Abstract
Conflicts of interest: none declared. Madam, One of the key features of atopic dermatitis (AD) is increased transepidermal water loss (TEWL),1, 2 a phenomenon attributable partly to impaired barrier function of the skin due to some genetic defects such as filaggrin gene (FLG) mutations, or to inflammatory status in AD.1 Remarkable loss of body fluid would induce a series of systemic regulatory reactions. The functional antidiuretic hormone (ADH)–aquaporin (AQP)‐2 axis is a major regulatory system to keep water balance. AQP‐2 mediates water transport across the apical plasma membrane of the renal collecting ducts. Kidney AQP‐2 expression can be estimated quantitatively by urinary excretion of AQP‐2. Moreover, the amount of urinary AQP‐2 (u‐AQP‐2) is positively correlated with the plasma levels of ADH in normal subjects.3 Increased serum ADH was detected in severe AD, a result possibly due to a dehydrated state caused by increased TEWL in these patients.2 Therefore, it is possible that u‐AQP‐2 is altered in AD. We conducted a case–control study to measure the u‐AQP‐2 level in paediatric patients with AD, and assessed its correlation with several clinical and laboratory parameters.
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