Endocrine Abstracts

A 54-year-old female presented with muscle cramps and arterial hypertension. She was taking spironolactone 25 mg for hypertension. Her K+ level at first visit was 2.5 mmol/l. She was recommended to stop spironolactone, start potassium suplements, and measure Aldosterone, Renin, and K+ levels after 4 weeks. The Patient is a medical doctor. By her own decision CT of the abdomen was performed that showed 6.5 cm mass in left adrenal gland. The density was +28 HU. Some hypo-perfusion lesions were described in the liver. Full hormonal evaluation of the adrenal glands was performed. Metanephrines and cortisol were normal. Aldosterone – 25 ng/l (11.7–2236), Renin <1 ng/l (1.7–23.9), Aldosterone : Renin ration >25 (<20); It seemed tumor was secreting precursors of the aldosterone (deoxycorticosterone, corticosterone) and not the aldosterone itself. Testosterone – 0.66 (<0.41); Androstenedione – 5.6 (<0.82) 17(OH), Progesterone – 3.6 (<0.53); DHEA-Sulfate – 2.27 (0.5–5.5); At the same time patient was diagnosed with thyroid papillary microcarcinoma. She was advised to perform open surgery for adrenal mass and then thyroidectomy. However, she decided to undergo a simultaneous laparoscopic adrenalectomy and thyroidectomy with central prophylactic lymph node dissection. After surgery her potassium, adrenal androgens, renin, and aldosterone/renin ratio normalized. Postoperative MRI of the abdomen was unremarkable. On histologic examination, adrenal mass was 9×8×5 cm in size; Weiss score – 6; Ki67 – heterogeneous, up to 13% in hot spots. The thyroid nodule 0.5×0.4 cm – papillary carcinoma, follicular variant, sclerosing, infiltrative growth, with minimal ETE and focal lympho-vascular invasion. A total body 18F-FDG PET performed on 10/12/2019 was negative for pathologic uptakes. The stage of the ACC was defined as stage II, pT2pN0M0 low-to-intermediate risk of recurrence. The stage of PTC was defined as stage I, pT1apN0 M0, intermediate risk of recurrence, initial target TSH 0.1–0.5 IU/ml. Adjuvant therapy with mitotane and no RAI was recommended. Glucocorticoid replacement therapy (hydrocortisone 25 mg) was commenced simultaneously with mitotane treatment. The initial dose of mitotane was 500 mg uptitrated to 3000 mg. Mitotanemia measurement was recommended after 6–8 weeks from the initiation. Levothyroxine supressive therapy with 125 µg was prescribed. After 3 months TSH was fylly suppressed – 0.089, Tg – 0.5 (<0.2), anti-Tg <10 IU/ml. Neck US revealed a 5 mm round hypoechoic lymph node. Patient was recommended to adjust the dose of Levothyroxine to 112.5 µg and control of TSH, Tg, and Neck US in 2–3 months.