Vogelhalterlunge ohne Vogelhaltung[1]

Zusammenfassung:

Die Identifizierung des für das Krankheitsbild einer exogen allergischen Alveolitis (EAA) relevanten Allergens stellt im Einzelfall ein Problem dar, und nur über eine akribische Anamnese gelingt die Eingrenzung der Allergenquelle. Wir berichten über eine 32-jährige Patientin, bei der wir eine chronische EAA diagnostiziert haben, die über die Persistenz von Wellensittichallergen in einem Eigenheim vermittelt wurde, das sie seit zwei Jahren bewohnte und dessen Vorbesitzer über Jahre Wellensittiche gehalten hatten. Ergänzende Untersuchungen an Staubproben aus dem Wohnbereich der Patientin mit dem Nachweis präzipitierender Antikörper wie auch IgG-reaktiver Banden im Immunoblot machten die genannte Ätiologie hinreichend wahrscheinlich. Auch ohne Wohnungswechsel konnte innerhalb eines Jahres eine Normalisierung der initial bis auf etwa 50 % des Sollwertes eingeschränkten Vitalkapazität erreicht werden, was als Ausdruck einer rückläufigen Allergenlast anzusehen sein dürfte.

The identification of disease-inducing allergens in hypersensitivity pneumonitis can be very problematic, and only by a thorough analysis of anamnestic data can the source of allergen be identified. We report on a case of a 32-year-old female diagnosed with hypersensitivity pneumonitis caused by inhalation of budgerigar antigen in her home. She had been living there for two years and had never been a birdkeeper at all. The former proprietor of the house was a budgerigar keeper for years. When we detected precipitating antibodies against different antigens including pigeon and budgerigar antigens as well as hay and Aureobasidium pullulans, the source of antigen exposition was not definitely clear. In the serum of our patient we found precipitating antibodies against protein structures extracted from dust samples from the patient's home, which were not detected in the serum of her husband. Using Western blots of budgerigar serum and of the dust sample from the patient's home we could demonstrate an IgG-reactive banding pattern in our patient's serum. The banding pattern against budgerigar serum correlated very closely to that of a control patient, who was a budgerigar keeper with hypersensitivity pneumonitis. The patient's husband reacted neither against budgerigar serum nor against the dust sample, while he and his wife showed double banding at about 9 kDA when their serum was exposed to dust from a home free of birdkeeping. These results point to the fact that the house dust sample of our patient contained budgerigar antigen, leading to an indirect antigen exposure causing hypersensitivity alveolitis. Our patient received a prolonged treatment with corticosteroids, and after about one year, vital capacity of the lungs which was reduced by 50 % at the beginning of treatment, returned to normal. The patient is still living in her home. Although she has been off medication for one year, lung function tests have not deteriorated. This fact points to a reduction of the amount of antigen in the patient's home.

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1 Die Kasuistik wurde als Poster anlässlich der 10-jährigen Jubiläumstagung der Arbeitsgemeinschaft exogen-allergische Alveolitis in Königswinter am 4. September 1999 präsentiert.