Endocrine Abstracts

Background: Clinically relevant pituitary adenomas (Pit PA) affect approximately 1:1200 of the general population, and may manifest with hormone hypersecretion, hypopituitarism and compression of the visual pathways. Primary aldosteronism (Adr PA) is now recognised to account for 5–14% of all cases of hypertension and is associated with excess morbidity when compared with primary hypertension. Here, we report a patient who was noted to have a history suggestive of Adr PA whilst being investigated for Pit PA.

Case: A 45-year-old man attended his primary care physician with a 6-month history of reduced sexual function. Laboratory investigation demonstrated partial hypogonadotrophic hypogonadism [LH 2.6 U/l (RR 1.5–9.3); FSH 8.8 U/l (RR 1.4–18.1); total testosterone 6.7 nmol/l (RR 7.2–31.3)], with associated mild hyperprolactinaemia [prolactin 719 mU/l (RR 45–375)] and possible partial central hypothyroidism [Free T4 10.3 pmol/l (RR 10.5–21.0); TSH 0.7 mU/l (RR 0.35–5.5)]. Serum cortisol was normal with no evidence of Cushing’s syndrome clinically or biochemically (UFC 42 nmol/24 h; LNSC 0.5 and 0.9 nmol/l) Serum calcium was normal. Formal visual field testing with perimetry showed a left temporal defect, and subsequent pituitary MRI revealed a 34×26×19 mm macroadenoma with suprasellar extension. Whilst being investigated for Pit PA, parallel investigations were initiated for suspected Adr PA based on the patient’s history of hypertension (treated with amlodipine) and unprovoked hypokalaemia. Plasma renin concentration (PRC) was low (3 mU/l), which coupled with a plasma aldosterone concentration (PAC) of 790 pmol/l, yielded a markedly raised aldosterone: renin ratio (263.3). Adrenal MRI demonstrated a possible nodule in the body of the left adrenal gland, with thickening of the medial limb; the right adrenal appearances were unremarkable. Subsequent ACTH-stimulated adrenal vein sampling (AVS) indicated a bilateral origin of PA (Ttable 1): The patient was changed to mineralocorticoid receptor antagonist (MRA) therapy with good control of blood pressure and correction of hypokalaemia. At trans-sphenoidal surgery, a macroadenoma was resected, with immunohistochemistry showing positivity for FSH. Transcription factor expression is negative. Genetic screening for a familial syndrome is awaited.

Conclusions: Although, the co-occurrence of Pit PA and Adr PA in our patient may represent a simple coincidence, the possibility that they are linked [either through an underlying genetic predisposition (e.g., MEN1) or a novel pathophysiological pathway (as previously proposed for macroprolactinomas and Adr PA – Williams et al., JCEM, 2015)] remains.