| pubmed-article:2869566 | pubmed:abstractText | This study covers current knowledge concerning the risks of tachyphylaxis induced by prolonged use of beta-mimetics in the asthmatic. The organization of the adrenergic membrane system is reviewed, as well as the various mechanisms which may lead to desensitization. Experimental evidence of the latter is described. The most extensive studies have involved circulating cells and, more precisely, lymphocytes and polynuclear neutrophils. Clinical trials are then dealt with. Studies concerned with bronchomotility and the possible loss of sensitivity of the bronchi after a therapeutic sequence using a sympatho-mimetic. No definite conclusion concerning this aspect can be made by review of the literature, because of contradictory results, and this regardless of the beta-mimetic used. However, it would seem that relative tachyphylaxis may develop in the bronchi. Nevertheless, the latter would not seem to be sufficiently marked in order to have clinical manifestations. Studies concerned with lymphocytes and polynuclears. Published studies are more in agreement here, demonstration of tachyphylaxis by measurement of cellular cyclic AMP or measurement of the density of receptors after impregnation by a beta-adrenergic being constant. The practical consequences of this risk is discussed, but cannot yet be accurately fixed. Therapeutic deductions from the findings described are then discussed. The protective role of corticosteroid therapy and of Ketotifen against the risk of tachyphylaxis is emphasized in particular. | lld:pubmed |
