 End-inspiratory rales	Increased A-a gradient	Elevated ESR Serologic testing for ANA, RF, ANCA & ASCA may be positive	Reticular and/or nodular opacities Honeycomb appearance (late finding)	Bilateral reticular and nodular interstitial infiltrates	↓	Video-assisted thoracoscopic lung biopsy
Lymphocytic Interstitial Pneumonia[9]		+	+	+	+	Autoimmune Lymphoproliferative disorders	–	+	–	–	Wheezing Rales	Increased A-a gradient	Polyclonal hypergammaglobulinemia Increased LDH	Bibasilar interstitial or micronodular infiltrates	Determines the degree of fibrosis Cysts (characterstic)	N	Open lung biopsy
Obesity[10][11]		+	+	–	–	Overweight Diabetes mellitus Asthma	–	–	–	+	Wheezing	–	Increased hematocrit	X ray findings are often limited due to body habitus	CT findings are variable and depends upon severity of obesity	N	Clinical
Pulmonary Eosinophilia[12]		+	+	+	+	Infections Parasitic Fungal Mycobacterial	+	–	+	+	Wheezing Rales	Increased A-a gradient	Leukocytosis with eosinophilia (> 250/µL)	Interstitial or diffuse nodular densities	Determines extent and distribution of the disease Interstitial infiltrates Cysts and nodules	↓	Biopsy of lesion (skin or lung)
Neuromuscular disease	Scoliosis	–	+	–	–	Postural abnormality	–	–	–	–	Decreased breath sounds	In severe scoliosis, the rib cage may press against the lungs making it more difficult to breathe.	R/0 genetic conditions Marfan’s syndrome Edward’s syndrome Total lymphocyte count (should be >1500/μL) Nutritional status must be assessed	Accurate depiction of the true magnitude of the spinal deformity can be assessed by supine anteroposterior (AP) and lateral spinal radiographs	N/A	N	Clinical Radiographs
	Muscular dystrophy	–	+	–	–	Proximal muscle weakness	–	–	–	–	Decreased breath sounds	Rash	Elevated CPK and aldolase +ANA +Anti-Jo abs Elevated ESR, CRP and RF	N/A	N/A	N	Muscle biopsy
	ALS	–	+	–	–	Muscle weakness Neurological deficit	–	–	–	–	Decreased breath sounds	Symptoms begin with limb involvement diue to muscle weakness and atrophy.  Cognitive or behavioral dysfunction Sensory nerves and the autonomic nervous system are generally unaffected	N/A	Not significant/diagnostic	Not significant/diagnostic	–	Clinical diagnosis Nerve conduction studies and needle electromyography (EMG)
	Myasthenia gravis	–	+	–	+	H/O of difficulty getting up from chair Combing Difficulty in swallowing	–	–	–	–	Decreased breath sounds	Extraocular, bulbar, or proximal limb muscles. Breathing as rapid and shallow Respiratory muscle weakness can lead to acute respiratory failure may require immediate intubation.	Anti–acetylcholine receptor (AChR) antibody (Ab) test +	Thymoma as an anterior mediastinal mass.	Thymoma as an anterior mediastinal mass.	N	Electromyography

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sargun Singh Walia M.B.B.S.[2]

The incidence and prevalence of hypersensitivity pneumonitis varies depending on various factors like season, occupation etc.Hypersensitivity pneumonitis usually affects patients in fourth to sixth decade of life.The mean age at diagnosis is 53 +/- 14 years.There is no racial predilection to hypersensitivity pneumonitis. Hypersensitivity pneumonitis affects men and women equally. Death due to Hypersensitivity pneumonitis is reported more in men.

• The incidence rate of hypersensitivity pneumonitis varies depending on various factors like season, occupation etc. ^[1]
  • The incidence of hypersensitivity pneumonitis among farmers is approximately 8 – 540 per 100,000 individuals worldwide.
  • The incidence of hypersensitivity pneumonitis pigeon breeders is approximately 6000 to 21,000 per 100,000 individuals worldwide.

• The prevalence of hypersensitivity pneumonitis varies based on exposure/occupation.
• These are as following:
  • Farmers:
    • US: 8-540 cases per 100,000 persons per year among those at risk.^[2]
    • UK: 420-3000 cases per 100,000 persons per year among those at risk.^[3]
    • France: 4370 cases per 100,000 persons per year among those at risk.^[4]
    • Finland: 1400-1700 cases per 100,000 persons per year among those at risk.^[5]
  • Pigeon Breeders: 6000-21,000 cases per 100,000 persons per year
  • Bird Fanciers: 20-20,000 cases per 100,000 persons per year

• Hypersensitivity pneumonitis usually affects patients in fourth to sixth decade of life.
• The mean age at diagnosis is 53 +/- 14 years.^[6]

• There is no racial predilection to hypersensitivity pneumonitis.

• Hypersensitivity pneumonitis affects men and women equally.
• Death due to Hypersensitivity pneumonitis is reported more in men.^[7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sargun Singh Walia M.B.B.S.[2]

The incidence and prevalence of hypersensitivity pneumonitis varies depending on various factors like season, occupation etc.Hypersensitivity pneumonitis usually affects patients in fourth to sixth decade of life.The mean age at diagnosis is 53 +/- 14 years.There is no racial predilection to hypersensitivity pneumonitis. Hypersensitivity pneumonitis affects men and women equally. Death due to Hypersensitivity pneumonitis is reported more in men.

• The incidence rate of hypersensitivity pneumonitis varies depending on various factors like season, occupation etc. ^[1]
  • The incidence of hypersensitivity pneumonitis among farmers is approximately 8 – 540 per 100,000 individuals worldwide.
  • The incidence of hypersensitivity pneumonitis pigeon breeders is approximately 6000 to 21,000 per 100,000 individuals worldwide.

• The prevalence of hypersensitivity pneumonitis varies based on exposure/occupation.
• These are as following:
  • Farmers:
    • US: 8-540 cases per 100,000 persons per year among those at risk.^[2]
    • UK: 420-3000 cases per 100,000 persons per year among those at risk.^[3]
    • France: 4370 cases per 100,000 persons per year among those at risk.^[4]
    • Finland: 1400-1700 cases per 100,000 persons per year among those at risk.^[5]
  • Pigeon Breeders: 6000-21,000 cases per 100,000 persons per year
  • Bird Fanciers: 20-20,000 cases per 100,000 persons per year

• Hypersensitivity pneumonitis usually affects patients in fourth to sixth decade of life.
• The mean age at diagnosis is 53 +/- 14 years.^[6]

• There is no racial predilection to hypersensitivity pneumonitis.

• Hypersensitivity pneumonitis affects men and women equally.
• Death due to Hypersensitivity pneumonitis is reported more in men.^[7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sargun Singh Walia M.B.B.S.[2]

If left untreated, patients with hypersensitivity pneumonitis may progress to develop flu like syndrome, cough, fatigue and malaise.Common complications of hypersensitivity pneumonitis include deterioration of lung function, hypoxemia, pulmonary hypertension and heart failure. Prognosis of hypersensitivity pneumonitis is generally excellent, and total lung recovery occurs in most cases but may take several years.

• The symptoms of hypersensitivity pneumonitis usually develop in within hours if significant exposure occurs.
• If the exposure to antigen is removed then the symptoms resolve within hours to days.
• If left untreated, patients with hypersensitivity pneumonitis may progress to develop flu like syndrome, cough, fatigue and malaise.

• Common complications of hypersensitivity pneumonitis include:
  • Deterioration in lung function
    • This occurs due to severe fibrosis.
    • Lungs are unable to oxygenate blood properly during normal breathing.
  • Hypoxemia^[1]
  • Pulmonary hypertension.^[2]
    • Pulmonary hypertension occurs due to damage to blood vessels in the lung.
  • Heart failure.

• Prognosis of hypersensitivity pneumonitis is generally excellent.
• Total lung recovery occurs in most cases but may take several years.^[3]
• Surgical lung biopsy can be done to check for fibrosis which is an indicator of poor prognosis.^[4]
• Prediction of prognosis can be done using high resolution CT scan.^[5]
• A study done among old patients suffering from hypersensitivity pneumonitis with no signs of air trapping on CT scan but desaturation with exercise showed poor survival rates.^[6]

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