Thereafter, the mitotane dose was tailored according to plasma levels. A progressive increase in plasma mitotane concentrations was observed during treatment, and a highly significant linear correlation was found between plasma drug levels and the total mitotane dose. Toxicity was manageable in all but one patient, who discontinued treatment. This approach is able to provide therapeutic mitotane concentrations and limit the unwanted effects. The present data provide a rationale to change the approach to mitotane treatment in patients with adrenocortical carcinoma from high dose to low dose regimens.
Adrenocortical carcinoma manifesting pure hyperaldosteronism is extremely rare.
Computed tomographic scan showed 4.5x5.3 cm lobulated mass with tiny calcification, while there was no significant uptake of 131I-iodomethyl norcholesterol in the tumor. This is the first report of a case of primary aldosteronism due to adrenocortical carcinoma, in which expression of all sets of steroidogenic enzymes required for aldosterone synthesis was proven. Distinction of adrenocortical carcinoma from benign adrenocortical lesions by standard criteria is often difficult. The only significant loss of material concerned the distal part of 9p. A subset of the CGH data was independently confirmed by interphase cytogenetics.