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• W2938656383 abstract "Abstract Background Infants with atopic dermatitis who developed hyponatremia and hyperkalemia with raised aldosterone have been repeatedly described in the Japanese‐language literature, but similar reports from other countries are scarce. Methods We collected reports of atopic dermatitis complicated with hyponatremia (≤130 mE q/L), written either in English or in Japanese, to delineate the characteristics and to elucidate the pathophysiology of this condition. Results Of a total of 36 patients, 35 were Japanese. All patients were infants younger than 9 months. Mean height SD score ( SDS ) at presentation was −2.1 ± 1.4 ( n = 25), with mean body mass index 14.1 ± 1.7 kg/m 2 ( n = 28). Mean sodium was 120.7 ± 6.1 mE q/L. While 28 patients had hyperkalemia, seven patients had normokalemia. Elevated aldosterone was documented in 15 patients. Nutrition mainly with breast‐feeding (97%), parental refusal of steroid ointment (77%), and the association of hypoalbuminemia (73%) were frequent findings. Diminished urinary sodium was verified in all 12 patients tested, indicating that sodium loss from the skin exudates, with limited supply of sodium from breast milk, is the primary cause of hyponatremia. Hyperkalemia seems to result from decreased delivery of sodium to the distal nephron and from the mechanism of the so‐called “aldosterone paradox”, which inhibits potassium secretion. In addition, physiological aldosterone insensitivity during infancy, low muscle volume, and impaired Na + ,K + ‐ ATP ase function due to protein deficiency seems to exaggerate the hyperkalemia. Conclusions Hyponatremia secondary to severe atopic dermatitis is an age‐dependent manifestation, elicited by inappropriate treatment that leads to sodium loss from the damaged skin and resultant hyperkalemia via multifaceted mechanisms." @default.
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• W2938656383 date "2019-06-01" @default.
• W2938656383 modified "2023-09-25" @default.
• W2938656383 title "Hyponatremia secondary to severe atopic dermatitis in early infancy" @default.
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• W2938656383 doi "https://doi.org/10.1111/ped.13865" @default.
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