SAT-110 Hypopituitarism and Diabetes Insipidus as Clinical Manifestations Leading to Sarcoidosis Diagnosis

Abstract Disclosure: T. Vega: None. J. Barbosa: None. S. Cruz: None. N. Aristizabal: None. C. Aguilar: None. J.L. Torres: None. S. Herrera: None. S. Osorio: None. Sellar and parasellar lesions can present with preoperative central diabetes insipidus (CDI) in 20% of cases, from which 70% are associated with adenohypophysis deficits. Even though neurosarcoidosis accounts for <3% of CDI cases, it can present with CDI in up to 55% of the cases and highlighting thoracic involvement in up to 70% of them. Here, we describe an unusual case of sarcoidosis presenting with hypopituitarism and CDI. A 28-year-old female without a past medical history, except for an inpatient visit for a parotitis episode in the previous semester, presented with 7 months of cephalea, vision changes, weight loss, and amenorrhea. She was referred for surgery after an MRI documented a mass-like structure above the hypophysis compressing the optic chiasm. Her labs from the previous month were compatible with hypogonadotropic hypogonadism, without any other hormonal imbalances. Nonetheless, pre-operative labs, were as follows: basal cortisol <1 ug/dl (3.7-19.4), FSH 0.58 mUI/ml (1.1-26.3), LH < 0.12 mIU/ml, estradiol <24 pg/ml, TSH 0.54 uUI/ml (0.4-4) T4L 0.75 ng/dl (0.8-2) and IGF-1 58.17 ng/ml (107.8-246.7) indicating hypopituitarism. In addition, she had hyperprolactinemia, (prolactin 98.16 ng/ml (0-25)), assumed to be secondary to the stalk effect, after a negative dilution test (1:100 107.55 ng/ml), which ruled out a hook effect. During inpatient care, she developed polydipsia, polyuria, (urine outputs around 6L per day) and hypernatremia (149.8 meq/L), whereby CDI was diagnosed, and treatment with sublingual desmopressin started. Considering a pituitary adenoma rarely causes CDI, a multidisciplinary board decided to biopsy through transsphenoidal surgery. Pathology showed infundibuloneurohypophysitis, dismissing lymphocytic etiology, lacking fibrosis suggestive of IGG-4 disease, or any other specific features leading to a precise etiology. Additional findings in a second MRI included pituitary stalk thickening, hypothalamic, pachymeningeal and VI cranial pair enhancement, and residual bilateral parotitis. After these results, a systemic cause was presumed, and a PET/CT was ordered, revealing mediastinal lymph node enlargement with abnormally increased metabolism. Pathology from mediastinoscopy reported chronic non-necrotizing granulomatous inflammation, and after ruling out tuberculosis infection, probable sarcoidosis was diagnosed. Pulse steroid therapy was started with subsequent treatment with prednisone and methotrexate. Conclusion: In patients presenting with hypophysitis and CDI, we suggest a chest-CT as part of the initial diagnosis line-up, looking for signs suggestive of sarcoidosis as in the above reported case, or other etiologies such as metastasis from lung or breast carcinoma, lymphoproliferative diseases, or other granulomatous disease, that may alter the interventions to follow. Presentation: Saturday, July 12, 2025