Abstract
Allergic alveolitis (AA) is a group of diseases with an immunologic background evoked by chronic antigen inhalation. The diagnosis is difficult due to the diversity and non-specific character of symptoms and different clinical severity. AA is the third most often interstitial-lung-disease, comprising 4−15% of all interstitial diseases. It’s often related to professional exposure. Farmer’s lung, a hypersensitivity pneumonitis is the most common AA. By binding precipitins to form immunologic complexes, antigens trigger an early phase acute reaction in the lung tissue thus initiating disease’s progression. In the chronic phase endolobular fibrosis located in the upper lobes prevails. Disease differs in course depending the type and time of antigen exposition. Thus, avoiding antigen exposition is the first-line-therapy. Acute form is characterized by fever, chills, dyspnea, and cough. It usually starts 4-8 hours after intensive exposure. Early diagnosis leads to a good prognosis. When the exposition to the antigen stops, acute form of AA usually self-limits within 24−48 hours. Only in severe cases 0.5−1.0 mg/kg/d (up 60 mg/d) can be required for 1−2 weeks with a subsequent dose reduction. Long-term usually leads to chronic form with more serious deteriorations, including severe dyspnea and chronic cough (it takes months-years for them to develop, however). There is no effective therapy, in rapidly progressing cases 40−60 mg/g of prednisone repeated in 4-week-cycles can be recommended. Usually it does not stop the progression, and pulmonary fibrosis followed by respiratory insufficiency develop. Symptoms duration at diagnosis and effectiveness of antigen elimination are the known prognostic factors.
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