Hypersensitivity Pneumonitis

(Extrinsic allergic alveolitis)

Extrinsic allergic alveolitis is associated with cough, dyspnea and fatigue disorder that (often professional) is caused by sensitization and subsequent hypersensitivity to environmental antigens. There are acute, subacute and chronic courses; all forms are characterized by an acute interstitial inflammation and the development of granulomas and fibrosis during long-term exposure. The diagnosis is made by a combination of history, physical examination, imaging, BAL and biopsy. The short-term therapy is done with corticosteroids, the long-term is to antigen leave.

Extrinsic allergic alveolitis is associated with cough, dyspnea and fatigue disorder that (often professional) is caused by sensitization and subsequent hypersensitivity to environmental antigens. There are acute, subacute and chronic courses; all forms are characterized by an acute interstitial inflammation and the development of granulomas and fibrosis during long-term exposure. The diagnosis is made by a combination of history, physical examination, imaging, BAL and biopsy. The short-term therapy is done with corticosteroids, the long-term is to antigen leave. Etiology have been identified more than 300 antigens to trigger an exogenous allergic alveolitis (EAA), but exposures in the agriculture, birds and the contamination of water cause 75% of cases. The antigens are often by nature and profession distinguished (see Table: Examples of hypersensitivity pneumonitis); the prototype of a EAA is farmers lung caused by inhalation of Heustäuben containing thermophilic actinomycetes. There is a considerable overlap between EAA and chronic bronchitis in farmers. Independent of smoking status, chronic bronchitis in this occurs much more frequently is associated with exposure to thermophilic actinomycetes and leads to EAA similar study findings. Examples of hypersensitivity pneumonitis antigen source Agriculture Bagassose thermophilic actinomycetes Moldy bagasse (sugar cane) Cheese washers lung Aspergillus Penicillium casei clavatus Moldy cheese coffee workers lung coffee bean without dust coffee beans compost pulmonary Aspergillus sp compost farmer’s lung fungi, in particular Aspergillus sp Thermophilic actinomycetes vegetable compost (moldy grain, hay, silage) Mushroom worker’s lung Hypsizigus Marmoreus thermophilic actinomycetes mushroom compost “Potato riddler’s lung” Aspergillus sp thermophiles Aktinomyze th Moldy hay to potatoes around Mushroom workers lung Aspergillus sp scopulariopsis brevicaulis tobacco plants winemakers lung Botrytis cinerea Moldy grape water “hot tub lung” Cladosporium sp Mycobacterium avium complex Contaminated mist and mold on ceilings and around the tub “Humidifier lung” Aureobasidium sp Candida albicans thermophilic actinomycetes contaminated water in humidification and air conditioners sauna lung Aureobasidium sp Contaminated water in the sauna sewage workers lung Cephalosporium sp Contaminated Keller (waste water) birds breeders lung parakeet, pigeon, chicken, turkey, and proteins of ducks Vogelkot- or feather animals fish food lung Unknown fish feed fish meal workers lungfish flour dust fish flour dust furrier lung animal fur dust animal skins hypersensitivity pneumonitis in laboratory workers proteins of rodents Urine and skin of male rats Mummienherstellerlunge Unknown substance bind mummies “Pituitary snuff taker’s lung” Animal proteins “Heterologous (bovine, porcine) pituitary snuff” mold nalgiovense pulmonary disease among workers in the sausage making Penicillium of dried sausages grains Malzarbe iterlunge Aspergillus sp Moldy barley Müller lung Sitophilus granarius (wheat weevil) of weevil-infested flour milling and construction Sequoiosis Aureobasidium sp Graphium sp sawdust from Redwoods thatch lung Saccharomonospora viridis Dried grass and leaves “Wood pulp worker’s disease” Penicillium sp cord of oak and maple lumberjack lung Rhizopus sp Mucor sp contaminated timber forest workers lung Alternaria sp Bacillus subtilis dust from oak, cedar, pine, spruce and mahogany industrial chemical workers lung isocyanates polyurethane foam, coatings, L ack “Detergent worker’s lung” Bacillus subtilis B. subtilis enzymes in detergent Winzer lung copper sulfate using copper sulfate Others byssinosis (brown lung) mill dust (possibly related to endotoxin) Lycoperdonose dust from cotton, flax and hemp spores of Staubli nts (Lycoperdon) Alternative medicine or recreational overuse (confusion of Stäublingen with hallucinogenic mushrooms) Pathophysiology The disease seems to be IV allergic reaction type III and type in which repeated exposure to antigens in genetically predisposed people leads to an acute neutrophil and mononuclear alveolitis followed by an interstitial lymphocytic infiltration and granulomatous reaction. For continuous exposure fibrosis can occur with obliteration of the bronchioles. In the blood circulating precipitins (antigens sensitized antibodies) appear to play a primary etiological role. A positive history of allergy (such as asthma and hay fever) is not a predisposing factor. Cigarette smoking appears to be the development of the disease to delay or prevent, perhaps by a down-regulation of pulmonary immune response to inhaled antigens. Has the disease but once established, smoking leads to exacerbations. The hypersensitivity is similar in clinical appearance other diseases with different pathophysiology. The toxic syndrome caused by organic dust (pulmonary mycotoxicosis, grain fever) z. B., is a syndrome associated with fever, chills, muscle pain, and dyspnea, requires no sensitization and to be caused by the inhalation of toxic dust fungal or other contamination of organic dusts. The Silobefüller disease can cause respiratory failure, acute respiratory distress syndrome (ARDS) and bronchiolitis obliterans or cause bronchitis, but is caused by the inhalation of toxic nitrogen oxides produced by freshly fermented corn or alfalfa silage. Professional Contingent asthma leads in sensitized to inhaled antigens people dyspnea. Findings such as obstruction, airway eosinophilia and differing triggering antigens allow the differentiation of an EAA. Symptoms and signs The symptoms depend on the nature of the outbreak from acute therapy subacute chronic Only a small proportion of exposed individuals develop symptoms usually only after weeks or months of exposure and sensitization. Acute hypersensitivity pneumonitis The acute disease occurs in persons previously sensitized with acute exposure to highly concentrated antigens and manifests 4-8 h after exposure to fever, chills, cough, both sides würgeähnlichem tightness of chest and dyspnea. Cachexia, nausea and vomiting may also be present. On physical examination, tachypnea, diffuse fine to medium-bubble inspiratory RG and usually no wheezing auskultiert.Chronische hypersensitivity pneumonitis The chronic disease occurs in individuals with long-term low concentrations of antigen exposure on (as with bird owners) and begins insidiously over months to years with exertional dyspnea, productive cough , fatigue and weight loss. Few examination findings can be found; rarely occur clubbing; Fever is absent. In advanced cases, pulmonary fibrosis causes symptoms and symptoms of right heart failure and / or respiratory Insuffizienz.Subakute hypersensitivity Subacute disease is between the acute and chronic forms and manifests itself either by cough, dyspnea, fatigue and cachexia occur within days to weeks or as acute disease that is grafted to a chronic symptoms. Diagnostic chest X-ray and high-resolution CT (HRCT) lung function tests lavage Histological examination and serological tests Diagnosis requires a high rate of suspicion in patients with relevant symptoms and an appropriate professional, part-time or domestic exposure in the past. Chest x-ray, HRCT and lung function tests are performed routinely. Bronchoalveolar lavage and biopsy may be necessary when the results are inconclusive. The range of differential diagnosis is extensive and includes environmental lung disease, sarcoidosis, bronchiolitis obliterans, lung disease in rheumatic diseases and other interstitial lung diseases. Among the notes in the history Recurrent atypical pneumonia symptom onset belong to changing jobs or moving to a new home whirlpool, sauna, swimming pool or other sources of standing water or water damage in your home or regular contact with it elsewhere birds as pets exacerbations and symptom relief in and outside special environments The physical examination is diagnostically often groundbreaking, although pathological lung sounds and clubbing may be present. Imaging techniques Imaging techniques are usually performed in patients with such a history, symptoms and complaints. A chest x-ray recording is neither sensitive nor specific and often normal in patients with acute and subacute forms for diagnosis. Especially in symptomatic cases reticular and nodular drawings may be present. The radiographs of patients with chronic disease often show reticular and nodular drawings in the upper lobes with reduced lung volume and wabigem reconstruction, similar to idiopathic pulmonary fibrosis. In HRCT pathological changes are found more frequently so that the HRCT showing parenchymal changes in EAA has become the diagnostic standard. The most typical findings in HRCT in acute and subacute disease is the detection of numerous poorly demarcated smallest centrilobular nodules. Occasionally frosted glass opacity is the most obvious or only finding. Normally, this is diffusely distributed, but sometimes the periphery of the second patch may be recessed. Areas with increased radiolucency similar to obliterative bronchiolitis, may be a prominent feature in some patients (e. B. mosaic-wise arranged reduction with transparency of retained air in the expiratory HRCT). When hypersensitivity pneumonitis occur findings of pulmonary fibrosis (z. B. reduced lobe volume, linear / reticular pattern or honeycomb lung), and it can centrilobular node be present. Some non-smoking patients with hypersensitivity to emphysema found in the upper lobes. Mediastinal lymphadenopathy is unusual, so that the hypersensitivity pneumonitis may be differentiated from sarcoidosis. Chronic hypersensitivity pneumonitis Image courtesy of Harold R. Collard, M.D. var model = {thumbnailUrl: ‘/-/media/manual/professional/images/chronic_hypersensitivity_pneumonitis_high_de.jpg?la=de&thn=0&mw=350’ imageUrl: ‘/-/media/manual/professional/images/chronic_hypersensitivity_pneumonitis_high_de.jpg?la = en & thn = 0 ‘, title:’ Chronic hypersensitivity pneumonitis ‘description:’ u003Ca id = “v37893164 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003eIn this high-resolution CT scan can be seen findings of fibrosis such as irregular networking and Traktionsbronchiektasen. The areas of reduced density in the lung corresponding regions with airway obstruction. These findings in their combination to a extrinsic allergic alveolitis out u003c / p u003e u003c / div u003e ‘credits’. Image courtesy of Harold R. Collard

Health Life Media Team

Leave a Reply