In view of the prevalence of D. pteronyssinus in this country and its high allergenic potency, it is considered that this mite is an important factor in allergic asthma. IntroductionThe importance of the house-dust mite as a cause of allergic disease has only recently been recognized (Voorhorst et al.,
Patients with atopic disease since infancy and who had had infantile eczema were found to react readily to all the challenge tests; nevertheless, even in these highly allergic subjects the titres of the positive reactions were no higher than those of other patients.The possibility that sensitization of some of the patients might have been promoted by the repeated skin, nasal, and bronchial challenge tests has to be considered. The blood samples were therefore taken before the serial in-vivo challenge tests in a random 10 patients. Some of the strongest positive serum and leuoocyte reactions were found in these 10 patients, and in only one were the blood tests weak or negative. These findings indicate that sensitization was unlikely to have been promoted by the testing procedures in the rest of the patients.The negative tests for precipitins suggest that the late bronchial reactions seen in six patients were not mediated by precipitins (as such reactions are in allergic alveolitis) and are not manifestations of Arthus-like type III immune responses in the lung. The mechanism of these late reactions in asthmatic patients has not been established, though such reactions have been described in detail previously and have been estimated to occur in about 30%,' of patients with house dust asthma (Herxheimer, 1952; McAllen, 1Q61). It seems possible that they may be due to cell-mediated immune responses (delayed hypersensitivity).Perhaps the most significant finding in our experiments is that the actual amount of antigen required to produce a tissue reaction both in vitro and in vivo is so extremely small. This is of the order of 0 05 to 1 jig. in the bronchi and 0-5 to 20 ug. in the nose; it would thus be possible under natural conditions for an allergic reaction. to be caused by the inhalation of mite material such as faecal pellets or parts -of dead mites in an amount weighing less than one whole live mite.It is concluded that the negative findings in the control tests and the high titres of sensitivity in the challenge tests on the allergic subjects establish that the mite D. pteronyssinus contains a very potent antigen. This antigen can cause high levels of reaginic antibody and can stimulate histamine release from leucocytes of sensitized patients when brought into direct contact with them in very weak dilution. It is also able to react with sensitized tissues in the skin, the nasal mucosa, and the bronchi in allergic subjects, and can cause symptoms from inhalation of very small quantities. It would therefore appear likely that the mite D. pteronyssinus is an important factor in the causation of perennial allergic asthma in this country.We Positive results were obtained in over 90% of patients, whereas the tests were either negative or very weakly positive in the control subjects. A significant degree of correlation was found between the. two tests used, but pronounced differences were observed in a few instances.Confirmation of the role of IgE in tissue sensitization was obtained from tests with anti-IgE serum on ...
SummaryBetamethasone valerate aerosol is a new compound for the treatment of asthma. Its clinical effectiveness was established in a double-blind cross-over trial in nonsteroid-dependent asthmatic patients. At a dosage of 400 to 800 tsg/day for three months there was no evidence of suppression of hypothalamic-pituitary-adrenal function, as assessed by tetracosactrin and insulin stress tests.A 12-month follow-up study of 120 patients using steroid aerosols (betamethasone valerate or beclomethasone dipropionate) indicated that tolerance does not develop and that a daily maintenance dose of 200 tsg/day was adequate in most patients. Temporary lack of response was observed during episodes of sputum production or of heavy exposure to antigen.There were no observed side effects other than fungal infections of the respiratory tract. However, the incidence of candidiasis ofthe pharynx (13%) and particularly of the larynx (5%) in apparently immunologically normal patients was disturbing. These infections were not seen in pauents taking 200 ,ug/day. Though there is yet no eviaence that fungal infections associated with steroid aerosols may penetrate the trachea and bronchi the possibility of this indicates that caution should be exercised in their use, particularly in long-term high dosage.
Summary The changes in a wide variety of in vivo and in vitro tests following a long course of low antigen dosage hyposensitization therapy in fifteen asthmatic patients with house dust mite allergy are reported. Evidence of clinical improvement was shown by decreased bronchodilator requirement. Bronchial challenge testing showed a significant increase in bronchial tolerance to mite antigen. Nasal and skin tests with mite extract, however, did not show a significant change. In contrast to the development of bronchial tolerance and to the clinical improvement, some of the in vitro tests seemed to provide evidence of hypersensitization. The leucocyte test, for example, showed increased sensitization to the mite antigen, as well as an increase in histamine release by anti‐IgE serum. Total serum IgE was also increased, but this was apparently due to non‐allergen specific IgE. Although the leucocyte test showed increased sensitization to mite antigen, serum reaginic activity as measured by the passive sensitization of human lung did not show any increase. Thus, there seemed to be a difference in the affinity of allergen‐specific IgE for leucocytes as compared with lung tissue. It also appeared that leucocyte response to antigen bore no relationship to sensitization of other tissues, particularly the bronchial tree. The mechanism of clinical hyposensitization by low dosage immunotherapy is discussed. It is suggested that apart from the development of blocking antibodies, other mechanisms seem likely. Among these are a change in the affinity of IgE antibodies for different tissues, and a competition between non‐specific IgE (produced in excess as a result of immunotherapy) and allergen‐specific IgE.
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