A significant relationship between the severity of allergic rhinitis and various allergic inflammatory markers was found but could account for only a minor part of the variation in the patients' evaluation of their disease.

The new microfibre method for allergy testing is based on basophil histamine release after challenge with suspected allergens in samples of 50 microliter washed blood cells. Released histamine is bound to microfibres and measured after removal of interfering substances by washing. The microfibre method was compared with the conventional leukocyte histamine release assay in 18 allergic patients tested with 10 different allergens. It was found that the same individuals responded with histamine release to the same allergens in both assays, and the number of responders was almost identical. Also the dose-response curves and the cell sensitivity were almost identical, which further substantiated identity between the results obtained by the new microfibre method and the conventional assay. A comparison between the microfibre method and in vivo provocation tests showed good agreement when comparing the number of positive and negative responses in these test. The new method overcomes the problems in allergy testing, where only small amounts of blood are available and many tests have to be carried out.

IgE against SEs may contribute to the pathogenesis of CSU in a subpopulation of patients. Its role and relevance in the pathophysiology of CSU need to be further analysed.

Apparently, there exists a pool of histamine in the human nose that can be transferred to lavage fluid during glandular hypersecretion. The source of this histamine is yet to be identified. As the level of histamine seems to be affected by the secretory activity of nasal glands, we question the use of this single mediator as an index of mast cell/basophil activation in nasal lavage studies.

IgE was removed from human basophils of 4 nonatopic persons and 10 hay fever patients allergic to timothy grass pollen by treating the cells with buffer to adjusted pH 4. IgE could be removed and refixed to the same cells. Refixation was demonstrated by immunofluorescence and by the ability of basophils to release histamine on exposure to timothy pollen. Removed total IgE and specific IgE directed against timothy pollen were estimated, and a linear correlation to the level of total IgE and specific IgE in serum was found. The total number of IgE molecules per basophil was calculated to be in the range of 30,000 to 300,000, and timothy‐specific IgE constituted 4%‐15% of the total IgE molecules on the cells. It was furthermore established that specific cell‐bound IgE was linearly correlated to the pollen concentration releasing 20% of the histamine contents of the basophils. Separated IgE from sensitized and nonsensitized basophils could be bound to basophils from other patients, resulting in a change in cell sensitivity. This could be ascribed to additional binding to free cell receptors as well as to a partial replacement of bound IgE. Basophils from nonatopic persons could not be sensitized by incubation with surface IgE from atopic persons. The results indicate that acid treatment is a simple method suitable for removing IgE from basophils. This IgE is intact and can be quantitated.