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Notes: Short-lived occupational skin symptoms of irritant or urticarial nature were commonly reported among 253 attendants in a clinical study on occupational dermatitis in Danish gardeners and greenhouse workers. Aimed prick or scratch-patch testing for immediate skin and mucosal symptoms was performed in 105 persons with plants as is. 35 persons (33%) had at least 1 positive reaction and a family history of, or personal, atopy was significantly more prevalent among these compared to attendants with negative reactions. Positive histamine release tests made immunologic etiology probable in Schlumbergera cacti, Stephanotis floribunda, Euphorbia pulcherrima and Gerbera reactions. Other new species implicated in immediate-type reactions included Ficus pumila, Gardenia jasminoides, Hibiscus rosa-sinensis, Campanula, Columnea, Epipremnum aureum, Pelargonium and Primula vulgaris. Because of the high prevalence of short-lived skin symptoms and because contact urticaria may present itself as a dermatitis, it is recommended that one supplement patch tests with tests for immediate reactions.

Notes: We have earlier suggested that bacteria-induced histamine release is caused by different mechanisms, including allergic and non-immunological mechanisms, and that the latter probably depends on lectin-mediated reactions. Two possibilities of lectin-mediated reactions were examined in this study, bacterial surface lectins bind to sugars on the basophil cell membrane leading to histamine release, and the reverse reaction where bacterial aminosugars react with lectins on the basophil cell surface. In the bacterial histamine release caused by the Staph. aureus strain Wood 46 it was possible to demonstrate a reverse reaction, but not a bacterial lectin-mediated reaction. The reaction seems to be complex, as lower concentrations of sugars might potentiate the release of histamine by binding to the target cell or bacteria, while the release is inhibited by higher concentrations.

Notes: Background The mediator mechanisms of the cutaneous wheal and flare response, which underlies allergic skin and urticarial conditions, are controversial. The wheal results primarily from a direct effect of histamine on the local vascular bed, but to what extent does histamine diffuse within the wheal? The flare is neurogenic in origin, being disseminated within the dermis by axon reflexes, but do the neuropeptides released from the nerve endings cause the vasodilatation directly or do they induce the further release of histamine which then transduces the fiare?Objective We have addressed these questions by inserting 216 μm diameter microdialysis fibres into the dermis within the different areas of the wheal and flare to monitor changes in histamine levels provoked by intradermal injections of histamine, allergen, codeine and substance P. Twenty-one subjects participated in the investigations.Results The histamine concentration in unprovoked skin was 10.5 ± 0.6 nM. As the dialysis efficacy was 50%, this equates to tissue concentrations of 20 nM. All provicants released large amounts of histamine at the injection site, maximum histamine levels being 337–1293 nM. Diffusion of histamine within the wheai was poor, levels at 2.3 mm and 3.7 mm from the site of injection being 4–22% and 0.2–3.7% respectively of those 1 mm from the injection site. No increased histamine levels were detected in the flare with any provicant. Atraumatic delivery to the skin of histamine in infusion concentrations of 30–10000 nM caused concentration-related effects, at least 100 nM being necessary to induce a significant increase in skin blood flow, a threshold of 300–1000 being required to stimulate a visible flare and a measurable erythema, and 3000–10000 nM being the minimum for induction of a wheal. Thus the skin blood vessels and nerves are responsive to histamine, but at relatively high concentrationsConclusions These data support the theory that the flare reaction to local histamine injection or release is a neurogenic reflex not involving histamine release at its effector end.

Notes: Background At present, several in vitro tests for immunoglobulin E (lgE)-mediated food allergy are available. An estimation of the diagnostic accuracy of the various tests used in predicting clinical sensitivity to codfish in a well-characterized allergic material is necessary.Objectives To compare the diagnostic value of four specific IgE tests, and histamine release from basophils (HR) in identifying clinical type I allergy to codfish. As a true diagnosis, double-blind, placebo-controlled food challenges (DBPCFC) were employed.Methods Eight clinically codfish-allergic adult patients were investigated together with 30 codfish-tolerant control subjects for evidence of codfish-specific reactivity by Phadebas RAST® (PHA). Pharmacia CAP System RAST® (CAP), Magic® Lite (ML) and HR. To characterize the diagnostic properties of a freshly prepared raw codfish extract, experiments were conducted employing an in-house radioallergosorbent test (RAST). the Maxisorp RAST (MAXI) and HR. Finally, protein profile and IgE-reacting allergens were detected by means of sodium dodecyl sulfate-polyacrylamide gel elcctrophoresis (SDS-PAGE) and immunoblotting.Results The sensitivities of HR with commercial extract and the three commercially available specific IgE analyses were 0.83 and 1.00 respectively. Specificities were 1.00 (H R) and 0.87-1.00 (specific IgE tests). Ereshly prepared codfish extracts improved the sensitivity of HR. SDS-PAGE revealed ∼29 bands (〈 14.3-200 kDa) including a band of 12-13 kDa. and in immunoblotting 18 sera identified 17 IgE-binding bands. The protein migrating at 12-13 kDa was identified in the fresh codfish extract tested with gen from all clinical codfish allergies, while no significant reaction was seen in the control subjects.Conclusion Based on the small number of adult patients included in our study, the in vitro assays with commercial and fresh extracts have high sensitivity and are acceptable for screening for codfish allergy. Specificity of Phadebas. CAP. and our in-house RAST was less than unity, whereas ML and strong binding of IgE to a 12-13kDa protein completely matches DBPCFC results, and thus seems sufficient for establishing the diagnosis.

Notes: Levels of specific serum IgE to cow's milk, whole hen's egg, egg white, and egg yolk were compared to the outcome of double-blind, placebo-controlled food challenge ‘DBPCFC) with fresh egg and/or milk in 21 adults with a case history of immediate hypersensitivity to egg and/or milk. Specific serum IgE was measured by four different commercially available tests and by an inhouse Maxisorp RAST using freshly prepared food extracts. Sensitivities and negative predictive accuracies were generally high with egg white and milk, but low with egg yolk. Specificities and positive predictive accuracies were low for all allergens and tests. Changing the cutoff levels did not improve the ability of the tests to predict clinical allergy. Among commercially available test allergens, egg white gave the most consistent results in levels and class scores, and the highest degree of concordance with DBPCFC, whereas egg yolk and milk varied more. Applying freshly prepared food extracts in Maxisorp RAST did not improve diagnostic value. Measuring specific serum IgE levels in control subjects tolerant to egg/milk showed that false positive reactions occurred frequently among patients with another food allergy and atopic dermatitis, whereas most tests were likely to be negative in pollen-allergic and nonallergic volunteers. In conclusion, specific IgE measurements with egg white and milk were useful for exclusion of symptomatic hypersensitivity to egg and milk in patients with a positive history, whereas DBPCFC is still mandatory in patients with positive history and positive test. Measuring egg-yolk-specific IgE or using freshly prepared food extracts for specific IgE measurements added no further diagnostic information. The rate of clinically insignificant positive test results seems to be influenced by the prevalence of other food allergies and/or atopic dermatitis in the population under study.

Notes: The possibility of autoimmune type I reactions to cellular constituents was investigated in 22 patients with ulcerative colitis, 12 with Crohn's disease, and in 22 healthy volunteers Nuclear components and colon mucosa fragments were tested as potential antigens by the basophil histamine release technique One of 12 patients with ulcerative colitis responded to sonicated leukocyte nuclei and one of 12 patients with Crohn's disease responded to both nuclei and RNA. Increased serum levels of total IgE and antinuclear antibodies of IgE class were found in one and three of the 24 patients, respectively Histamine release caused by colon mucosa fragments was not observed in a separate study consisting of 10 ulcerative colitis patients and 10 healthy volunteers. Autoimmune type I allergy to cellular‘constituents does not seem to be of significance for chronic inflammatory bowel disease and thus could not explain the involvement of tissue mast cells and eosinophils in this condition

Notes: In vitro formation of immune complexes was studied by 3H-serotonin release from human platelets by P. aeruginosa antigens in the presence of serum From 22 cystic fibrosis patients. chronically infected with mucoid P. aeruginosa (CF + P) and with a pronounced antibody response against these bacteria, and in 24 patients without P. aeruginosa (CF-P). All CF + P patients responded with 3H -serotonin release (16–34%), whereas CF-P patients released less than 15%. In the group of CF4-P patients the number of P. aeruginosa precipitins was correlated to the serotonin liter. Time courses indicated that SH-serotonin release was maximal between 2 and 5 min, and that no further release was observed up to 20 min. There was a gradual increase in 3H -serotonin release with higher platelet concentrations The response was not changed by complement inactivation. and fractionation of serum demonstrated that the serotonin release was dependent on the presence of the immuno-globulin fraction. These experiments support the suggestion of a type 111 reaction being invoked in the lung damage in CF + P patients and also suggest a possible involvement of serotonin in the inflammatory reaction during chronic P. aeruginosa lung infection.

Notes: A double-antibody radioimmunoassay for measurement of grass pollen antigen-specific IgG in serum is described. Grass pollen antigens were used to show a correlation between the results obtained by this method and those obtained by measuring blocking antibodies by inhibition of antigen-induced leukocyte histamine release. The new technique described is convenient, sensitive, specific and reproducible and can be recommended for clinical use.

Notes: We studied the polyethylene (PEC) precipitability of monomeric human IgE, and of human IgE artificially complexed with rabbit anti-human IgE. At conditions where precipitation of monomeric IgE did not occur, from 0.2 to 20% of the complexed IgE was precipitated. The PEG precipitability of the complexes was inversely related to the IgE/anti-IgE ratio used for preparation of the complexes. From 1.5 to 19.2% of the IgE in the redissolved precipitates could be detected by use of a two-site IgE immunoradiometric assay, the percentage being highest for complexes formed at equivalence. We conclude that exact quantitation of circulating IgE immune complexes (IC) probably is impossible by any PEC precipitation assay. However, the optimized assay was found to be useful for identification of IgE IC in sera with total IgE concentrations below 5,000 U/ml. IgE IC were found in 5/20 sera from patients with Felty's syndrome, in 5/39 sera from patients with extrinsic allergy and high levels of specific IgE, and in 1/17 sera from immunized wasp allergies. No IgE IC were found in 20 normal human sera.