Hypersensitivity pneumonitis

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Hypersensitivity pneumonitis
Classification and external resources
Histology of chronic hypersensitivity pneumonitis.jpg
This is a high magnification photomicrograph from a lung biopsy taken from a patient with chronic hypersensitivity pneumonitis (hematoxylin-eosin stain). It shows mild expansion of the alveolar septa (interstitium) by lymphocytes. A multinucleated giant cell, seen within the interstitium to the right of the picture halfway down, is an important clue to the correct diagnosis.
ICD-10J67
ICD-9495
DiseasesDB4630
MedlinePlus000109
eMedicinemed/1103 ped/2577
MeSHD000542
 
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Hypersensitivity pneumonitis
Classification and external resources
Histology of chronic hypersensitivity pneumonitis.jpg
This is a high magnification photomicrograph from a lung biopsy taken from a patient with chronic hypersensitivity pneumonitis (hematoxylin-eosin stain). It shows mild expansion of the alveolar septa (interstitium) by lymphocytes. A multinucleated giant cell, seen within the interstitium to the right of the picture halfway down, is an important clue to the correct diagnosis.
ICD-10J67
ICD-9495
DiseasesDB4630
MedlinePlus000109
eMedicinemed/1103 ped/2577
MeSHD000542

Hypersensitivity pneumonitis (HP; also called extrinsic allergic alveolitis, EAA) is an inflammation of the alveoli within the lung caused by hypersensitivity to inhaled organic dusts. Sufferers are commonly exposed to the dust by their occupation or hobbies.

Pathophysiology[edit]

Hypersensitivity pneumonitis involves inhalation of an antigen. This leads to an exaggerated immune response (hypersensitivity). Type III hypersensitivity and type IV hypersensitivity occur in hypersensitivity pneumonitis.[1]

Symptoms[edit]

Hypersensitivity pneumonitis (HP) is categorized as acute, subacute, and chronic based on the duration of the illness.[2]

Acute[edit]

In the acute form of HP, symptoms may develop 4–6 hours following heavy exposure to the provoking antigen. Symptoms include fever, chills, malaise, cough, chest tightness, dyspnea, and headache. Symptoms resolve within 12 hours to several days upon cessation of exposure.[3]

Acute HP is characterized by poorly formed noncaseating interstitial granulomas and mononuclear cell infiltration in a peribronchial distribution with prominent giant cells.[3]

On chest radiographs, 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 high-resolution CT scans, ground-glass opacities or diffusely increased radiodensities are present. Pulmonary function tests show reduced diffusion capacity of lungs for carbon monoxide (DLCO). Many patients have hypoxemia at rest, and all patients desaturate with exercise.[3]

Subacute[edit]

Patients with subacute HP gradually develop a productive cough, dyspnea, fatigue, anorexia, weight loss, and pleurisy. Symptoms are similar to the acute form of the disease, but are less severe and last longer. On chest radiographs, micronodular or reticular opacities are most prominent in mid-to-lower lung zones.[3] Findings may be present in patients who have experienced repeated acute attacks.

The subacute, or intermittent, form produces more well-formed noncaseating granulomas, bronchiolitis with or without organizing pneumonia, and interstitial fibrosis.[3]

Chronic[edit]

In chronic HP, patients often lack a history of acute episodes. They have an insidious onset of cough, progressive dyspnea, fatigue, and weight loss. This is associated with partial to complete but gradual reversibility. Avoiding any further exposure is recommended. Clubbing is observed in 50% of patients. Tachypnea, respiratory distress, and inspiratory crackles over lower lung fields often are present.[3]

On chest radiographs, 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.[3]

Chronic forms reveal additional findings of chronic interstitial inflammation and alveolar destruction (honeycombing) associated with dense fibrosis. Cholesterol clefts or asteroid bodies are present within or outside granulomas.[3]

In addition, many patients have hypoxemia at rest, and all patients desaturate with exercise.

Diagnosis[edit]

The diagnosis is based upon a history of symptoms after exposure to the allergen and clinical tests. A physician may take blood tests, seeking signs of inflammation, a chest X-ray and lung function tests. The sufferer shows a restrictive loss of lung function.

Although overlapping in many cases, hypersensitivity pneumonitis may be distinguished from occupational asthma in that it is not restricted to only occupational exposure, and that asthma generally is classified as a type I hypersensitivity.[4][5] Unlike asthma, hypersensitivity pneumonitis targets lung alveoli rather than bronchi.[6]

Lung biopsy[edit]

Low magnification view of the histology of chronic hypersensitivity pneumonitis. The interstitium is expanded by a chronic inflammatory infiltrate. Two multinucleated giant cells can be seen within the interstitium at left, and a plug of organizing pneumonia at bottom left.

Lung biopsies can be diagnostic in cases of chronic hypersensitivity pneumonitis, or may help to suggest the diagnosis and trigger or intensify the search for an allergen. The main feature of chronic hypersensitivity pneumonitis on lung biopsies is expansion of the interstitium by lymphocytes accompanied by an occasional multinucleated giant cell or loose granuloma. [7] [8]

When fibrosis develops in chronic hypersensitivity pneumonitis, the differential diagnosis in lung biopsies includes the idiopathic interstitial pneumonias.[9] This group of diseases includes usual interstitial pneumonia, non-specific interstitial pneumonia and cryptogenic organizing pneumonia, among others. [10] [11]

The prognosis of some idiopathic interstitial pneumonias, e.g. idiopathic usual interstitial pneumonia (i.e. idiopathic pulmonary fibrosis), are very poor and the treatments of little help. This contrasts the prognosis (and treatment) for hypersensitivity pneumonitis, which is generally fairly good if the allergen is identified and exposures to it significantly reduced or eliminated. Thus, a lung biopsy, in some cases, may make a decisive difference.

Types[edit]

Hypersensitivity pneumonitis may also be called many different names, based on the provoking antigen. These include:

Type[12]Specific antigenExposure
Bird fancier's lung
Also called bird breeder's lung, pigeon breeder's lung, and poultry worker's lung
Avian proteinsFeathers and bird droppings [13]
BagassosisThermophilic actinomycetes[13]Moldy bagasse (pressed sugarcane)
Cephalosporium HPCephalosporiumContaminated basements (from sewage)
Cheese-washer's lungPenicillum casei[13] or P. roquefortiCheese casings
Chemical worker’s lung - Isocyanate HPToluene diisocyanate (TDI), Hexamethylene diisocyanate (HDI), or Methylene bisphenyl isocyanate (MDI)Paints, resins, and polyurethane foams
Chemical worker's lung[13] - Trimellitic anhydride (TMA) HPTrimellitic anhydride[13]Plastics, resins, and paints
Coffee worker's lungCoffee bean proteinCoffee bean dust
Compost lungAspergillusCompost
Detergent worker's diseaseBacillus subtilis enzymesDetergent
Familial HP
Also called Domestic HP
Bacillus subtilis, puffball sporesContaminated walls
Farmer's lungThe moldsMoldy hay
Hot tub lungMycobacterium avium complexMist from hot tubs
Humidifier lungThe bacteria
  • Thermoactinomyces candidus
  • Bacillus subtilis
  • Bacillus cereus, and Klebsiella oxytoca;
  • Thermophilic actinomycetes[13]

the fungi

and the amoebae

  • Naegleria gruberi,
  • Acanthamoeba polyhaga, and
  • Acanthamoeba castellani.
Mist generated by a machine from standing water
Japanese summer house HP Also called Japanese summer-type HP
Trichosporon cutaneumDamp wood and mats
Laboratory worker's lungMale rat urine proteinLaboratory rats
LycoperdonosisPuffball sporesSpore dust from mature puffballs[14]
Malt worker's lungAspergillus clavatus[13]Moldy barley
Maple bark diseaseCryptostroma corticale[13]Moldy maple bark
Metalworking fluids HPNontuberculous mycobacteriaMist from metalworking fluids
Miller's lungSitophilus granarius (wheat weevil)[13]Dust-contaminated grain[13]
Mollusc shell HPAquatic animal proteinsMollusc shell dust
Mushroom worker's lungThermophilic actinomycetesMushroom compost
Peat moss worker's lungCaused by Monocillium sp. and Penicillium citreonigrumPeat moss
Pituitary snuff taker's lungPituitary snuffMedication
Sauna worker's lungAureobasidium, Graphium sppContaminated sauna water
SequoiosisAureobasidium, Graphium sppRedwood bark, sawdust
Streptomyces HPStreptomyces albusContaminated fertilizer
SuberosisPenicillium glabrum (formerly known as Penicillium frequentans)Moldy cork dust
Tap water HPUnknownContaminated tap water
Thatched roof diseaseSaccharomonospora viridisDried grass
Tobacco worker's lungAspergillus sppMoldy tobacco
Wine-grower's lungBotrytis cinerea moldMoldy grapes
Woodworker's lungAlternaria, Penicillium sppWood pulp, dust

Of these types, Farmer's Lung and Bird-Breeder's Lung are the most common. "Studies document 8-540 cases per 100,000 persons per year for farmers and 6000-21,000 cases per 100,000 persons per year for pigeon breeders. High attack rates are documented in sporadic outbreaks. Prevalence varies by region, climate, and farming practices. HP affects 0.4-7% of the farming population. Reported prevalence among bird fanciers is estimated to be 20-20,000 cases per 100,000 persons at risk." [3]

Treatment[edit]

The best treatment is to avoid the provoking allergen, as chronic exposure can cause permanent damage. Corticosteroids such as prednisolone may help to control symptoms but may produce side-effects.[15]

Additional images[edit]

References[edit]

  1. ^ Mohr LC (September 2004). "Hypersensitivity pneumonitis". Curr Opin Pulm Med 10 (5): 401–11. doi:10.1097/01.mcp.0000135675.95674.29. PMID 15316440. 
  2. ^ http://www.ucsfhealth.org/adult/medical_services/pulmonary/ild/conditions/hp/signs.html signs and symptoms
  3. ^ a b c d e f g h i Sharma, Sat. Hypersensitivity Pneumonitis. eMedicine, June 1, 2006.
  4. ^ "Lecture 14: Hypersensitivity". Retrieved 2008-09-18. 
  5. ^ "Allergy & Asthma Disease Management Center: Ask the Expert". Retrieved 2008-09-18. 
  6. ^ Page 503 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). Robbins Basic Pathology (8th ed.). Philadelphia: Saunders. ISBN 1-4160-2973-7. 
  7. ^ Mukhopadhyay, Sanjay. "Pathology of Hypersensitivity Pneumonitis", Retrieved on 3 May 2013.
  8. ^ Mukhopadhyay S, Gal AA. (2010). "Granulomatous lung disease: an approach to the differential diagnosis". Archives of Pathology and Laboratory Medicine 134 (5): 669–690. doi:10.1043/1543-2165-134.5.667. PMID 20441499. 
  9. ^ Ohtani Y, Saiki S, Kitaichi M, et al. (August 2005). "Chronic bird fancier's lung: histopathological and clinical correlation. An application of the 2002 ATS/ERS consensus classification of the idiopathic interstitial pneumonias". Thorax 60 (8): 665–71. doi:10.1136/thx.2004.027326. PMC 1747497. PMID 16061708. 
  10. ^ Mukhopadhyay, Sanjay. "Pathology of Hypersensitivity Pneumonitis", Retrieved on 3 May 2013.
  11. ^ Mukhopadhyay S, Gal AA. (2010). "Granulomatous lung disease: an approach to the differential diagnosis". Archives of Pathology and Laboratory Medicine 134 (5): 669–690. doi:10.1043/1543-2165-134.5.667. PMID 20441499. 
  12. ^ Enelow, RI (2008). Fishman's Pulmonary Diseases and Disorders (4th ed.). McGraw-Hill. pp. 1161–72. ISBN 0-07-145739-9. 
  13. ^ a b c d e f g h i j k l Kumar 2007, Table 13-5
  14. ^ Munson EL, Panko DM, Fink JG. (1997). "Lycoperdonosis: Report of two cases and discussion of the disease". Clinical Microbiology Newsletter 19 (3): 17–24. doi:10.1016/S0196-4399(97)89413-5. 
  15. ^ [1]