Abstract

The present chapter considers only one aspect of glucocorticoid therapy of patients with systemic lupus erythematosus (SLE): a possibility of using blood level of tyrosine for monitoring glucocorticoid therapy. Thus, problems of SLE etiology and pathogenesis, as well as numerous schemes of SLE therapy are beyond the limits of this chapter. In the сhapter normal catabolism of tyrosine and some congenital disturbances in catabolism of this amino acid are considered. But in the great majority of cases, specific features of tyrosine catabolism allow us to admit that tyrosine content in blood should be determined by the liver functional competence, in particular, its ability to synthesize an adaptive enzyme tyrosine aminotransferase and by entrance into the liver of glucocorticoids, natural hormones or glucocorticoid preparations. This сhapter also presents experimental data obtained on adrenalectomized rats and observations on children with adrenogenital syndrome which clearly demonstrate blood tyrosine dependence on glucocorticoids and support the idea of using blood tyrosine content as a promising laboratory parameter for monitoring glucocorticoid therapy, similar to blood glucose for insulin. Some observations on glucocorticoid therapy in patients with SLE compared with changes in their blood tyrosine level which were earlier published only in Russian are presented, as well as the imaginary tyrosine-based monitoring of these cases.

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