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SUN-082 Panhypopituitarism Due to Empty Sella Syndrome: An Overlooked Etiology of Hyponatremia

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Abstract Disclosure: J. Mulayamkuzhiyil: None. J. Joseph: None. J. Auguste: None. J. Ma: None. D. Yepez Romero: None. N.I. De Souza: None. Introduction: Severe hyponatremia as the presenting manifestation of Empty Sella Syndrome (ESS) is rare. We describe a case of severe hyponatremia due to secondary adrenal insufficiency resulting from panhypopituitarism caused by ESS. Case Presentation A 53-year-old female with a past medical history of hypertension and hypothyroidism presented with leg cramps and altered mental status. Vital signs were stable and physical examination was unremarkable. Lab results were significant for Sodium 118 mmol/L, BUN 13 mg/dL, Creatinine 0.9 mg/dL, TSH 3.49 mIU/mL, fT4 0.44 ng/dL, Serum osmolality 253 mOsm/kg, Urine osmolality 660 mOsm/kg, Urine sodium 161 mmol/L. The patient was on Levothyroxine 50 mcg at home, which was increased to 75 mcg due to a low fT4 level. The patient was treated with salt tablets, fluid restriction, 3% saline, and fludrocortisone. However, the hyponatremia was initially resistant to these measures, raising suspicion for a central cause. Further workup revealed hormonal deficiencies of FSH 3.0 mIU/mL, LH 0.4 mIU/mL, Estradiol <2 pg/mL, Prolactin 2.3 ng/mL, IGF-1 <10 ng/mL, Cortisol 2.72 µg/dL, ACTH 12 pg/mL. Patient was diagnosed with panhypopituitarism and started on IV hydrocortisone. This led to an improvement in the sodium level and the patient’s symptoms. An MRI of the brain revealed an empty sella with no evidence of any sellar or suprasellar mass, with a thin rim of enhancing pituitary glandular tissue along the floor of the sella, measuring 1.5 mm in thickness. An ACTH stimulation test was abnormal, with cortisol levels increasing to only 8.1 µg/dL at 60 minutes, suggesting secondary adrenal insufficiency. The patient was discharged home on oral hydrocortisone (10 mg QAM and 5 mg QHS), levothyroxine 75 mcg daily, fludrocortisone 100 µg daily, and salt tablets. Discussion: This case depicts severe hyponatremia as the presenting manifestation of Empty Sella Syndrome. ESS is characterized by the herniation of the subarachnoid space into the sella turcica, resulting in flattening of the pituitary gland and partial or complete filling of the sella with cerebrospinal fluid (CSF). Hyponatremia in this case could have easily been misdiagnosed as SIADH, given the low serum osmolality and high urine osmolality and sodium. Treatment resistance to standard measures used in treating SIADH prompted further investigation into central causes of adrenal insufficiency. Cortisol is a physiological inhibitor of ADH, and hypocortisolism due to low ACTH levels from the pituitary leads to inappropriate increases in ADH secretion causing euvolemic hypoosmolar hyponatremia. Treatment with glucocorticoids resolved the hyponatremia in this case. This case highlights the importance of considering secondary adrenal insufficiency due to empty sella syndrome as a potential etiology of severe hyponatremia, especially when it is resistant to standard SIADH treatments. Presentation: Sunday, July 13, 2025
Title: SUN-082 Panhypopituitarism Due to Empty Sella Syndrome: An Overlooked Etiology of Hyponatremia
Description:
Abstract Disclosure: J.
Mulayamkuzhiyil: None.
J.
Joseph: None.
J.
Auguste: None.
J.
Ma: None.
D.
Yepez Romero: None.
N.
I.
De Souza: None.
Introduction: Severe hyponatremia as the presenting manifestation of Empty Sella Syndrome (ESS) is rare.
We describe a case of severe hyponatremia due to secondary adrenal insufficiency resulting from panhypopituitarism caused by ESS.
Case Presentation A 53-year-old female with a past medical history of hypertension and hypothyroidism presented with leg cramps and altered mental status.
Vital signs were stable and physical examination was unremarkable.
Lab results were significant for Sodium 118 mmol/L, BUN 13 mg/dL, Creatinine 0.
9 mg/dL, TSH 3.
49 mIU/mL, fT4 0.
44 ng/dL, Serum osmolality 253 mOsm/kg, Urine osmolality 660 mOsm/kg, Urine sodium 161 mmol/L.
The patient was on Levothyroxine 50 mcg at home, which was increased to 75 mcg due to a low fT4 level.
The patient was treated with salt tablets, fluid restriction, 3% saline, and fludrocortisone.
However, the hyponatremia was initially resistant to these measures, raising suspicion for a central cause.
Further workup revealed hormonal deficiencies of FSH 3.
0 mIU/mL, LH 0.
4 mIU/mL, Estradiol <2 pg/mL, Prolactin 2.
3 ng/mL, IGF-1 <10 ng/mL, Cortisol 2.
72 µg/dL, ACTH 12 pg/mL.
Patient was diagnosed with panhypopituitarism and started on IV hydrocortisone.
This led to an improvement in the sodium level and the patient’s symptoms.
An MRI of the brain revealed an empty sella with no evidence of any sellar or suprasellar mass, with a thin rim of enhancing pituitary glandular tissue along the floor of the sella, measuring 1.
5 mm in thickness.
An ACTH stimulation test was abnormal, with cortisol levels increasing to only 8.
1 µg/dL at 60 minutes, suggesting secondary adrenal insufficiency.
The patient was discharged home on oral hydrocortisone (10 mg QAM and 5 mg QHS), levothyroxine 75 mcg daily, fludrocortisone 100 µg daily, and salt tablets.
Discussion: This case depicts severe hyponatremia as the presenting manifestation of Empty Sella Syndrome.
ESS is characterized by the herniation of the subarachnoid space into the sella turcica, resulting in flattening of the pituitary gland and partial or complete filling of the sella with cerebrospinal fluid (CSF).
Hyponatremia in this case could have easily been misdiagnosed as SIADH, given the low serum osmolality and high urine osmolality and sodium.
Treatment resistance to standard measures used in treating SIADH prompted further investigation into central causes of adrenal insufficiency.
Cortisol is a physiological inhibitor of ADH, and hypocortisolism due to low ACTH levels from the pituitary leads to inappropriate increases in ADH secretion causing euvolemic hypoosmolar hyponatremia.
Treatment with glucocorticoids resolved the hyponatremia in this case.
This case highlights the importance of considering secondary adrenal insufficiency due to empty sella syndrome as a potential etiology of severe hyponatremia, especially when it is resistant to standard SIADH treatments.
Presentation: Sunday, July 13, 2025.

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