A B Tonnel, M Joseph, B Gosselin, P Gosset, E Fournier
{"title":"[Secondarily infected pneumatocele, eosinophilia and excess production of IgE manifesting as Buckley's syndrome in an adult].","authors":"A B Tonnel, M Joseph, B Gosselin, P Gosset, E Fournier","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The hyper IgE syndrome develops in childhood and leads to repeated infectious episodes, usually of staphylococcus aureus origin and affecting mainly the skin and pulmonary parenchyma. It may be associated with a predominantly facial atypical dermatitis and more rarely with allergic manifestations. Biological tests show mainly an eosinophilia and a hypergammaglobulinemia E alone without modifications in other immunoglobulin types. Disorders of neutrophil and monocyte chemotaxis are inconstant findings. The initial mechanism of the affection appears related to a deficit in suppressive T function selectively acting on the IgE isotype.</p>","PeriodicalId":76107,"journal":{"name":"Le Poumon et le coeur","volume":"39 2","pages":"95-100"},"PeriodicalIF":0.0000,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Le Poumon et le coeur","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
The hyper IgE syndrome develops in childhood and leads to repeated infectious episodes, usually of staphylococcus aureus origin and affecting mainly the skin and pulmonary parenchyma. It may be associated with a predominantly facial atypical dermatitis and more rarely with allergic manifestations. Biological tests show mainly an eosinophilia and a hypergammaglobulinemia E alone without modifications in other immunoglobulin types. Disorders of neutrophil and monocyte chemotaxis are inconstant findings. The initial mechanism of the affection appears related to a deficit in suppressive T function selectively acting on the IgE isotype.