Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
Fever and syndrome of inappropriate antidiuretic hormone secretion in a patient with multiple system atrophy after treatment with duloxetine.
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Zhao Wen, Shi Jinyu, Sarma Anand Karthik, Lin Jianwen, Wang Cui, Xie Lushuang, Liu Yi
Аннотация
BACKGROUND: Multiple system atrophy (MSA) is a neurodegenerative disease that affects the extrapyramidal, cerebellar, and autonomic nervous systems. In some patients, hypothalamic involvement can lead to impaired thermoregulation and hyponatremia. Duloxetine, a serotonin-norepinephrine reuptake inhibitor used for chronic pain, has rarely been linked to fever and syndrome of inappropriate antidiuretic hormone secretion (SIADH).
CASE PRESENTATION: A 66-year-old man with clinically probable MSA and baseline hyponatremia (serum sodium 121.6 mmol/L) started duloxetine 30 mg/day for migrating pain. Within 24 h, he developed high fever (38.0-39.5 °C) without sweating, and serum sodium fell to 117 mmol/L despite oral sodium supplementation. Findings supported SIADH, with low plasma osmolality (269 mOsm/kg), inappropriately concentrated urine (404 mOsm/kg), and high 24-h urinary sodium (444.5 mmol). The infectious workup was largely unremarkable, and antibiotics did not improve either fever or hyponatremia. After duloxetine was discontinued, body temperature gradually returned to normal, sweating resumed, and serum sodium increased. He later developed aspiration-related pneumonia and died despite intensive care.
CONCLUSIONS: Duloxetine may trigger fever and worsen hyponatremia due to SIADH in patients with MSA, possibly by increasing hypothalamic stress. Duloxetine should be used cautiously in MSA, with close monitoring of temperature and serum sodium, particularly in patients with pre-existing hyponatremia or suspected hypothalamic involvement.
CASE PRESENTATION: A 66-year-old man with clinically probable MSA and baseline hyponatremia (serum sodium 121.6 mmol/L) started duloxetine 30 mg/day for migrating pain. Within 24 h, he developed high fever (38.0-39.5 °C) without sweating, and serum sodium fell to 117 mmol/L despite oral sodium supplementation. Findings supported SIADH, with low plasma osmolality (269 mOsm/kg), inappropriately concentrated urine (404 mOsm/kg), and high 24-h urinary sodium (444.5 mmol). The infectious workup was largely unremarkable, and antibiotics did not improve either fever or hyponatremia. After duloxetine was discontinued, body temperature gradually returned to normal, sweating resumed, and serum sodium increased. He later developed aspiration-related pneumonia and died despite intensive care.
CONCLUSIONS: Duloxetine may trigger fever and worsen hyponatremia due to SIADH in patients with MSA, possibly by increasing hypothalamic stress. Duloxetine should be used cautiously in MSA, with close monitoring of temperature and serum sodium, particularly in patients with pre-existing hyponatremia or suspected hypothalamic involvement.