Endocrine Abstracts

Aldosterone is a steroidal hormone that specifically binds to the mineralocorticoid receptor (MR). Production and secretion of aldosterone is triggered by changes in blood pressure (BP). Primary aldosteronism (PA) is an important cause of secondary hypertension. The effects of aldosterone have been described in renal and vascular tissue but recent studies have shown that MR is also expressed in non- epithelial cells such as those of the immune system. A 29-year-old Afro-Carribbean man was referred to clinic with treatment-resistant stage 2 hypertension and an elevated renin-aldosterone ratio. He was initially seen in cardiology clinic for palpitations, atypical chest pain and a BP 185/123 mmHg. Indapamide 2.5 mg daily was initiated. He had no history of headaches, dizziness, nausea or vomiting. Hypertension screen demonstrated an elevated aldosterone renin ratio (ARR) >1850. There were no features to suggest Cushing’s or acromegaly and no evidence of goitre although the patient complained of recent weight gain and symptoms suggestive of hypothyroidism. Thyroid function tests (TFTs) performed at his initial visit were consistent with primary thyroid disease (free thyroxine 9 pmol/l, thyroid stimulating hormone 27.52 Miu/l) necessitating treatment with levothyroxine 50 mcg twice daily. His BP control remained suboptimal and Doxazosin 2 mg twice daily was added. The patient was reviewed in 4 months at which point his BP had improved to 139/77 mmHg. A saline infusion test was suggestive of primary disease (baseline aldosterone 750 pmol/l with a 4 h aldosterone suppression result of 430 pmol/l). Magnetic resonance imaging of the adrenal glands showed no evidence of adrenal adenoma. Adrenal venous sampling indicated bilateral secretion of aldosterone. Repeat TFT’s on levothyroxine showed adequate replacement (TSH 5.37 Miu/l, free T3 5.6 pmol/l, free thyroxine 9.7 pmol/l) and very high titres of thyroid peroxidase antibodies 1579 u/Ml. The patient was started on Spironolactone 50 mg daily. Autoimmune diseases are more common in women with a more Th2- predominant immune response, whereas a Th1 response and inflammation is usually more severe in men. Chronic thyroiditis is classified as a Th1 disorder. There has been evidence to suggest that mineralocorticoids have been strongly associated with the modulation of various cells of the immune system. This is the first reported case of PA in a man exacerbating the course of autoimmune thyroid disease. For patients presenting with PA, it would be wise to consider the possibility of coexistent autoimmune disease.