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Endocrine Abstracts (2025) 110 P50 | DOI: 10.1530/endoabs.110.P50

ECEESPE2025 Poster Presentations Adrenal and Cardiovascular Endocrinology (169 abstracts)

Pseudohypoaldosteronism in infantile atopic dermatitis: a case series

Aimee Jacquemot 1 , David Taylor 2 , Emily Derrick 3 & Ritika R Kapoor 4,5


1Evelina Children’s Hospital, Paediatric Nephrology, London, UK; 2King’s College Hospital NHS Foundation Trust, Department of Clinical Biochemistry (Synnovis), London, UK; 3University Hospital Lewisham, London, UK; 4Variety Children’s Hospital, King’s College Hospital NHS Foundation Trust, Department of Paediatric Endocrinology, London, UK; 5King’s College London, Faculty of Medicine and Life Science, London, UK


JOINT1137

Recent literature has highlighted a potential association between severe atopic dermatitis (AD) in infancy and biochemical disturbances resembling pseudohypoaldosteronism (PHA), though the mechanisms behind these disturbances remain poorly understood. We present a case series of three children, aged three to seven months, who were admitted with severe exudative eczema and were found to be hyponatraemic (sodium levels 115–129 mmol/l) and hyperkalaemic (potassium levels 6.3–7.4 mmol/l) on routine blood testing. Screening for PHA revealed elevated aldosterone levels with hyperreninaemia and increased urinary corticosterone and aldosterone metabolites providing further evidence of activation of the renin–angiotensin system (RAS). In each case, these biochemical and hormonal disturbances resolved after optimising dermatological and nutritional management of their atopic presentations. Trans-epidermal sodium loss driving volume depletion has commonly been hypothesised to determine both hyponatraemia and RAS activation in severe eczema, but direct evidence in support of this mechanism remains sparse. In all three cases, the patients exhibited low urinary sodium levels despite elevated aldosterone and renin, suggesting a compensatory response to hypovolaemia rather than renal tubular resistance to aldosterone. We also explore other potential contributing factors, including gastrointestinal protein and sodium loss due to increased permeability in the gastrointestinal tract, which is common in children with severe eczema and food allergies. Chronic inflammatory states associated with severe AD may also induce dilutional hyponatraemia and disrupt potassium handling in the kidneys. Furthermore, age-related factors such as low muscle mass and the physiological unresponsiveness to aldosterone in infancy may exacerbate electrolyte imbalances and complicate the clinical picture. This case series contributes to the sparse but growing body of literature on pseudohypoaldosteronism-like disturbances in severe infantile atopic dermatitis. The findings underscore the multi-system impact of severe eczema, highlighting the importance of considering not only dermatological management but also biochemical and hormonal factors in the comprehensive treatment of infantile AD. These cases reinforce the need for a holistic, multidisciplinary approach to early management in order to prevent severe complications, including electrolyte imbalances and nutritional deficiencies, that can arise in the context of this chronic inflammatory condition.

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

European Society of Endocrinology 
European Society for Paediatric Endocrinology 

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