Endocrine Abstracts

Introduction: The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is characterized by hypotonic and euvolemic hyponatremia along with urinary hyperosmolarity, resulting from antidiuretic hormone (ADH) release in the absence of adequate stimuli.

Case report: A 59-year-old woman, presented with complaints of constant thirst, general weakness, memory loss, episodes accompanied by headaches, leg cramps, increased blood pressure. From the anamnesis-for the first time hyponatremia 114-123 mmol/l (135-145), was revealed during hospitalization for fainting 5 years ago, this episodes repeated several times a year. At the same time, a pituitary non-active macroadenoma of 22*12*9 mm (Knosp 2) was found, without indications for surgical treatment during yearly observation by MRI. All diagnostic criteria for SIADH were met in the form of repeatedly confirmed hypotonic hyponatremia with urine osmolality exceeding the blood plasma osmolality (412-520 mOsm/kg), and normal urinary sodium excretion of 92-162 mmol/l and GFR> 60 ml/min. Hypothyroidism and adrenal insufficiency were excluded. Cardiac, hepatic and renal functions were normal. Medications included azilsartan 40 mg and amlodipine 5 mg. To search for the source of a possible ADH-secreting tumor, an oncological search was performed with ultrasound of the thyroid gland, abdominal cavity, CT of the lungs with contrast, gastro- and colonoscopy. She also underwent PET/CT ‘whole body’ with 68Ga-DOTATATE, according to which no pathological formations were detected. According to the results of which, a node of the right lobe of the thyroid gland 11 x 10 mm was revealed, with a fine-needle aspiration biopsy - Bethesda II. Drinks about 2000 ml (of which 300-400 ml is 0.9% saline), releases 1700-1800 ml of urine per day. Copeptin (Phoenix) -1.659 ng/ml (0.178-2.578 ng/ml), Oxytocin (BMA Biomedicals) -2.668 ng/ml (0-12.821 ng/ml), Apelin-12 (Phoenix) -2.026 ng/ml (0.620-2.095 ng/ml), BNP (RayBiotech)-981.63 pg/ml (646.3-2033.4 pg/ml). Since the synthesis of ADH occurs in the nuclei of the hypothalamus, and the hormone is only stored and secreted in the posterior lobe of the pituitary gland, then the pituitary adenoma per se presumably cannot be a source of ADH (the patient refused the proposed adenectomy).

Conclusions: The modern diagnostic arsenal is not sufficient to identify the source of inadequate secretion of ADH. Fluid restriction and oral saline administration are effective and well tolerated long-term therapeutic interventions.