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Critical care
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Transepithelial nasal potential difference in patients with, and at risk of acute respiratory distress syndrome
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  • Published on: 17 November 2022
    Reply to: CFTR dysfunction as a cause for increased epithelial sodium channel function in acute respiratory distress syndrome
    • Kiran Reddy, Clinical Research Fellow Queen's University Belfast
    • Other Contributors:
      • Rob MacSweeney, Consultant
      • Daniel F McAuley, Professor of Medicine

    We have read with interest the letter from Dr. Eisenhut in this issue of the Journal and thank him for his comments on our work. The theory regarding reduced Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) dysfunction in acute respiratory distress syndrome (ARDS) is interesting, though remains speculative at present. While some rationale exists to explain why transmembrane ion channels may be dysregulated in inflammation,1 we did not directly examine CFTR function in our original work.2 To test this hypothesis, direct augmentation of CFTR function during a nasal potential difference reading, or measurement of sweat chloride concentration, or another surrogate measure of CFTR function, would need to additionally be incorporated into our study design. We are not aware of any published studies of directly measured CFTR function in adults with ARDS.

    References

    1. Eisenhut M, Wallace H. Ion channels in inflammation. Pflugers Arch 2011; 461(4): 401-21.
    2. MacSweeney R, Reddy K, Davies JC, et al. Transepithelial nasal potential difference in patients with, and at risk of acute respiratory distress syndrome. Thorax 2021; 76(11): 1099-107.
    3. Davis PB, Del Rio S, Muntz JA, Dieckman L. Sweat chloride concentration in adults with pulmonary diseases. Am Rev Respir Dis 1983; 128(1): 34-7.

    Conflict of Interest:
    KR reports grants from the Wellcome Trust ICAT programme outside the submitted work.
    RM reports no competing interests.
    Outside the submitted work, DFM reports personal fees from consultancy for GlaxoSmithKline, Boehringer Ingelheim, Bayer, Novartis, SOBI and Eli Lilly, and from sitting on a DMEC for Vir Biotechnology and Faron Pharmaceuticals. In addition his institution has received funds from grants from the NIHR, Wellcome Trust, Innovate-UK and NI HSC R&D division as well as from Novavax and Randox. In addition, DFM has a patent issued to his institution for a treatment for ARDS. DFM was a Director of Research for the Intensive Care Society and is MRC/NIHR EME Programme Director. His spouse has received personal fees from the California Inst for Regenerative Medicine outside the submitted work.
  • Published on: 24 October 2022
    CFTR dysfunction as a cause for increased epithelial sodium channel function in acute respiratory distress syndrome

    MacSweeney et al. in their recent report of transepithelial nasal potential difference measurements in patients at risk of acute respiratory distress syndrome documented that the amiloride response of nasal respiratory epithelium was significantly greater in patients who progressed to develop ARDS compared to those who did not (1). It was also greater in patients who died with ARDS compared to survivors. This is consistent with an increased epithelial sodium channel function in patients at risk of ARDS and its associated mortality. We previously conducted nasal potential difference measurements in children with and without meningococcal septicemia associated pulmonary edema and controls on a Pediatric Intensive Care Unit (2). We found that the amiloride response was greater in patients with pulmonary edema compared to controls but this effect did not reach statistical significance which may have been due to the small number of patients we could enrol (n=4 with pulmonary edema, n=2 with septicemia without pulmonary edema and 8 controls) (2). Despite this small number of patients we found that the nasal potential response to a low chloride solution in patients with septicemia associated pulmonary edema compared to controls was significantly reduced indicating a concomitant dysfunction of respiratory epithelial chloride channels.
    It is known from in vitro studies that the epithelial sodium channel is inhibited by the Cystic Fibrosis Transmembrane Conductance Regulator (...

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    Conflict of Interest:
    None declared.