Abstract
Excess aldosterone is associated with the increased risk of
cardio-/cerebrovascular events as well as metabolic comorbidities
not only due to its hypertensive effect but also due to its proinflammatory
action. Autonomous cortisol secretion (ACS) in the setting of primary
aldosteronism (PA) is known to worsen cardiovascular outcome and potentially
exhibit immunosuppressive effects. The aim of this study was to determine
the impact of ACS status in patients with PA on kinetics of thyroid
autoantibodies (anti-TPO, anti-TG) pre and post therapy initiation.
Ninety-seven PA patients (43 unilateral, 54 with bilateral PA) from the
database of the German Conn’s Registry were included. Anti-TPO and
anti-TG levels were measured pre and 6–12 months post therapeutic
intervention. Patients were assessed for ACS according to their 24- hour
urinary cortisol excretion, late night salivary cortisol and low-dose
dexamethasone suppression test. Abnormal test results in line with ACS were
identified in 74.2% of patients with PA. Following adrenalectomy,
significant increases in anti-TPO levels were observed in patients with at
least one abnormal test (p = 0.049), adrenalectomized patients with
at least two pathological ACS tests (p = 0.015) and adrenalectomized
patients with pathologic dexamethasone suppression tests (p =
0.018). No antibody increases were observed in unilateral PA patients
without ACS and in patients with bilateral PA receiving mineralocorticoid
antagonist therapy (MRA). Our data are in line with an immunosuppressive
effect of mild glucocorticoid excess in PA on thyroid autoantibody titers.
This effect is uncovered by adrenalectomy, but not by MRA treatment.
Key words
primary aldosteronism - auto-immune disease - adrenalectomy - thyroid - cortisol secretion
- auto-antibodies