Thyroid cysts: a new extra-adrenal site of aldosterone synthase expression and increased aldosterone content

Background The rapid re-accumulation of fluid following aspiration of thyroid cystic lesions suggests that active transport of sodium and water may be involved in volume regulation of these lesions. In this study we address the possibility that aldosterone may take part in this process.

Subjects and methods Thirty-one patients (29 women and two men), with a mean age of 52·7 ± 13·2 years (range: 27–77 years) underwent evaluation for thyroid nodules that had a sonographic cystic component. Cystic fluid obtained by FNA biopsy was sent for cytological examination and biochemical measurements. In 10 patients, material was collected for RNA extraction and determination of aldosterone synthase expression by RT-PCR amplification.

Results All lesions were benign, cystic, colloid nodules. Cyst fluid aldosterone levels as measured by routine radioimmunoassay (RIA) were elevated above the normal plasma levels in all but five patients. Mean aldosterone levels were 27·1 ± 22·9 ng/dl (SD) (range: 5·9–117·5 ng/dl). In contrast, cyst cortisol values were in the low, low normal serum range (6·2 ± 2·9 µg/dl, range: 0·2–10·2 µg/dl). Sodium, chloride and potassium levels were 137 ± 4·7 mEq/l, 98 ± 5 mEq/l and 4·9 ± 1·4 mEq/l, respectively. Plasma aldosterone levels were normal in all patients tested. To confirm these results, 12 samples were assayed after extraction and chromatography using a highly specific antibody. Cyst aldosterone levels in this group were elevated above the normal serum range in all but one patient (mean concentration: 24·5 ± 14·6 ng/dl, range: 8·72–40·1 ng/dl). In this group, 18(OH)B levels were within the normal plasma range (12–55 ng/dl) in all but one patient (34·9 ± 17 ng/dl). Furthermore, aldosterone synthase mRNA expression was found in aspirates of four of 10 patients.

Conclusions The increased aldosterone concentration and the presence of aldosterone synthase expression suggest that aldosterone may be locally produced and secreted in thyroid tissue. The pathophysiological implications of this finding remain to be established.