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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: 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: 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: Cord blood cells were incubated (passively sensitized) with sera from 27 patients with previous systemic reactions to insect stings. Histamine release (HR) from these cells was measured following exposure to venom extracts at increasing concentrations. The aim was to see whether this parameter could predict more efficiently than RAST and skin test the outcome of a subsequent re-sting. Results showed that HR from passively sensitized cells tended to reflect skin sensitivity and specific IgE levels. If patients were not re-stung during the follow-up period, HR from the passively sensitized cells frequently decreased whereas an increase was seen (in 6/13) when using sera collected after re-sting. In conclusion HR from passively sensitized cord blood cells could not satisfactorily predict re-sting reactions in the serum donors.

Notes: We report the results of an open, prospective study on the efficacy of systemic ranitidine in the treatment of psoriasis. Twenty patients suffering from moderate to severe psoriasis were included in the study. The median pretreatment PASI score was 15·7 (range 6·0-24·7). The patients were treated with oral ranitidine 300 mg twice a day for 6 months; no other medication was allowed during the study period. Eighteen patients completed the study. The median PASI score was reduced from 15·7 to 14·5. 9·1 and 5·7. after 1, 3 and 6 months of treatment, respectively (P〈0·00001). A significant reduction in PASI score was evident at 3 months of treatment. A mild to moderate deterioration occurred in 15 patients within the first month of treatment, but this was followed by improvement during prolonged treatment in most patients. No other clinical and/or biochemical side-effects were observed. Eight patients continued therapy with ranitidine after the study was completed, and none of these patients relapsed during a follow-up period of 12–18 months. The results of the present study suggest that ranitidine may be a beneficial and safe treatment for psoriasis. In addition, high-dose, long-term ranitidine treatment appears to be free from severe adverse effects.

Notes: This study showed that under well-defined conditions all immunoglobulins could be removed from the rat mast cell surface. Surface immunoglobulins were examined by immunofluorescence technique, and cell function by the allergic reaction to antigen as judged by histamine release. Refixation of eluted surface Ig to the mast cell was easily accomplished. Furthermore, fixation of specific surface Ig to already sensitized cells resulted in inreased cell sensitivity to antigen, whereas fixation of nonspecific surface Ig resulted in decreased sensitivity. The results indicate that removed immunoglobulins are intact, have affinity for mast cells, and are able to compete with cell-bound Ig.

Notes: The histamine-releasing capability of lipopolysaccharides (LPS) was examined in human leukocyte suspensions. LPS alone did not release histamine, but was found to enhance the histamine release caused by anti-IgE. Also the IgE-mediated histamine release caused by specific antigens (allergens or bacteria) in sensitized individuals was enhanced by LPS. The potentiating effect of LPS was observed in grass pollen and dog dander allergic patients as well as in patients sensitized to E. coli or Staph, aureus bacteria. No potentiation was obtained by exposure to unspecific allergens or bacteria to which the persons were not sensitized. Bacteria can release histamine by immunological or nonimmunological mechanisms, and only the immunological histamine release was found to be potentiated by LPS. It is speculated that endotoxins reinforce release of histamine caused by allergens in allergic patients or by bacteria in persons sensitized to these microorganisms.

Notes: Several cell types, including mast cells, basophils, macrophages/monocytes, lymphocytes, platelets and eosinophils, may bind or contain IgE. To investigate the source of cell-associated IgE and its relation to spontaneous IgE synthesis, peripheral blood mononuclear cells from allergic and non-allergic donors were examined. Using a combination of different cell fractionation techniques and varying methods for extraction of cell-associated IgE, data were obtained indicating that monocytes constitute a major source of cell-associated IgE in human blood. The amount of cell-associated IgE in peripheral blood mononuclear cells from allergic and non-allergic donors varied more than 100-fold but correlated closely to the level of serum IgE (r = 0.84, p 〈 0.001, n= 38). Spontaneous and mitogen-induced in vitro syntheses of IgA, IgE and IgG were compared for allergic and non-allergic donors. Only one donor with very high serum IgE demonstrated spontaneous or mitogen-induced in vitro IgE synthesis despite synthesis of IgA and IgG.

Notes: The aim was to compare IgE and IgG4, RAST-inhibition assay (RI), monoclonal antibody ELISA (Mab-ELISA), counter current immuno electrophoresis (CCIE) and histamine release from basophil leukocytes (HR) for allegen quantification with special reference to aeroallergen detection. As components of indoor acroallergens, cat, dog, and Derm. pter. allergen extracts were selected for the experiments. To evaluate unspecific interference, these allergens were compared mutually and with Cladosporium herbarum. Allergen extracts in varying dilutions were mixed with crushed glass fibre filter materials, eluted, recovered by centrifugation, and allergen concentration quantified by the assays. Equal sensitivity was found for both IgE- and IgG4-RI assaying eat allergen (in the range 5 − 50 SQ-U/ml) and dog allergen (in the range 102− 103 SQ-U/ml). The IgG4-RI assaying Derm. pter, was more sensitive (50 SQ-U/ml) than IgE-RI (2*103 SQ-U/ml). The ranges of allergen detection limits for the Mab-ELISA were equal for cat and Derm. pter. (10 – 102 SQ-U/ml). The range of allergen detection limits for CCIE, assaying dog were 104− 105 SQ-U/ml. The ranges of allergen detection limits for HR were equal for eat and Derm. pter. (10 – 102 SQ-U/ml), and 102− 103 SQ-U/ML for dog. Because of cross-reactivity, a minor degree of interference was observed in the IgE-RI and the HR test for the highest concentration of cat and dog allergens.

Notes: To study the human intestinal mast cell of children and adults, we combined a sensitive glassfibre-based histamine assay with the enzymatic and mechanical dispersion of surgical specimens or mucosal biopsies. The method yields between 1.2 × 103 to 4.6 × 103 mast cells/mg tissue constituting 1.2% to 5.3% of total cell count. The mast cell yield, however, depends on the intestinal tissue specimen used for dispersion. Aliquots containing 1500 mast cells per sample are sufficient for measuring significant amounts of histamine (± 0.15 ng histamine per sample), thus making it possible, to carry out approximately 75 tests for four mucosal biopsies of 10 mg each. The intestinal mast cell releases histamine in a dose-dependent manner on challenge with anti-IgE (6–600 U/ml), ionophore A23187 (0.25–1.0 μM), and Concanavalin A (0.7–25.0 μg/ml). The histamine release shows interindividual variation with a net histamine release between 0 to 2.5 ng/samples dependent on the secretatogue. In general, it is not necessary to passively sensitize the mast cells to obtain a sufficient histamine release response to anti-IgE challenge, indicating the presence of intact and functional cell-bound IgE. However, it is shown that four of 10 non-atopic intestinal mast cell samples could be passively sensitized with human plasma containing either mite- or grass-specific IgE without stripping off the IgE first. This indicates the presence of free and preserved Fc-receptors on the dispersed mast cells in some subjects. In addition, it is found that the phorbolester TPA increases the histamine release response to A23187 and turns anti-IgE non-responding mast cells into responding mast cells, but TPA alone at 2 to 16 ng/ml has no histamine releasing effect. In patients with anti-IgE responding mast cells no additional effect of TPA is seen. Finally, no substantial differences between mast cells of children and adults are demonstrated.