Library

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.

Notes: The in vitro histamine release response of human intestinal mast cells and basophils challenged with anti-IgE, Concanavalin A, ionophore A23187 and food extracts was compared with skin prick test, RAST analysis and open food challenge. It was not possible to perform food challenge in all patients; however, seven children underwent open food challenge and in five the clinical diagnosis of “true” food allergy was confirmed. The intestinal mast cells were pooled from enzymatically dispersed duodenal biopsies obtained by duodenoscopy from 15 selected children suspected of food allergy, and five age-matched controls. In nine of 10 patients classified as “food allergic” intestinal mast cells released histamine to various food extracts in a dose-dependent fashion. From the mast cells of the nine food-allergic patients compared with non-allergics, the anti-IgE mediated mast cell histamine release was increased. Additionally, at 1000 U/ml anti-IgE the mast cell histamine release was increased compared with their corresponding basophils. However, in non-allergic subjects the histamine release of basophils was increased compared with their corresponding mast cells. Histamine release from basophils was positively correlated to the test scores of the RAST analysis, skin prick test, and food challenge. No apparent correlation between tests scores obtained from histamine release of intestinal mast cell and the other tests was demonstrated, except in children with diarrhoea as only symptom. However, the study gives evidence that duodenal mast cells actually are sensitized with specific IgE and thus may play a pathophysiological role in food hypersensitivity. In addition, the study shows that the ability of different stimuli, including food extracts, to trigger basophil histamine release does not correlate with their potency to induce histamine release from mast cells.

Notes: The aim of the study is to compare the glass fibre-based basophil histamine release test with skin test (Phazet®), RAST (Phadebas®) and bronchial provocation test in children with allergic asthma. The study comprised 68 selected children with a case history of extrinsic allergic asthma to danders (cat and dog) and house-dust mite. Skin prick test, RAST, and histamine release were performed in all children and the bronchial provocation test was used as a reference of “true allergic asthma”. A total of 81 allergen bronchial challenges were performed and 44 children experienced 49 positive provocations. In 2.9% (2/68) of the children histamine release could not be performed due to technical difficulties (low histamine release with anti-IgE). Concordances in the range 76–87 % were observed with no significant difference between the tests. The highest concordance (87%) was found between histamine release and bronchial provocation test followed by skin prick test vs bronchial provocation (84 %) and RAST vs bronchial provocation (80%). The sensitivity and specificity were calculated for each test. All tests showed sensitivities in the range 90–94 % and no significant difference between them was observed. The specificity of histamine release, skin prick test, and RAST was 0.78, 0.69, and 0.63, respectively. The specificity of histamine release was better than RAST demonstrated by 95% confidence intervals. In conclusion, it was found that the histamine release test is a convenient diagnostic method and the study indicates a diagnostic value comparable to the common diagnostic methods in clinical allergy.

Notes: It has been speculated whether the recently developed non-sedating antihistamines may possess other properties than merely being antagonists at the H1-receptors. To investigate this suggestion 12 patients with strictly seasonal allergic rhinitis participated in a double-blind placebo controlled randomized cross-over study outside the pollen season. At steady state levels of 10 mg loratadine, a new non-sedating antihistamine, the patients were challenged with methacholine. This was followed by a nasal challenge with increasing doses of allergen. 24 h later the patients were rechallenged nasally with the same methacholine dose as the day before. The volume of the methacholine-induced nasal secretion was measured and the response to allergen was determined by scoring technique. In returned nasal lavage fluid the levels of histamine and TAME-esterase activity were measured. It was found that loratadine significantly reduced the immediate allergic nasal symptoms compared with placebo (P 〈 0.01). Loratadine also reduced the allergen-induced release of histamine into the nasal cavity after the strongest allergen dose, from 9.6±1.5 (mean ± SEM) to 6.4±1.4 ng/ml (P 〈 0.05). A similar decrease in the TAME-esterase activity after treatment with loratadine was observed. The TAME-esterase activity decreased from 11.6 *103±2.47 *103 to 5.60 *103±1.45 */103 CMP (P 〈 0.05). There were no significant changes between the active and placebo treatments regarding the methacholine-induced secretory response. This was true for the initial methacholine challenge as well as the secretory response 24 h later. This study shows that loratadine is an effective drug in the suppression of immediate allergic nasal symptoms. One of the beneficial effects of this drug could be a reduction in allergen-induced histamine release. A finding which further implicates that antihistamines may possess other effects than just a blocking of the H1-receptor.

Notes: Magsat data have been used to design scalar magnetic anomaly maps in an area that covers about half of Europe on both sides of the north-south directed European Geotraverse (EGT). The two maps refer to different altitudes and are intended to place recent compilations of aeromagnetic surveys along the EGT (Wonik et al. 1992) into global perspective.The presentation of the magnetic anomalies and their compatibility with the aeromagnetic data required (i) a suitable reference field for subtraction from the measured total field, which was derived from the field model M102089 by Cain, and (ii) a proper function of time reduction to the epoch 1980.0, which has been obtained from the actual satellite data. Because of the considerable noise in the data only those anomalies have been chosen for mapping, which show up in all Magsat tracks independent of altitude and epoch of measurement. The anomaly maps are based upon the less disturbed dawn track data, but a few dusk tracks have also been used as tie lines.The anomalies are interpreted in terms of a magnetization model, which divides the Earth's lithosphere in Europe into blocks of extension 1°N-S by 2°E-W and attributes to each block the ‘Depth Integrated Magnetization' of the magnetized layer, i.e. the magnetization integrated over the vertical extension of the block. Each block is represented by a dipole parallel to the inducing core field, and the calculated model field is adjusted to the anomaly maps by trial and error, starting with an initial coarse distribution that seems plausible from the anomalies and from local geomagnetic surveys. For a realistic model field in the EGT area a rather large portion of the Earth's magnetized lithosphere outside the area under investigation must be included in the calculation.In order to check, whether the features of the magnetization model are necessary for the interpretation of the field anomalies, they are compared with the distribution of magnetization that is obtained by the application of linear inverse theory.Prominent features of the model of crustal magnetization are the contrast between high values over the East European Platform and low values in the younger parts of Europe, maxima at the iron ore districts of Kiruna and Kursk, a broad minimum centred at St Petersburg, and only small differences between the Mediterranean Sea and the adjacent continental areas. There is a fairly good agreement of these anomaly maps with the corresponding maps presented by Cain et al. (1989a).