Non-Functioning Pituitary Macroadenoma Leading to Secondary Adrenal Insufficiency and Exacerbated SIADH With Severe Symptomatic Hyponatremia: A Complex Endocrine Case

Document Type

Conference Proceeding

Publication Date

10-2025

Publication Title

Journal of the Endocrine Society

Abstract

Introduction: Non-functioning pituitary adenomas (NFPAs) are benign adenohypophyseal tumors without hormonal hypersecretion, accounting for 10-20% of intracranial tumors, and are discovered incidentally. NFPAs are classified by pituitary hormone and transcription factor expression to differentiate silent from null cell adenomas. Symptoms arise from mass effect, such as headaches, visual disturbances, and hormonal deficiencies including central hypogonadism, hypothyroidism, and adrenal insufficiency due to compression of the pituitary or stalk. Rarely, pituitary apoplexy presents initially. Electrolyte abnormalities like severe hyponatremia can occur, often due to SIADH driven by increased ADH in response to cortisol deficiency. This case illustrates SIADH and severe hyponatremia due to secondary adrenal insufficiency (SAI) from NFPA compression. Case: A 60-year-old female presented with nausea, weakness, headache, and peripheral vision loss. She was hypertensive with bitemporal hemianopsia on presentation. The laboratory studies showed Na of 110, glucose of 52, serum osmolality of 229, urine osmolality of 448, and urine Na of 41. Hormone profile showed FSH of 1.4, LH of 0.1, prolactin of 34.5 with no hook effect, IGF-1 < 15, TSH of 1.5, free T4 of 0.7, ACTH of 6, A.M. cortisol of 2.2, DHEA-S < 5—consistent with hypopituitarism. MRI showed a 3.1 x 2.9 x 2.7 cm sellar mass with suprasellar extension compressing the optic chiasm with invasion of cavernous sinuses. Treatment involved correction of hyponatremia with hypertonic saline requiring desmopressin and dextrose to slow correction, stress dose steroids, and levothyroxine. She underwent transsphenoidal resection with vision improvement and was discharged on hydrocortisone and Synthroid. Conclusion: Hyponatremia is a common electrolyte abnormality in adrenal insufficiency due to hypocortisolism. In secondary adrenal insufficiency (SAI), sodium levels are typically near normal, but this can vary due to the complex relationship between cortisol and antidiuretic hormone (ADH). Cortisol inhibits ADH; thus, in hypocortisolism, ADH increases in response to hypovolemia and CRH-mediated stimulation. Cortisol deficiency also heightens renal sensitivity to ADH by upregulating aquaporin-2 channels. Recognizing severe hyponatremia due to adrenal insufficiency is critical for timely glucocorticoid replacement. This case highlights SIADH as an exaggerated physiologic response to SAI from compressive effects of a nonfunctioning pituitary adenoma (NFPA).

Volume

9

Issue

Suppl 1

First Page

A767

Last Page

A767

Comments

ENDO 2025 Endocrine Society Annual Meeting, July12-15, 2025, San Francisco, CA

DOI

10.1210/jendso/bvaf149.1455

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