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Asthma and autoimmune diseases apparently have little to share except for the involvement of the immune system in both types of disorder. However, epidemiological studies have shown that asthma and Type 1 diabetes, a typical autoimmune disease, are associated at the population level, and some experimental findings have suggested that autoimmune mechanisms might be operating in asthma as well. Female preponderance, increased incidence of antinuclear autoantibodies and detection of autoantibodies against either bronchial epithelial antigens or endothelial antigens in patients with nonallergic asthma suggest that the disease may have an autoimmune basis. Approximately 50% of patients with nonallergic asthma react to intradermal injection of autologous serum, indicating the presence of circulating vasoactive factors and suggesting an autoreactive mechanism. Recent findings in experimental animals support the involvement of an autoreactive mechanism in allergic asthma as well, indicating that human a-nascent polypeptide-associated complex, identified as an IgE-reactive autoantigen, has the potential to sensitize and induce immediate skin reactions and airway inflammation. In summary, asthma is a heterogeneous disorder characterized by chronic inflammation of the respiratory airways that can be triggered by allergen exposure or by other mechanisms, possibly autoreactive/autoimmune. The autoimmune hypothesis is further, indirectly, supported by the response to immunosuppressive drugs. [ABSTRACT FROM AUTHOR]

The objective of the study was to compare triggers for asthma attacks in a group of intrinsic (IA) and extrinsic asthmatic (EA) subjects. We included 205 asthmatic patients divided, according to skin-prick tests, in a group (n=63) of IA and a group (n=142) of EA. The questionnaire provided information on associated conditions (nasal polyps and intolerance to aspirin) as well as on allergenic and nonallergenic triggers. Data analysis demonstrated that in IA, some airborne nonallergenic factors were significantly more often involved. In addition, this association did hold true when comparing subgroups of patients with normal baseline FEV[SUB1] values. For those subjects, PC[SUB20] and the slopes of the dose-response curves to metacholine were comparable. In conclusion, the higher sensitivity of a group IA subjects to some nonallergenic factors is not related to a lower baseline spirometric value in this subgroup. It may be hypothesized that, in these patients, sensitivity of airways irritant receptors might be increased. [ABSTRACT FROM AUTHOR]