[Cortisone therapy today].

Abstract

Five decades of experimental and clinical experience have changed corticoid therapy thoroughly. Corticoides have two modes of action. The first is a genomic effect through which anti-inflammatory proteins are formed which inhibit pro-inflammatory cytokines. This effect is initiated even by small doses, but is of late onset. The use of high doses initiates non-genomic effects through alterations of the cell membrane; these effects are found early after initiation of treatment. The risk of adverse corticoid effects are extremely rare when modern application forms and therapy regimens are used: Very high doses for a short time in case of acute states of illness, very low doses in long-term therapy of chronic illnesses, and the use of topical substances wherever this is possible. As for the dose regimen, one should start with an initial dose which suffices to treat the acute state, and subsequently reduce the dosage after the first positive results are obtained. In long-term therapy a daily dose of 5 mg prednisolone should not be exceeded; usually even lower doses are sufficient. These very low doses can only be reached by reducing in steps of one half to one milligram over very long periods of time. During long-term therapy osteoporosis prophylaxis is mandatory. Due to these new therapeutic concepts treatment of rheumatoid arthritis with corticoids is experiencing a revival. Low-dose corticoid therapy is of lower risk than nonsteroidal antirheumatic treatment and slows down disease progression, i.e. joint destruction is significantly inhibited. Corticoids have also undergone a new development in the treatment of asthma. Previously used only in acute systemic therapy, they have now been established in basic therapy, i.e. long term therapy using special topic applications.