Syndrome of inappropriate antidiuretic hormone secretion following immune effector cell–associated neurotoxicity syndrome during blinatumomab therapy: a case report

Background Blinatumomab (BLINA) causes immune-related toxicities, such as cytokine release syndrome and immune effector cell–associated neurotoxicity syndrome (ICANS). Although hyponatremia associated with interleukin (IL)-6–mediated vasopressin secretion has been reported with chimeric antigen receptor T-cell therapy, similar reports with bispecific antibodies are scarce. Case presentation A woman in her 60s with B-cell acute lymphoblastic leukemia developed grade 3 ICANS on day 3 of the second BLINA cycle. On day 13, the patient experienced grade 4 hyponatremia (serum sodium, 106 mmol/L). Treatment with 3% saline and tolvaptan improved symptoms. No other causes, such as central nervous system disease, adrenal insufficiency, or thyroid dysfunction, were identified. Based on the clinical findings and the exclusion of other etiologies, BLINA-induced syndrome of inappropriate antidiuretic hormone secretion (SIADH) was diagnosed. After confirming a decrease in IL-6 levels, tolvaptan was tapered and discontinued, and no recurrence of hyponatremia was observed. Conclusions BLINA may be involved in SIADH development, potentially via increased central IL-6 levels following ICANS treatment, which may promote arginine vasopressin secretion. In patients who develop ICANS during BLINA therapy, close monitoring of serum sodium levels may be a useful part of neurological assessment. If hyponatremia occurs, clinicians should promptly consider SIADH and initiate the appropriate management.