MON-009 - An Atypical Presentation of Arginine Vasopressin Deficiency Secondary to Partial Empty Sella Syndrome in the Setting of COVID-19-Associated Multifocal Pneumonia and Hypopituitarism

Arginine vasopressin deficiency (AVP-D) results from impaired synthesis or release of arginine vasopressin from the posterior pituitary gland, causing inability to concentrate urine and subsequent polyuria, polydipsia, and hypernatremia. Early recognition is essential, particularly in hospitalized patients with persistent hypernatremia.

We report a 71-year-old man with prednisone-dependent pulmonary sarcoidosis and hypothyroidism admitted with acute hypoxic respiratory failure due to COVID-19 associated multifocal pneumonia. During hospitalization, he developed progressive hypernatremia from 148 to 157 mmol/l (135-145) despite hypotonic intravenous fluids. Serum osmolality was elevated at 333 mOsm/kg (275-295). Urine studies showed inappropriately dilute urine with specific gravity 1.007 (1.005-1.030), urine osmolality 214 mOsm/kg (300-900), and urine sodium 24 mmol/L ( < 20), consistent with hypotonic polyuria concerning for AVP-D. There was no lithium exposure or other causative medication use.

A modified water deprivation protocol was performed. Baseline testing revealed serum sodium 151 mmol/L with urine osmolality 128 mOsm/kg. Following intravenous desmopressin (DDAVP) 2 mcg, urine osmolality increased to 326 mOsm/kg within two hours, with improvement in serum sodium to 144 mmol/L, indicating adequate renal sensitivity. Copeptin was < 2 pmol/L ( < 2.6), confirming AVP deficiency. Clinically, thirst and polyuria improved.

Brain MRI demonstrated a partially empty sella without pituitary adenoma, mass lesion, or granulomatous disease. Given the underlying sarcoidosis, neurosarcoidosis was considered but deemed unlikely after a multidisciplinary review due to the absence of radiographic CNS involvement. Comprehensive pituitary evaluation demonstrated hypopituitarism, including secondary hypothyroidism, hypogonadotropic hypogonadism, growth hormone deficiency, and secondary adrenal insufficiency. Despite transient correction with fluids, hypernatremia recurred and stabilized only with scheduled DDAVP therapy, confirming AVP-D.

AVP-D is uncommon in empty sella syndrome and occurs less frequently than anterior pituitary hormone deficiencies. Hypopituitarism affects approximately 34-52% of patients, most commonly involving gonadotropins and growth hormone. In partial empty sella, milder hormonal dysfunction is present. AVP-D may be unmasked after glucocorticoid replacement, as cortisol enhances renal free water clearance.

This case highlights AVP-D in the setting of partial empty sella syndrome and hypopituitarism with COVID-19 infection as a potential contributing factor. Emerging literature suggests hypothalamic-pituitary injury from viral invasion, immune-mediated hypophysitis, or vascular mechanisms, although this remains rare. Dynamic testing remains essential to establish the diagnosis and guide therapy.

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