Hypersensitivity pneumonitis 2303500 216736144 2008-06-02T23:51:19Z 99.128.119.90 /* Types */ {{Infobox_Disease | Name = {{PAGENAME}} | Image = | Caption = | DiseasesDB = 4630 | ICD10 = {{ICD10|J|67||j|60}} | ICD9 = {{ICD9|495}} | ICDO = | OMIM = | MedlinePlus = | eMedicineSubj = med | eMedicineTopic = 1103 | eMedicine_mult = {{eMedicine2|ped|2577}} | MeshID = D000542 | }} '''Hypersensitivity pneumonitis''' (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. == Types == Hypersensitivity Pneumonitis (HP) may also be called many different names, based on the provoking [[antigen]]. These include: ; Bird-Breeder's Lung : Also called [[Bird fancier's lung]], Pigeon-Breeder's Lung, and Poultry-Worker's Lung. Caused by avian proteins. Exposure is from feathers and bird droppings. ; Farmer's Lung : Caused by the [[mold]]s ''Thermophilic [[actinomycetes]]'', ''[[Aspergillus]] species'', ''[[Saccharopolyspora rectivirgula]]'', and ''[[Micropolyspora faeni]]''. Exposure is generally from moldy hay but may be found elsewhere. ; Bagassosis : Caused by ''[[Thermophilic actinomycetes]]''. Exposure is from moldy bagasse (pressed sugarcane). ; Malt Worker's Lung : Caused by ''Aspergillus clavatus''. Exposure is from moldy barley. ; Humidifier Lung : Caused by the bacterias ''T. candidus'', ''Bacillus subtilis'', ''B. cereus'', and ''Klebsiella oxytoca''; the fungus ''[[Aureobasidium pullulans]]''; and the amoebae ''Naegleria gruberi'', ''Acanthamoeba polyhaga'', and ''Acanthamoeba castellani''. Exposure is from mist from standing water. ; Mushroom Worker's Lung : Caused by ''Thermophilic actinomycetes''. Exposure is from mushroom compost. ; Compost Lung : Caused by ''[[Aspergillus]]''. Exposure is from [[compost]]. ; Peat Moss Worker's Lung : Caused by ''Monocillium sp.'' and ''Penicillium citreonigrum''. Exposure if from peat moss. ; Suberosis : Caused by ''Penicillum frequentans''. Exposure is from moldy cork dust. ; Japanese Summer-Type HP : Caused by ''[[Trichosporon cutaneum]]''. Exposure is from damp wood and [[mats]]. ; Cheese-Washer's Lung : Caused by ''Pencillum casei'' or ''P.roqueforti''. Exposure is from [[cheese casings]]. ; Metalworking Fluids HP : Caused by Nontuberculous Mycobacteria. Exposure is from mist from metalworking fluids. ; Hot Tub Lung : Caused by ''[[Mycobacterium avium]]'' complex. Exposure is from mist from [[hot tub]]s. ; Mollusc Shell HP : Caused by aquatic animal proteins. Exposure is from mollusc shell dust. ; Isocyanate HP : Caused by TDI, HDI, and MDI. Exposure is from paints, resins, and polyurethane foams. ; TMA HP : Caused by Trimellitic anhydride. Exposure is from plastics, resins, and paints. ; Beryllium: Caused by [[Beryllium]]. Exposure in the electronics industry. ; Wine-grower's lung: From Botrytis cinerea mold on grapes. 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." <ref name="Sharma">Sharma, Sat. [http://www.emedicine.com/med/topic1103.htm/ Hypersensitivity Pneumonitis]. ''eMedicine'', June 1, 2006.</ref> == Symptoms == Hypersensitivity Pneumonitis (HP) is categorized as acute, subacute, and chronic based on the duration of the illness. '''Acute''' In the [[Acute (medical)|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.<ref name="Sharma"/> Acute HP is characterized by poorly formed noncaseating interstitial [[granuloma]]s and mononuclear cell infiltration in a peribronchial distribution with prominent giant cells.<ref name="Sharma"/> On [[chest radiograph]]s, 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 scan]]s, ground-glass opacities or diffusely increased radiodensities are present. Pulmonary function tests show "diffusing capacity of lungs for carbon monoxide. ... Many patients have hypoxemia at rest, and all patients desaturate with exercise.<ref name="Sharma"/> '''Subacute''' Patients with [[subacute]] HP gradually develop a [[productive cough]], dyspnea, [[fatigue (physical)|fatigue]], [[anorexia (symptom)|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-upper lung zones.<ref name="Sharma"/> 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]].<ref name="Sharma"/> '''Chronic''' In chronic HP patients often lack a history of acute episodes. They have an insidious onset of cough, progressive dyspnea, fatigue, and weight loss. Removing exposure results in only partial improvement. ... Clubbing is observed in 50% of patients. [[Tachypnea]], respiratory distress, and inspiratory crackles over lower lung fields often are present.<ref name="Sharma"/> 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.<ref name="Sharma"/> Chronic forms reveal additional findings of chronic interstitial inflammation and alveolar destruction ([[honeycombing]]) associated with dense fibrosis. Cholesterol clefts or [[Asteroid body|asteroid bodies]] are present within or outside granulomas.<ref name="Sharma"/> In addition, many patients have hypoxemia at rest, and all patients desaturate with exercise. == Diagnosis == 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. == Management == The best treatment is to avoid the provoking allergen, as chronic exposure can cause permanent damage. Sufferers might try a face mask if they cannot avoid the allergen. [[Corticosteroids]] such as [[Prednisolone]] may help to control [[symptoms]] but may produce side-effects. ==References== {{Reflist}} *Oxford Handbook of Clinical Medicine {{Respiratory pathology}} {{Allergic conditions}} [[Category:Pulmonology]] [[es:Alveolitis alérgica extrínseca]] [[nl:Allergische alveolitis]] [[ja:過敏性肺臓炎]] [[pl:Alergiczne zapalenie pęcherzyków płucnych]]