SUN-313 - Immune Checkpoint Inhibitor-Induced Thyroiditis with Dramaticbiphasic Thyroid Dysfunction during Durvalumab Therapy Formuscle Invasive Bladder Cancer

Background
Immune checkpoint inhibitors (ICI) are widely used across multiple
malignancies and are associated with immune mediated endocrine adverse
events, most commonly thyroid dysfunction. While ICI-induced thyroiditis is
well described with programmed cell death protein one inhibitors, fewer cases
have been reported with durvalumab, a programmed death ligand one inhibitor,
potentially leading to under recognition.

Case Presentation
A woman in her seventies with muscle invasive urothelial carcinoma received
neoadjuvant gemcitabine, split-dose cisplatin, and durvalumab beginning in
2025. Baseline thyroid function was normal. Within four weeks of
immunotherapy initiation, she developed symptomatic thyrotoxicosis with heat
intolerance and palpitations, accompanied by suppressed TSH ≤0.01 µIU/mL
and peak FT4 3.45 ng/dL, FT3 4.57 pg/mL. Thyroid peroxidase antibodies
720.7 IU/mL, thyroid stimulating immunoglobulin 1.80 IU/L, and TSH receptor
antibodies 2.12 IU/L. Despite autoantibody positivity, radioactive iodine uptake
was low, supporting ICI-induced destructive thyroiditis rather than Graves
disease. Symptomatic treatment with beta adrenergic blockade was initiated,
and durvalumab was continued. Over subsequent weeks, thyroid function
rapidly transitioned to severe hypothyroidism with TSH >46.0 µIU/mL and FT4
0.30 ng/dL, necessitating levothyroxine replacement. The patient completed
neoadjuvant therapy, underwent definitive surgical management, and resumed
adjuvant durvalumab with stable thyroid function.

Discussion
This case demonstrates the marked and rapid biochemical variability of
thyroiditis, including severe thyrotoxicosis followed by profound
hypothyroidism. It underscores the importance of serial thyroid monitoring and
endocrine involvement to allow safe continuation of life-prolonging
immunotherapy without unnecessary interruption.

Conclusion & Learning Points
●Autoantibody positivity does not reliably distinguish Graves disease
from destructive thyroiditis
●Symptomatic management and close biochemical monitoring often
allow continuation of life saving immunotherapy
●Early endocrine involvement prevents unnecessary treatment delays
and optimizes outcomes

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