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SAT-047 Immunotherapy-Related Hypophysitis: A Case Report

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Abstract Disclosure: R.E. Sevilla: None. A. Aguilar-Garcia: None. E.G. Duran Perez: None. J.S. Calzada: None. Introduction: Immunotherapy-related hypophysitis is characterized by the deficiency of one or more anterior pituitary hormones, with or without involvement of the posterior pituitary. It is now recognized for its association with anti-PD1/PD-L1 immunotherapy, being more prevalent with combined therapy including anti-CTLA-4 agents.Case Report: A 67-year-old woman presented to the emergency department with holocranial headache, vomiting, somnolence, and the following vital signs: BP 70/36 mmHg, HR 55 bpm, Temp 36.3°C. Initial laboratory findings showed serum sodium of 109 mEq/L and glucose of 64 mg/dL, leading to the suspicion of an adrenal crisis, prompting the initiation of hydrocortisone treatment. Urinary sodium and osmolality levels were measured, yielding values of 32 mEq/L and 111.12 mOsm/kg, respectively. This prompted the evaluation of endocrine causes. Hormonal profile testing revealed TSH 0.6 mIU/mL, FT4 <0.4 ng/dL, cortisol 1.6 mcg/dL, ACTH 3.7 pg/mL, LH 0.25 U/L, and FSH 4.2 U/L, consistent with hypopituitarism. As part of the diagnostic workup, the patient’s medical history revealed acral melanoma stage IIIB treated with Ipilimumab and Nivolumab, receiving three cycles, with the last dose administered two months before the clinical presentation.A brain MRI was performed, showing no anatomical causes of hypopituitarism, leading to a diagnosis of immunotherapy-related hypophysitis. Treatment was adjusted with glucocorticoids and levothyroxine, achieving evident clinical improvement. The patient was discharged, and immunotherapy was resumed by the oncology team.At follow-up in the endocrinology clinic three months later, the patient was clinically stable but showed persistent hormonal levels consistent with adrenal insufficiency and central hypothyroidism. Permanent pituitary damage was considered, and hormonal replacement therapy was continued.Discussion: Immunotherapy-induced hypophysitis typically occurs within the first 8 to 12 weeks, as observed in this case, within the expected range after the last immunotherapy cycle. Only 0.5% of cases develop severe adrenal insufficiency. MRI is the diagnostic tool of choice, although up to one-third of cases show no abnormalities, as in this case. Conclusion: This case highlights the importance of prolonged endocrine monitoring in patients undergoing immunotherapy. Clinical and biochemical diagnosis was essential despite the absence of radiological findings. Early hormonal therapy improved the clinical condition, although permanent pituitary damage was established. Presentation: Saturday, July 12, 2025
Title: SAT-047 Immunotherapy-Related Hypophysitis: A Case Report
Description:
Abstract Disclosure: R.
E.
Sevilla: None.
A.
Aguilar-Garcia: None.
E.
G.
Duran Perez: None.
J.
S.
Calzada: None.
Introduction: Immunotherapy-related hypophysitis is characterized by the deficiency of one or more anterior pituitary hormones, with or without involvement of the posterior pituitary.
It is now recognized for its association with anti-PD1/PD-L1 immunotherapy, being more prevalent with combined therapy including anti-CTLA-4 agents.
Case Report: A 67-year-old woman presented to the emergency department with holocranial headache, vomiting, somnolence, and the following vital signs: BP 70/36 mmHg, HR 55 bpm, Temp 36.
3°C.
Initial laboratory findings showed serum sodium of 109 mEq/L and glucose of 64 mg/dL, leading to the suspicion of an adrenal crisis, prompting the initiation of hydrocortisone treatment.
Urinary sodium and osmolality levels were measured, yielding values of 32 mEq/L and 111.
12 mOsm/kg, respectively.
This prompted the evaluation of endocrine causes.
Hormonal profile testing revealed TSH 0.
6 mIU/mL, FT4 <0.
4 ng/dL, cortisol 1.
6 mcg/dL, ACTH 3.
7 pg/mL, LH 0.
25 U/L, and FSH 4.
2 U/L, consistent with hypopituitarism.
As part of the diagnostic workup, the patient’s medical history revealed acral melanoma stage IIIB treated with Ipilimumab and Nivolumab, receiving three cycles, with the last dose administered two months before the clinical presentation.
A brain MRI was performed, showing no anatomical causes of hypopituitarism, leading to a diagnosis of immunotherapy-related hypophysitis.
Treatment was adjusted with glucocorticoids and levothyroxine, achieving evident clinical improvement.
The patient was discharged, and immunotherapy was resumed by the oncology team.
At follow-up in the endocrinology clinic three months later, the patient was clinically stable but showed persistent hormonal levels consistent with adrenal insufficiency and central hypothyroidism.
Permanent pituitary damage was considered, and hormonal replacement therapy was continued.
Discussion: Immunotherapy-induced hypophysitis typically occurs within the first 8 to 12 weeks, as observed in this case, within the expected range after the last immunotherapy cycle.
Only 0.
5% of cases develop severe adrenal insufficiency.
MRI is the diagnostic tool of choice, although up to one-third of cases show no abnormalities, as in this case.
Conclusion: This case highlights the importance of prolonged endocrine monitoring in patients undergoing immunotherapy.
Clinical and biochemical diagnosis was essential despite the absence of radiological findings.
Early hormonal therapy improved the clinical condition, although permanent pituitary damage was established.
Presentation: Saturday, July 12, 2025.

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