Popper H, Pongratz M, Lanzer G
Allergol Immunopathol (Madr). 1982 May-Jun;10(3):177-84.
A case of severe therapy-resistant asthma in a young girl with a duration of two years prior to death is reported. At autopsy antibodies of the IgA2-subtype were demonstrated in the lungs on the alveolar basement membranes. We were able to demonstrate intracellular virus-like structures by electron microscopy; this virus infection is taken to be the cause of antibody production. Following antigen-antibody reaction a non-complement-mediated eosinophilic pneumonia with numerous macrophages developed. This inflammatory reaction showed the injurious effect of eosinophilic granulocytes causing fibrinoid necrosis; this is confirmed by the pronounced depletion of the Charcot-Leyden-granules, equivalent to the release of the major basic protein and the Charcot-Leyden crystal protein. Death was caused by IgA2 deposition in the myocardial vessels with consequent eosinophilic myocarditis.
报告了一名年轻女孩严重的难治性哮喘病例,在死亡前病程长达两年。尸检时在肺的肺泡基底膜上发现了IgA2亚型抗体。我们通过电子显微镜能够证明细胞内有病毒样结构;这种病毒感染被认为是抗体产生的原因。抗原 - 抗体反应后,出现了伴有大量巨噬细胞的非补体介导的嗜酸性粒细胞性肺炎。这种炎症反应显示了嗜酸性粒细胞导致纤维蛋白样坏死的损伤作用;夏科 - 莱登晶体颗粒的明显减少证实了这一点,这相当于主要碱性蛋白和夏科 - 莱登晶体蛋白的释放。死亡是由IgA2沉积在心肌血管中并随之引发嗜酸性粒细胞性心肌炎所致。