MON-338 - Novel Case of Teclistamab-Associated Thyroiditis in A Patient with Multiple Myeloma

Introduction

Teclistamab, a bispecific antibody targeting BCMA and CD3, has significantly improved outcomes in relapsed/refractory multiple myeloma. However, endocrine immune-related adverse events are rare. We report, seemingly, the first case of thyroiditis associated with teclistamab therapy.

Case Description

An 85-year-old man with IgA κ multiple myeloma on teclistamab presented with weakness. He endorsed one month of nonproductive cough and a resolved sore throat two weeks prior, but he denied diarrhea, constipation, chest pain, palpitations, tremors, or weight loss. He last received his weekly scheduled teclistamab around two weeks prior, his fourth in total. His most recent scheduled dose was held given symptoms, new acute kidney injury, liver test abnormalities, and elevated c-reactive protein (CRP). Initial evaluation considered infection versus cytokine release syndrome due to recent immunotherapy exposure. Empiric pneumonia treatment was given, though infectious workup was negative.

Endocrinology was consulted for newly abnormal thyroid function tests: TSH < 0.05 (prior 1.02) and free FT4 2.8 . He had no personal or family history of thyroid disease. Thyroid peroxidase antibodies were negative, and thyroid ultrasound demonstrated homogeneity without nodules or hypervascularity. Findings were inconsistent with Graves’ disease. A low T3:T4 ratio (6.4) and elevated CRP supported a diagnosis of thyroiditis.

Given the low likelihood of sustained hormone overproduction, methimazole was held and beta-blockade was given for symptom control. Teclistamab was held indefinitely due to concern for immunotherapy-related immune dysregulation. The patient was started on IVIG for recurrent infections and post-teclistamab immunoparesis. Repeat thyroid studies in 3 months showed return to normal levels: TSH 1.31 and FT4 1.0.

Discussion / Conclusion

This case describes transient thyroiditis temporally associated with teclistamab, likely driven by early T-cell activation and cytokine release. Interestingly, BCMA-directed T-cell engager therapy has shown efficacy in refractory antibody-mediated autoimmune diseases, including Graves’ disease, through depletion of autoreactive plasma cells. In contrast, the thyroiditis observed here appears cytokine-mediated rather than autoantibody-driven, highlighting distinct immunologic effects of BCMA-targeted therapy. Although a recent upper respiratory illness raises consideration of post-viral thyroiditis, the timing during active teclistamab therapy, lack of neck pain or overt thyrotoxic symptoms, systemic immune dysregulation, and resolution after drug cessation support a drug-related effect. This case suggests endocrine toxicity may be a rare or underrecognized complication of teclistamab. Awareness of this association is important, as management is supportive, and prognosis is favorable.

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