[Treatments of allergic asthma].
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Biomedical subjects
Publications and source records attributed to J Charpin.
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Six patients who had suffered a reaction to the administration of muscle relaxants at the time of induction of general anaesthesia were explored using skin tests, the Prausnitz-Küstner reaction, the blastic transformation test, the Shelley test and the basophil histamine release test. Fifteen normal subjects were used as controls. The patients who had suffered a reaction showed considerable cutaneous hypersensitivity to muscle relaxants. None of the biological tests carried out revealed an immunological mechanism.
The effect of aerosolized prostaglandin F2alpha (PGF2alpha) on specific airway resistance (SRaw) has been measured in patients with common (n = 10) or aspirin-sensitive asthma (n = 5). In all subjects PGF2alpha caused a dose-related increase in SRaw, but considerable individual differences in sensitivity were observed. The patients with aspirin intolerance did not differ from regular asthmatics in terms of their response to PGF2alpha. Two types of reactions to PGF2alpha could be distinguished from their time-course: immediate and short-lasting (3 cases) or delayed and long-lasting (12 cases). Inhalation of a beta-adrenergic drug rapidly and completely reversed the effect of PGF2alpha, suggesting that the increase in SRaw was due to bronchospasm. In 7 subjects the inhalation of an anticholinergic drug (SCH 1000) prior to PGF2alpha inhibited to a large extent the effect of the latter, suggesting that the cholinergic system played an important role in the bronchial response to PGF2alpha. In 9 subjects no correlation was found between the bronchial sensitivity to carbachol and PGF2alpha.
The effect of Paragerm spray from either a hand pressurized can or from a general room mist device (MCR device) on mattress mite populations was compared with the effect of a control spray. After 1 month a reduction in mite population due to the cleaning procedures was evident in the control treated mattresses; Paragerm treated mattresses had significantly fewer mites, notably those treated with the aerosol can spray, nine out of fifteen of which were mite free. Dissection of the mattresses showed that some mites survive and they could form the nucleus from which reinfestation could occur.
A plane-tree pollen allergen was obtained by ion exchange and gel filtration chromatography. It is a glycoprotein with a molecular weight of 22,000. By isoelectrofocusing, two isomers with a high cross-allergenicity were obtained. The results suggest that this fraction is not the only allergen but certainly the most active.
By constructing cumulative dose-response curves to inhaled carbachol in 12 normal and 17 asthmatic subjects with comparable baseline specific airway conductance, we have shown that there were wide variations among subjects in the dose of carbachol needed to cause a 25 per cent decrease in specific airway conductance (bronchial sensitivity) and in the slopes of the curves (bronchial reactivity). Furthermore, there was no significant correlation between these 2 characteristics of the bronchial response to carbachol. The mean dose-response curves of the asthmatic and the normal subjects were widely divergent, indicating that the asthmatic subjects differed from normal subjects more in terms of bronchial reactivity than in bronchial sensitivity. This suggests that different mechanisms determine the sensitivity and reactivity of the bronchial tree, and that hyper-reactivity is the main feature of the asthmatic response. Both should be assessed when the bronchial response to bronchoconstrictor agents is measured.
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Spirometric indices such as the forced expiratory volume in one second (FEV1), the maximal expiratory flow rate (MEFR) and the maximal midexpiratory flow rate (MMFR) can be criticized for use with bronchial provocation tests since they are either partly effort-dependent or dependent on the forced vital capacity (FVC). These criticisms can be avoided by the use of a new index corresponding to the volume of air expired in one second starting at 75% of the control FVC, called the (FEV1)-25. This study was performed to evaluate the relative sensitivity of the (FEV1)-25 and the classical FEV1 in detecting airway obstruction caused by an inhaled carbachol aerosol in 20 asthmatic subjects. The mean fall in (FEV1)-25 of 46% following carbachol inhalation compared with a mean fall in FEV1 of 35% indicates that, in addition to its theoretical advantages, the (FEV1)-25 is a sensitive index for use with bronchial provocation tests.
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A theoretical study of the basic principles involved in Radioallergosorbent test (RAST) showed that: 1) When a given serum is tested, the significance of the numerical value obtained with RAST depends upon the serum assayed and the allergosorbent preparation, in a rather unpredictable way. Three factors can be measured: a) The percentage of specific IgE antibodies among all allergen-specific antibodies; b) The specific IgE antibody level; c) The product of the specific IgE antibody level and its affinity constant. 2) Simple graphical techniques allow a straightforward determination of all these factors if four dilutions of each serum are assayed at the same time. The results are expressed in two constant parameters (arbitrary IgE unit and allergosorbent capacity). It is concluded that these theoretical calculations may give a fair account of a lack of correlation between specific IgE antibody levels (as assayed with RAST) and several clinical and biological parameters. Furthermore, they provide a simple procedure which makes such tedious manipulations as specific IgE antibody purification quite necessary.
Deuterium oxide (D2O) is known to potentiate non-cytotoxic histamine release in vitro. It has been shown (5) that D2O could also potentiate in vivo immediate-type hypersensitivity in dogs and monkeys. Present studies demonstrate potentiation in vivo by D2O of the cutaneous reactivity in 48/80, PHA and Dermatophagoides cutaneous reactions in human beings. PHA histamine release from human leucocytes is also potentiated by D2O in vitro.
Our purpose was to determine whether exposure to a realistic concentration of nitrogen dioxide (NO2) could increase the bronchial sensitivity of asthmatic patients to bronchoconstrictor agents. We established dose-response curves for changes in specific airway resistance (SRaw) in response to aerosolized carbachol in 20 asthmatics after each had spent 1 h in an exposure chamber breathing on one occasion unpolluted air and on a separate occasion 0.1 ppm NO2: sequence of exposures to unpolluted air and to low levels of NO2 were randomized in a single-blind fashion. NO2 induced a slight but significant increase in initial SRaw and enhanced the bronchoconstrictor effect of carbachol in 13 subjects: curves were shifted to the left and the mean dose of carbachol producing a twofold increase in initial SRaw was decreased from 0.66 mg to 0.36 mg (P less than 0.001). In contrast, NO2 neither modified the initial SRaw nor the bronchoconstrictor effect of carbachol in seven subjects. In 4 out of the 20 subjects, exposure to a higher concentration of NO2 (0.2 ppm) yielded variable results. Potentiation of the carbachol bronchoconstrictor response by NO2 could not be related to any physical or clinical characteristics of the subjects tested. Although the mechanisms underlying the NO2 effect remain controversial, the present results demonstrate that very low levels of NO2 can adversely affect some asthmatics.
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