It is widely accepted that asthma is a clinical manifestation of atopy. Specially relevant in children, this concept is less obvious in adults where there is the classic distinction between asthma "extrinsic" (allergic) and "intrinsic" (non-allergic). Intrinsic Asthma is deliberately late third, a female is classic, as well as association with a naso-sinus polyposis, an intolerance to aspirin and lower corti-cosensibilité requiring more frequent to-corticothéra Oral pie. These patients have no history of allergy, skin tests are negative for aero-allergens and concentrations of serum total IgE and specific are low. The majority of published works often lignent however the existence of biological or clinical markers of inflammation-question "allergic" in a broad sense in asthma, even seemingly intrinsic.
[...] Finally, some apparently intrinsic asthma questions likely result of occupational exposure unknown. Macrophage activation The only biological reported in Intrinsic Asthma Study are in favor of a particular cell activation during intrinsic asthma include bronchial infiltration rich cells of the lineage of monocytes / macrophages (recognized by the CD68 marker) This macrophage inflammation is associated with increased expression of cytokines promoting the accumulation of these cells (especially interleukin-3 and Granulocyte- Macrophage Colony Stimulating Factor or GM-CSF). Finally, the GM-CSF receptor (GM-CSFR) is expressed in the mucosa in non-allergic asthmatics. [...]
[...] It may nevertheless con-rise developments pejorative with the risk of acute severe asthma in allergic massive exposures or a severe asthma harder to treat, especially when the foreclosure action are poorly understood or poorly implemented. The non- allergic asthma "intrinsic" has also some special clinics. It often appears in their forties or later. A female is classic, and the association with a naso-sinus polyposis, an intolerance to aspirin and a reduced sensitivity to inhaled treatments requiring more frequent oral corticosteroids. [...]
[...] The Marseille group found a mean age at onset of asthma of 23 years with dix-allergic asthma in September against 43 years in September dix-asthmatic non allergic. Similarly intrinsic asthmatics that we have analyzed in the Intrinsic asthma study were so- gnificativement older than allergic asthma (53 years (39-62) against 33 years p [...]
[...] Is intrinsic asthma a heriditary disease? Allergy 1991; 46: 367- Vervloet Charpin D. Intrinsic asthma. In Holgate ST, Lockhart Marsh DG (eds). Genetics of asthma. Oxford: Blackwell Scientific Publications 93- Lock Kay AB, Barnes N. Double-blind, placebo-controlled study of cyclosporin A as a corticosteroid-sparing agent in corticosteroid-dependent asthma-ma. Am J Respir Crit Care Med 1996; 153: 509- Humbert Grant JA, Taborda-Barata et al. High affinity IgE receptor (FceRI)-bearing cells in bronchial biopsy sies from atopic and non-atopic asthma. Am J Respir Crit Care Med 1996; 153: 1931- Humbert Durham SR, Ying et al. [...]
[...] Immunoglobulin E Intrinsic Asthma is characterized by serum levels of IgE in normal limits. In practice, it focuses particularly on the fact that the diagnosis of intrinsic asthma is retained in the absence of clinical allergy and immediate reaction to skin tests. In scientific studies, the criteria are more Drast-making. Thus in our study Intrinsic asthma requiring negative skin tests (and a positive test to histamine) and RAST negativity of a battery of twenty-five aero-allergens common. Note however that, despite these precautions, and normal levels of IgE , concentrations of total IgE in non-allergic asthmatics of Intrinsic asthma study were significantly higher than those of the group of subjects non-asthmatics (66 IU / ml 108) against 12 IU / ml (3-29 p [...]
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