# Thyroid and cortisol endocrinopathies and survival in cancer patients treated with immune checkpoint inhibitors in UAE

**Authors:** Mohamed Alqedra, Bara Fahmayee, Lina Wahba, Jawaher Ansari, Romona D Govender, Saif Al-Shamsi, Raya Almazrouei

PMC · DOI: 10.1210/jendso/bvag037 · Journal of the Endocrine Society · 2026-02-17

## TL;DR

This study found that thyroid and cortisol-related side effects in cancer patients treated with immune checkpoint inhibitors are linked to better survival rates.

## Contribution

The novel contribution is identifying a favorable survival trend associated with thyroid and cortisol endocrinopathies in ICI-treated cancer patients.

## Key findings

- Thyroid-related events were all post-thyroiditis hypothyroidism, and cortisol-related events were ACTH deficiency.
- Patients with endocrinopathies showed improved overall survival compared to those without.
- Endocrinopathies occurred most frequently in patients treated with anti–PD-1 agents.

## Abstract

Immune checkpoint inhibitors (ICIs) are associated with immune-related adverse events (irAEs) of which endocrinopathies are among the most frequent. This study aimed to identify thyroid and cortisol-related endocrine-related adverse events (ERAEs) in a cohort of patients treated with ICIs and to examine survival differences between patients who developed endocrinopathies and those who did not.

We conducted a retrospective review of electronic medical records of adult patients who received ICIs between 2018 and 2023. Data were collected specifically on thyroid and cortisol-related ERAEs.

Among 616 patients, 59 (9.6%) developed thyroid or cortisol-related ERAEs. The mean time to onset was 22.7 weeks. All thyroid-related events were post-thyroiditis hypothyroidism (n = 55), while all cortisol-related events were due to adrenocorticotropic hormone (ACTH) deficiency (n = 11). The majority of these events occurred in patients treated with anti–PD-1 agents, the most commonly used therapy in this cohort. Patients who developed ERAEs demonstrated improved overall survival during the follow-up period compared to those without endocrine toxicity.

In this cohort, systematic monitoring identified thyroid- and cortisol-related ERAEs in 9.6% of patients, consisting exclusively of post-thyroiditis hypothyroidism and ACTH deficiency. The occurrence of these endocrinopathies was associated with a favorable survival trend, underscoring the importance of early recognition and management of endocrine irAEs in patients receiving ICIs.

## Linked entities

- **Diseases:** cancer (MONDO:0004992)

## Full-text entities

- **Genes:** CTLA4 (cytotoxic T-lymphocyte associated protein 4) [NCBI Gene 1493] {aka ALPS5, CD, CD152, CELIAC3, CTLA-4, GRD4}, CD274 (CD274 molecule) [NCBI Gene 574058] {aka PDL1}, PDCD1 (programmed cell death 1) [NCBI Gene 100533201], CD274 (CD274 molecule) [NCBI Gene 29126] {aka ADMIO5, B7-H, B7H1, PD-L1, PDCD1L1, PDCD1LG1}, POMC (proopiomelanocortin) [NCBI Gene 5443] {aka ACTH, CLIP, LPH, MSH, NPP, OBAIRH}, PDCD1 (programmed cell death 1) [NCBI Gene 5133] {aka ADMIO4, AIMTBS, CD279, PD-1, PD1, SLEB2}, CTLA4 (cytotoxic T-lymphocyte associated protein 4) [NCBI Gene 397286]
- **Diseases:** glucocorticoid deficiency (MESH:C565974), anterior pituitary disorders (MESH:D010900), died (MESH:D003643), Post-thyroiditis hypothyroidism (MESH:D007037), ERAE (MESH:D002318), endocrinopathies (MESH:C567425), post (MESH:D000094025), endocrine toxicities (MESH:D004700), Thyroid and cortisol endocrinopathies (MESH:C535280), Thyroid dysfunction (MESH:D013959), type 1 diabetes (MESH:D003922), dysfunction (MESH:D006331), gonadal abnormalities (MESH:D006058), renal cell carcinoma (MESH:D002292), melanoma (MESH:D008545), hypophysitis (MESH:D000072659), ACTH deficiency (MESH:C535668), Lung cancer (MESH:D008175), Diabetes mellitus (MESH:D003920), adrenal insufficiency (MESH:D000309), Cancer (MESH:D009369), autoimmune toxicities (MESH:D001327), hyperthyroidism (MESH:D006980), Subclinical hypothyroidism (MESH:D058345), post-thyroiditis (MESH:D013966), hypoparathyroidism (MESH:D007011)
- **Chemicals:** FT4 (-), T4 (MESH:D013974), TSH (MESH:D013972), pembrolizumab (MESH:C582435), steroid (MESH:D013256), durvalumab (MESH:C000613593), nivolumab (MESH:D000077594), cortisol (MESH:D006854), atezolizumab (MESH:C000594389), ipilimumab (MESH:D000074324)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

22 references — full list in the complete paper: https://tomesphere.com/paper/PMC12954486/full.md

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Source: https://tomesphere.com/paper/PMC12954486