Hypersensitivity Pneumonitis Workup

  • Author: Marine Demirjian, MD; Chief Editor: Zab Mosenifar, MD   more...
 
Updated: May 19, 2010
 

Laboratory Studies

Blood tests are of limited utility. Leukocytosis and neutrophilia, elevated erythrocyte sedimentation rate, and increased levels of quantitative immunoglobulins and C-reactive protein are observed in many patients. Precipitating immunoglobulin G antibodies against potential antigens indicate prior exposure and sensitization but do not necessarily represent disease. Many patients with clinical disease have no detectable antibodies, owing either to testing with an inappropriate antibody or to cessation of exposure.

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Imaging Studies

Chest radiography

In acute hypersensitivity pneumonitis, a diffuse micronodular interstitial pattern (at times with ground-glass density in the lower and middle lung zones) may be observed. Findings are normal in approximately 10% of patients.

In subacute hypersensitivity pneumonitis, micronodular or reticular opacities are most prominent in mid-to-upper lung zones.[29] Note the image below:

A 60-year-old dairy farmer had an 8-year history oA 60-year-old dairy farmer had an 8-year history of intermittent dyspnea. Chest radiograph shows bilateral reticulonodular interstitial infiltration secondary to subacute hypersensitivity pneumonitis.

In chronic hypersensitivity pneumonitis, progressive fibrotic changes with loss of lung volume particularly affect the upper lobes. Nodular or ground-glass opacities are not present. Features of emphysema are found on significant chest films and CT scans. Note the image below:

Chest radiograph of a patient with chronic hyperseChest radiograph of a patient with chronic hypersensitivity pneumonitis from pigeon breeder's disease. Bilateral reticulonodular densities are present.

High-resolution CT scanning [30]

Ground-glass opacities or diffusely increased radiodensities are present in the acute phase of disease. Note the image below:

High-resolution CT scan of lungs shows ground-glasHigh-resolution CT scan of lungs shows ground-glass opacification in the acute phase of hypersensitivity pneumonitis.

In subacute disease, diffuse micronodules, ground-glass attenuation, focal air trapping, and mild fibrotic changes are observed.

In chronic hypersensitivity pneumonitis, several patterns may be observed, including multiple centrilobular nodules with some ground-glass attenuation, radiolucency or air trapping, extensive fibrosis, and honeycombing.[31] Note the images below:

The chronic phase of hypersensitivity pneumonitis The chronic phase of hypersensitivity pneumonitis shows honeycombing in the right upper lung and traction bronchiectasis. High-resolution chest CT scan of a patient with suHigh-resolution chest CT scan of a patient with subacute hypersensitivity pneumonitis demonstrates centrilobular nodules. These nodules are unlike those of sarcoidosis, in which the nodules are subpleural and along bronchovascular bundles.
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Other Tests

Pulmonary function studies

A restrictive ventilatory pattern, with reduced forced vital capacity, total lung capacity, and preserved airflow, is observed in acute or subacute disease. A restrictive (severe) or a mixed obstructive and restrictive pattern is common in chronic hypersensitivity pneumonitis. Diffusing capacity of lungs for carbon monoxide is reduced in all forms of hypersensitivity pneumonitis. Many patients have hypoxemia at rest, and all patients desaturate with exercise.

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Procedures

Inhalation challenge

Re-exposure to the environment of the supposed agent is recommended to establish a relationship between symptoms and the environment. Patients develop fever, malaise, headache, crackles upon chest examination, and decreased forced vital capacity 8-12 hours after exposure.

Bronchoalveolar lavage [32, 33]

BAL may provide supportive information for the diagnosis of hypersensitivity pneumonitis. A marked BAL lymphocytosis (more than 20%) is nonspecific but helpful. Elevation in the number of CD8+ T cells and a CD4+ -to-CD8+ ratio of less than 1 is diagnostic.[34] Abnormalities from bronchoalveolar lavage fluid (both cellular changes and specific antibodies) may be found in asymptomatic individuals with antigen exposure.

Lung biopsy

Pathologic examination of lung tissue has been proposed as a criterion for diagnosis of hypersensitivity pneumonitis. Transbronchial biopsies have good diagnostic yield in acute and subacute disease. Yield can be maximized with multiple samples from lobes most affected as observed on imaging studies. Surgical lung biopsies are suggested in chronic disease or when high-resolution CT scanning (HRCT) findings are not classic for hypersensitivity pneumonitis.[35] Video-assisted thoracic surgery has made this a less morbid and, hence, more commonly used, procedure.

Findings may reveal small, poorly formed noncaseating granulomas near respiratory or terminal bronchioles; these are associated with multinucleated giant cells. Patchy mononuclear cell infiltration (lymphocytes and plasma cells) of alveolar walls may be present. Large histiocytes with foamy cytoplasm may be present in the interstitium.

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Histologic Findings

Histologic findings for acute hypersensitivity pneumonitis, subacute hypersensitivity pneumonitis, and chronic hypersensitivity pneumonitis are as follows:

  • Acute hypersensitivity pneumonitis: Little is known about the gross pathologic features of acute hypersensitivity pneumonitis. The pathologic features of acute hypersensitivity pneumonitis in farmer’s lung include a neutrophil and eosinophil infiltration of the alveolar spaces, vessel vasculitis, and in some cases, diffuse alveolar damage. Additionally, immunopathologic studies have revealed immunoglobulin and complement deposition in the vessels.[1] Note the image below. Light microscopy shows mononuclear infiltration anLight microscopy shows mononuclear infiltration and noncaseating granulomas usually observed in association with acute hypersensitivity pneumonitis, but it also can be observed in subacute and chronic disease.
  • Subacute hypersensitivity pneumonitis: The histopathologics features of subacute hypersensitivity pneumonitis comprise a triad of lymphocyte-dominant interstitial inflammatory cell infiltration, poorly formed nonnecrotizing granulomas, and cellular bronchiolitis. Foci of bronchiolitis obliterans and intra-alveolar fibrosis also are described.[1]
  • Chronic hypersensitivity pneumonitis: The pathological features of chronic hypersensitivity pneumonitis include a usual interstitial pneumonia–like pattern with subpleural patchy fibrosis, alternating normal alveoli, and fibroblastic foci with centrilobular fibrosis. In contrast to pathological features of acute and subacute hypersensitivity pneumonitis, epithelioid cell granulomas are sparse or absent. Giant cells, however, can be seen in the interstitium. Bridging fibrosis between peribronchiolar areas and perilobular areas is a defining feature of chronic hypersensitivity pneumonitis.[1] Note the images below. Giant cells are a characteristic feature of hypersGiant cells are a characteristic feature of hypersensitivity pneumonitis. Chronic hypersensitivity pneumonitis shows interstChronic hypersensitivity pneumonitis shows interstitial inflammation associated with fibrosis.
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Staging

Hypersensitivity pneumonitis has been divided into 3 forms of diseases depending on the length of time of exposure. Note the following:

  • Acute hypersensitivity pneumonitis is due to a brief but intermittent intense exposure to an offending agent. Symptoms begin 4-8 hours after exposure and resemble the flu. Features include cough, dyspnea, fever, malaise, diaphoresis, headaches, and myalgias. Chest radiography shows an interstitial pattern, and HRCT demonstrates ground-glass opacities. Symptoms resolve in 12-24 hours, and the patient returns to his or her normal baseline state. If exposure is controlled, long-term sequelae are limited.
  • Subacute hypersensitivity pneumonitis is due to a low-level but prolonged exposure to an inciting agent. Symptoms resemble those of chronic bronchitis and include chronic cough, exertional dyspnea, malaise, anorexia, fatigue, and weight loss. Chest radiography shows a reticulonodular pattern in mid-to-upper lung fields. HRCT reveals micronodules, ground-glass opacities, and early fibrosis. With recognition and avoidance of the antigen, patients may have complete recovery. With continued exposure, however, more than half the patients progress to end-stage lung disease.
  • Chronic hypersensitivity pneumonitis is the final destination from uncontrolled acute or subacute disease. Signs and symptoms resemble those of end-stage interstitial pulmonary fibrosis. Radiographic findings include fibrosis and honeycombing. Prognosis is poor, with continued deterioration of lung function.
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Contributor Information and Disclosures
Author

Marine Demirjian, MD  Resident Physician, Department of Internal Medicine, Ronald Reagan University of California in Los Angeles Medical Center

Marine Demirjian, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Medical Women's Association, and California Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Nader Kamangar, MD, FACP, FCCP, FCCM  Associate Professor of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, University of California, Los Angeles, David Geffen School of Medicine, Olive View-UCLA Medical Center; Associate Program Director, Pulmonary and Critical Care Multi-Campus Fellowship Program, Cedars-Sinai/West Los Angeles Veterans Affairs/Los Angeles Kaiser Permanente/Olive View-UCLA Medical Center; Site Director, Pulmonary/Critical Care Fellowship Program, Olive View-UCLA Medical Center

Nader Kamangar, MD, FACP, FCCP, FCCM is a member of the following medical societies: American Academy of Sleep Medicine, American Association of Bronchology, American College of Chest Physicians, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, California Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC  Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael Peterson, MD  Chief of Medicine, Vice-Chair of Medicine, University of California, San Francisco, School of Medicine; Endowed Professor of Medicine, University of California, San Francisco-Fresno, School of Medicine

Michael Peterson, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Daniel R Ouellette, MD, FCCP  Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Pulmonary Disease and Critical Care Medicine Service, Henry Ford Health System

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society

Disclosure: Nothing to disclose.

Timothy D Rice, MD  Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, St Louis University School of Medicine

Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD  Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society

Disclosure: Nothing to disclose.

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A 60-year-old dairy farmer had an 8-year history of intermittent dyspnea. Chest radiograph shows bilateral reticulonodular interstitial infiltration secondary to subacute hypersensitivity pneumonitis.
Chest radiograph of a patient with chronic hypersensitivity pneumonitis from pigeon breeder's disease. Bilateral reticulonodular densities are present.
High-resolution CT scan of lungs shows ground-glass opacification in the acute phase of hypersensitivity pneumonitis.
The chronic phase of hypersensitivity pneumonitis shows honeycombing in the right upper lung and traction bronchiectasis.
High-resolution chest CT scan of a patient with subacute hypersensitivity pneumonitis demonstrates centrilobular nodules. These nodules are unlike those of sarcoidosis, in which the nodules are subpleural and along bronchovascular bundles.
Light microscopy shows mononuclear infiltration and noncaseating granulomas usually observed in association with acute hypersensitivity pneumonitis, but it also can be observed in subacute and chronic disease.
Giant cells are a characteristic feature of hypersensitivity pneumonitis.
Chronic hypersensitivity pneumonitis shows interstitial inflammation associated with fibrosis.
Table. Selected Etiological Agents for Hypersensitivity Pneumonitis
DiseaseSource of ExposureMajor Antigen
Farmer's lungMoldy haySaccharopolyspora rectivirgula



(Micropolyspora faeni)



BagassosisMoldy sugar cane fiberThermoactinomyces sacchari
Grain handler's lungMoldy grainS rectivirgula,Thermoactinomyces vulgaris
Humidifier/air-conditioner lungContaminated forced-air systems, heated water reservoirsS rectivirgula, T vulgaris
Bird breeder's lungPigeons, parakeets, fowl, rodentsAvian or animal proteins
Cheese worker's lungCheese moldPenicillium casei
Malt worker's lungMoldy maltAspergillus clavatus
Paprika splitter's lungPaprika dustMucor stolonifer
Wheat weevilInfested wheatSitophilus granarius
Mollusk shell hypersensitivityShell dustSea snail shells
Chemical worker's lungManufacture of plastics, polyurethane foam, rubberTrimellitic anhydride, diisocyanate, methylene diisocyanate
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