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Chronic intestinal ischaemia and Hirschsprung’s disease
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  • Published on:
    Reply to "Genetic mutations in Hirschprung's: cause or effect?"
    • Daniel B Hawcutt, Research fellow
    • Other Contributors:
      • Rebecca L. Venn, Richard M. Lindley, Simon E. Kenny.

    Dear Editor,

    The response by Fiddian-Green to our letter raises several interesting points that we would like to expand upon. He suggests that the well described mutations in enteric nervous system development genes we highlighted could be the result of ischaemia or decline in cellular energy charge [1].

    We do not believe this is the case, as the mutations in question are somatic (present in all cells...

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    Conflict of Interest:
    None declared.
  • Published on:
    Genetic mutations in Hirschprung's: cause or effect?

    Dear Editor,

    "Huge advances ..in understanding the molecular and genetic basis of Hirschsprung’s disease" have indeed been made in the past 13 years, as Hawcutt et al observe in their eLetter, but might not the specific mutations to which they refer all be the product of ischaemia and/or a decline in Daniel Atkinson energy charge? What too of the possibility of gene expression being dramatically changed by these me...

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    Conflict of Interest:
    None declared.
  • Published on:
    Response to “Chronic Intestinal Ischaemia and Hirschsprung’s Disease”
    • Daniel B Hawcutt, Research Fellow
    • Other Contributors:
      • Rebecca L Venn, Richard M Lindley, Simon E Kenny

    Dear Editor,

    The letter by R G Fiddian-Green [1] was accurate in reporting that there is evidence of prolonged carriage of Clostridium difficile in Hirschsprung’s disease (HSCR), and there may be abnormalities in the vasculature of the gut wall. However there is no evidence that these observations in themselves play a causative role in the pathogenesis of Hirschsprung’s disease. In the 13 years since the papers h...

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    Conflict of Interest:
    None declared.