Oxcarbazepine (OXC) associated SIADH with adrenocortical insufficiency: learnings from a complex hyponatraemic case with multifactorial aetiology

Mohamed Yousif; David Otuonye; Justin Lim Yuan Shen; Kelly Pendle; Naik Haya; Zeenat Banu; Craig Parkinson; Duncan Fowler; Damian Morris; Sanjeev Sharma

doi:10.1530/endoabs.109.P200

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Endocrine Abstracts (2025) 109 P200 | DOI: 10.1530/endoabs.109.P200

SFEBES2025 Poster Presentations Neuroendocrinology and Pituitary (48 abstracts)

Oxcarbazepine (OXC) associated SIADH with adrenocortical insufficiency: learnings from a complex hyponatraemic case with multifactorial aetiology

Mohamed Yousif , David Otuonye , Yuan Shen Justin Lim , Kelly Pendle , Naik Haya , Zeenat Banu , Craig Parkinson , Duncan Fowler , Damian Morris & Sanjeev Sharma

Author affiliations

East Suffolk and North Essex NHS Foundation Trust, Ipswich, United Kingdom

Introduction: OXC is a commonly used anti-epileptic drug with a reported prevalence of 29.9% hyponatraemia due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). We present a case of a 49-year-old man with refractory epilepsy on OXC who developed severe hyponatraemia following unilateral radical nephrectomy 4 weeks prior for focal renal cell carcinoma.

Initial presentation: He presented with status epilepticus with serum sodium (sNa⁺) between 115-120mmol/l. Osmolality studies showed serum 250-262mOsm/kg and urine 328-546mOsm/kg suggestive of SIADH but atypically high urine sodium at 64-112mmol/l. Short Synacthen Test showed a suboptimal 30-minute rise of cortisol level (76 to 395 mmol/l; ACTH normal:22ng/l). Rest of endocrine milieu and MRI brain were unremarkable. Concomitant medications included OXC, Levetiracetam, Perampanel and Citalopram.

Management: Initial management included 1L/day fluid restriction and hydrocortisone. As sNa⁺ levels dropped (112 mmol/l), Citalopram was stopped and Fludrocortisone was added despite normal ACTH. Neurology was hesitant to stop OXC due to fear of precipitating seizures but sNa⁺ persisted between 115 -120mmol/L and hence Tolvaptan was started at 7.5 mg OD. The latter showed a rise of sNa⁺ but plateaued at <125mmol/l. Following neurology consultation, OXC was guardedly weaned down without recrudescence of epilepsy resulting in sNa⁺ rising to 130-140mmol/l. Once OXC was completely stopped, Tolvaptan was next weaned down completely with sNa⁺ remaining stable at 132-138mmol/l.

Learning Points: SIADH can be challenging especially if there are multiple contributing aetiologies. In this case, the effect of low sNa⁺ on precipitating seizures, reticence to stop OXC and adrenocortical insufficiency, all contributed to a complex interplay needing prolonged inpatient stay. This case highlights that clinicians should be alert to OXC side effects and such cases need complex MDT approaches to achieve the best clinical outcome.