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Endocrine Abstracts (2025) 110 EP1168 | DOI: 10.1530/endoabs.110.EP1168

1Royal Children’s Hospital, Department of Endocrinology and Diabetes, Melbourne, Australia; 2Murdoch Children’s Research Institute, Melbourne, Australia.


JOINT1587

A 25 year-old woman with childhood onset panhypopituitarism after surgery, cranial radiation and chemotherapy for a midline germinoma presented to a rural hospital in a low-middle income country with acute confusion and vomiting, which occurred during attendance at a party. Despite administration of appropriate parenteral stress dosing of glucocorticoids by her friend, improvement did not occur. Assessment suggested a presumptive diagnosis of gastroenteritis. She was initially managed with crystalloid intravenous fluid resuscitation, without recognition of her diabetes insipidus (DI). Serum sodium was reported as 114 mmol/L. Contact was made with an endocrinologist who advised cessation of intravenous fluids. With fluid restriction, hyponatraemia, confusion and vomiting resolved. Throughout her presentation she remained afebrile, had no diarrhoea, nor any other infective symptoms and recovered rapidly. On return home she subsequently stated that she thought her "drink may have been spiked". Although the evidence is presumptive that ingestion of 3,4-methylenedioxymethamphetamine (MDMA) is likely to have been involved, the case is important in that it demonstrates potential hazards that need to be navigated when negotiating transition to adult care for young adults who have complex disorders, and the need for awareness of drug and alcohol interactions that may have potentially catastrophic outcomes if not recognized. There have been multiple reports of hyponatraemia in MDMA users since it was first described in 1993, predominantly affecting females. To our knowledge, there are no reported cases of hyponatraemia following MDMA use in patients with DI. The mechanism for hyponatraemia following MDMA ingestion is thought to be multifactorial with proposed mechanisms including syndrome of inappropriate anti-diuretic hormone release; MDMA-induced polydipsia and dry mouth (with subsequent thirst and ingestion of hypotonic fluid); and recommendations to remain well-hydrated after MDMA use to counter-act the risk of dehydration from increased diaphoresis and hyperthermia all postulated as a possible contributors. In this case, the patient’s DI excludes SIADH as an aetiology for her hyponatraemia and parenteral glucocorticoid administration was adequate. In conclusion, the case demonstrates an absolute need for meticulous transitional care and adequate advice for young adults with complex health issues for clinicians, both paediatric and adult.

References: Baggott, M. et al., 2016. MDMA Impairs Response to Water Intake in Healthy Volunteers. Adv Pharmacol Sci. Campbell, G. et al., 2008. The agony of ecstasy: MDMA (3,4-methylenedioxymethamphetamine) and the kidney. Clinical J Am Soc Nephrol, 3(6), pp.1852-1860. Maxwell, D. et al., 1993. Hyponatraemia and catatonic stupor after taking "ecstasy". BMJ, Volume 307, p.1399.

Volume 110

Joint Congress of the European Society for Paediatric Endocrinology (ESPE) and the European Society of Endocrinology (ESE) 2025: Connecting Endocrinology Across the Life Course

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