Bilateral Adrenal Adenomas in the Presence of Primary Aldosteronism
Presentation Number: SAT 375
Date of Presentation: April 1st, 2017
Min Ji Kim*, Eun Yeong Mo, Sung Dae Moon, Eun Sook Kim and Je Ho Han
Incheon St. Mary’s Hospital, The Catholic University of Korea, Incheon, Korea, Republic of (South)
Primary aldosteronism is mainly caused by either unilateral aldosterone-producing adenoma (APA) or bilateral adrenal hyperplasia (BAH). Usual diagnostic approaches in patients with primary aldosteronism are focused on differentiating unilateral APA and BAH. Bilateral adrenal cortical adenomas in the setting of primary aldosteronism are very rare, but possible.
A 48-year-old man was referred to our hospital with hypokalemia and poorly controlled hypertension despite four antihypertensive medications. Physical examination showed blood pressure of 180/100 mmHg. The serum potassium level was 3.0 mEq/L, arterial blood gas analysis revealed metabolic alkalosis. The Plasma aldosterone concentration (PAC) was 57.62 ng/dL (normal 1.3 to 14.5), and the Plasma rennin activity (PRA) was 0.26 ng/mL/hr (normal 0.32 to 1.84) with a calculated aldosterone to renin ratio was 221.6. Intravenous saline infusion test for confirmation failed to suppress plasma aldosterone level signiﬁcantly (pre-infusion PAC: 35.9 ng/dL, post-infusion PAC: 58.5 ng/dL), consistent with a primary aldosteronism. Upright posture for 240 minutes suppressed plasma aldosterone concentration. (Basal PAC: 50.1 ng/dL, after upright PAC: 38.7 ng/dL). Abdomen computed tomography (CT) demonstrated a 1.5 cm sized right adrenal mass and a 1.2 cm sized left adrenal mass both with less than 10 Hounsfield unit (HU) on pre-contrast image. The adrenal venous sampling was performed and revealed the following adrenal vein - inferior vena cava (IVC) ratio of cortisol was greater than 10, right - left adrenal vein ratio of aldosterone - cortisol ratio was 5.56, left adrenal vein - IVC ratio of aldosterone - cortisol ratio was 0.64. Although the right-sided hyper-functioning mass was suspected in the adrenal vein sampling, we planned to explore both adrenal glands due to discrete masses were existed on both adrenal glands on CT. Right total adrenalectomy and left partial adrenalectomy were performed by laparoscopic approach. The pathology confirmed the bilateral adrenal cortical adenomas with marked cytologic atypia and the sections from both sides shared a nearly identical appearance. 7 days after surgery, laboratory finding showed the normal basal PAC of 0.68 ng/dL, after intravenous saline infusion PAC was 0.23 ng/Dl and PRA was 0.2 ng/ml/hr. 14 Days after surgery, the patient was normotensive (130/80 mmHg) on a calcium channel blocker and a angiotensin ll receptor blocker (Nefidipine 90 mg, fimasartan 30 mg a day), and the serum potassium was 4.5 mEq/L without any potassium supplement.
In this case, unilateral hyperfunction was suspected in the adrenal vein sampling, but bilateral adrenal adenomas was presented on the CT and then confirmed by pathology. Clinicians should consider the possibility of bilateral adenomas in diagnosis and treatment with primary aldosteronism.
Nothing to Disclose: MJK, EYM, SDM, ESK, JHH