Volume 6, Number 36;  October 12, 2006 - Hypersensitivity Pneumonitis

 

Clinical Question: 

1) What is hypersensitivity pneumonitis and how is it diagnosed and managed?

 

Recommended reading:

Patient:

Session Handout:

 

Readings:

 

 

  

<7>

Unique Identifier [PMID]: 15331190

Authors: Selman M.

Institution: Instituto Nacional de Enfermedades Respiratorias, Tlalpan 4502, CP 14080, Mexico DF, Mexico. moiselman@salud.gob.mx

Title: Hypersensitivity pneumonitis: a multifaceted deceiving disorder. [Review] [144 refs]

 

Source: Clinics in Chest Medicine. 25(3):531-47, vi, 2004 Sep.

Abstract: Hypersensitivity pneumonitis (HP) represents a group of immunologically mediated lung disorders provoked by recurrent exposure to various environmental agents. HP is multifaceted and may mimic almost any interstitial lung disease, some infectious diseases,and even bronchiolar disorders. In the absence of a diagnostic gold standard,diagnosis of HP requires a combination of clinical, environmental, radiologic, physiologic,and pathologic findings that represent a diagnostic challenge for clinicians and-in the chronic form-even for experienced pathologists. Therapeutic approach includes avoiding further exposure and, depending on the clinical form, the administration of a course of prednisone. New anti-inflammatory, immunoregulatory, and antifibrotic drugs are urgently needed for this and other interstitial lung diseases. [References: 144]

Publication Type: Journal Article. Review.

 

 

<8>

Unique Identifier [PMID]: 15316440

Authors: Mohr LC.

Institution: Environmental Biosciences Program and Department of Medicine, Medical University of South Carolina, Charleston, South Carolina 29425, USA. mohrlc@musc.edu

Title: Hypersensitivity pneumonitis. [Review] [99 refs]

 

Source: Current Opinion in Pulmonary Medicine. 10(5):401-11, 2004 Sep.

Abstract: PURPOSE OF REVIEW: Hypersensitivity pneumonitis (HP), also known as extrinsic allergic alveolitis, is a granulomatous, inflammatory disease of the lungs caused by the inhalation of antigenic organic particles or fumes. The disease may present as an acute, subacute, or chronic illness. Episodes of acute and subacute HP usually resolve following cessation of antigen exposure. Chronic HP may be progressive, irreversible, and result in debilitating fibrotic lung disease. This review discusses current concepts regarding the diagnosis, pathogenesis, and treatment of HP. RECENT FINDINGS: The pathogenesis of HP involves both type III and type IV hypersensitivity reactions that are mediated by immune complexes and Th1 T cells, respectively. Proinflammatory cytokines and chemokines activate alveolar macrophages, cause an influx of CD8+ lymphocytes into the lungs, facilitate granuloma formation, and promote the development of pulmonary fibrosis. IFN-gamma is essential for the development of HP and IL-10 appears to modulate the severity of disease. TNF-alpha and TGF-beta have been implicated in development of the pulmonary fibrosis that is seen in chronic HP. It has been shown that pigeon fanciers with HP have an increase in the frequency of HLA-DRB1*1305 and HLA-DQB1*0501 alleles, a decrease in the frequency of the HLA-BRB1*0802 allele, and an increased frequency of the TNF-2 (-308) polymorphism of the TNF-alpha promoter gene. SUMMARY: A careful environmental and occupational history and establishment of exposure to a known inciting antigen are key factors in making the diagnosis of HP. Serum precipitating antibodies, bronchoalveolar lavage, and lung biopsy may be helpful in making the diagnosis. Avoidance of organic antigen exposure is the most important factor in the management of HP. Corticosteroids are indicated for the treatment of severe acute and subacute HP and for chronic HP that is severe or progressive. Long-term corticosteroid therapy for the treatment of chronic HP should be considered only if objective improvement in clinical signs, pulmonary function, or radiographic abnormalities is documented. [References: 99]

Publication Type: Journal Article. Review.

 

 

<9>

Unique Identifier [PMID]: 15316436

Authors: Agostini C. Trentin L. Facco M. Semenzato G.

Institution: Padua University School of Medicine, Department of Clinical and Experimental Medicine, Clinical Immunology, Padua, Italy. carlo.agostini@unipd.it

Title: New aspects of hypersensitivity pneumonitis. [Review] [32 refs]

 

Source: Current Opinion in Pulmonary Medicine. 10(5):378-82, 2004 Sep.

Abstract: PURPOSE OF REVIEW: Hypersensitivity pneumonitis (HP) represents a complex pulmonary disorder of varying intensity and clinical presentation, which is characterized by a diffuse Tc1 immune response of lung parenchyma and airways in patients previously sensitized to one of more than 300 etiologic agents that may favor the HP reaction. This review describes recent data that have clarified some of the events that govern the development of the hypersensitivity reaction following exposure to the causative agents involved in this disease. RECENT FINDINGS: A number of recent data clearly demonstrate that several cytokines and chemokines, which are secreted at sites of disease activity, participate in the pulmonary inflammatory responses taking place in the lung of patients with HP. SUMMARY: The past few years have seen outstanding advances in the understanding of immunologic and molecular events involved in the pathogenesis of HP. It is possible that these data could allow the discovery of therapeutic targets in individuals chronically exposed to HP antigens and evolving towards pulmonary fibrosis. [References: 32]

Publication Type: Journal Article. Review.

 

 

<10>

Unique Identifier [PMID]: 15021060

Authors: Girard M. Israel-Assayag E. Cormier Y.

Institution: Institute of Cardiology and Pneumology Research Centre, Laval University, Laval Hospital, Quebec, Canada.

Title: Pathogenesis of hypersensitivity pneumonitis. [Review] [47 refs]

 

Source: Current Opinion in Allergy & Clinical Immunology. 4(2):93-8, 2004 Apr.

Abstract: PURPOSE OF REVIEW: Hypersensitivity pneumonitis is a group of immunologically mediated diseases caused by an abnormal response to a wide variety of inhaled antigens. Its pathogenesis is complex and involves many immunological concepts. This review discusses recent advances in our understanding of the pathogenesis of hypersensitivity pneumonitis. RECENT FINDINGS: Over the last 3 years, several studies on the pathogenesis of hypersensitivity pneumonitis have been published. New antigens have been identified. We now have a better understanding of the role of inflammatory cells and mediators, and promoting and protective factors have been suggested. SUMMARY: Most of the mechanisms involved in the pathogenesis of hypersensitivity pneumonitis remain incompletely understood. Current and future findings will not only help our understanding of the disease and its prevention, but also improve its treatment. [References: 47]

Publication Type: Journal Article. Review.

 

 

 

Resident Report / Department of Medicine & Grady Branch Library

Emory University School of Medicine

2006 Edition

Participating Faculty:  Carlos Del Rio MD  / Joyce Doyle MD / Lorenzo Difrancesco MD / Joel Mermis MD / Maunank Shah MD

Contact: Karl Woodworth 

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