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due to the increasing importance of peripheral alpha-adrenoceptor stimulation once a maximal central effect has been reached. Differences in the sensitivities of central and peripheral alpha-adrenoceptors to clonidine have been reported." -13 Thus the balance of the evidence favours peripheral stimulation as the cause of drug resistance in patients on very high doses of clonidine. Our observations suggest that the use of high doses of clonidine may be associated with diminishing and not increasing hypotensive effects, and this should be borne in mind when the dose is being adjusted. SummaryThe relation between clinical and biochemical changes in thyrotoxicosis were studied in 12 patients with Graves's disease who were being treated with carbimazole. Clinical assessment (using the Crooks-Wayne index) was combined with the measurement of free thyroxine and triiodothyronine indices (FT4I and FT3I) and the assessment of two tissue markers of thyroid hormone actionsex-hormone-binding globulin (SHBG) levels and the thyrotrophin responses to TRH. In general the FT4I and FT3I fell rapidly once treatment was started, and returned to normal in one to four weeks, followed shortly by SHBG levels. The thyrotrophin response returned at this time in two patients, who still had borderline high levels of FT3I and SHBG. The clinical score fell more slowly and variably and was less closely related to any of the biochemical indices than these were to each other.During the early phase of treatment with antithyroid drugs the clinical evaluation may be an unreliable indicator of persisting thyroid hormone excess, and when the patient seems clinically but not biochemically thyrotoxic the symptoms should be treated on their own merits with beta-blocking drugs and not with increased doses of antithyroid drugs.