27%, p 0.0001) has been demonstrated. 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 BMS-794833 treatment. strong class=”kwd-title” Key words: primary aldosteronism, auto-immune disease, adrenalectomy, thyroid, cortisol secretion, auto-antibodies Introduction Primary aldosteronism (PA) represents the leading cause of endocrine hypertension 1 , accounting for 5C10% of all cases. Simultaneously, it is the most common endocrine form of hypertension that can be cured by surgery 2 . A large body of evidence exists implicating the increased risk of cardio- and cerebrovascular events as well as metabolic comorbidities in patients with aldosterone excess compared to patients with essential hypertension 3 4 5 . Interestingly, studies have suggested that the above mentioned complications are not only due to the hypertensive effect of excessive aldosterone but are also mediated by its proinflammatory action 6 . Recently, emphasis has been made on the effects of glucocorticoid co-secretion in the setting of PA revealing a higher incidence of metabolic syndrome and type 2 diabetes mellitus due to impaired insulin secretion 7 and insulin-sensitivity 8 further worsening the cardiovascular and metabolic burden in PA. Recent studies have investigated the implication of aldosterone in the development and/or progression of autoimmune disorders, as aldosterone is associated with the activation of circulating immune cells, reduced by mineralocorticoid receptor antagonists (MRA) 9 . Autoimmune thyroiditis also known as Hashimotos thyroiditis represents one of the most common disorders in the Rabbit Polyclonal to DNA Polymerase alpha general population, especially in women, with the incidence estimated at 3.5 cases/1000 women per year 10 11 . In the setting of autoimmunity, Hashimotos thyroiditis is characterized by the presence of specific autoantibodies (most specifically anti-TPO) 10 and by a lymphocytic infiltration 10 11 . In this study, we investigated the kinetics of anti-thyroid peroxidase (anti-TPO) and thyroglobulin antibody (anti-TG) in patients with primary aldosteronism and evaluated BMS-794833 the extent of concomitant autonomous cortisol secretion (ACS) on said antibodies pre- and post-therapy initiation. Patients and Methods Description of the patient cohort and diagnostic workup The study population consisted of 97 patients who were recruited at the Munich center of the German Conns Registry. The German Conns Registry is a multicenter-registry that investigates therapy, comorbidities and the long-term outcome in PA BMS-794833 patients throughout Germany since 2008 12 . The investigated cohort was studied between January 2014 and February 2019. The diagnosis of PA was established as stated in the Endocrine Society Practice Guidelines 2 . Diagnosis was established initially during screening by an elevated blood pressure (BP) and an elevated plasma aldosterone/renin ratio (ARR) (cutoff: 12.0 ng/U sitting position) 13 followed by an abnormal confirmatory test (saline infusion and/or captopril challenge test). Before conducting these tests (and complete testing for hypercortisolism) interfering antihypertensive medication was changed whenever possible ( 90% of patients). ACE inhibitors, beta blockers, central-alpha agonists, angiotensin receptor blockers (ARBs) were withdrawn for at least one week, and mineralocorticoid receptor antagonists (MRA) for at least four weeks prior testing. The diagnosis was then made on the basis of all clinical and laboratory findings. All patients in this study underwent adrenal venous sampling without cosyntropin stimulation as well as some form of adrenal imaging (computed tomography scanning or MRI) for subtype differentiation between unilateral and bilateral disease. The majority of patients ( 80%) had simultaneous bilateral adrenal BMS-794833 BMS-794833 venous sampling using a selectivity index of 2.0 and a lateralization index of 4.0 14 15 16 . All patients underwent complete testing for hypercortisolism, including 1 mg dexamethasone suppression test (DST), a 24-hour urinary free cortisol determination (UFC) and late.
