Article Text

Download PDFPDF

Rebuttal: ‘Obesity hypoventilation syndrome (OHS): does the current definition need revisiting?’
  1. Nicholas Hart1,
  2. Swapna Mandal1,
  3. Ari Manuel2,
  4. Babak Mokhlesi3,
  5. Jean-Louis Pepin4,
  6. Amanda Piper5,
  7. John Stradling6
  1. 1 Lane Fox Respiratory Unit, GSTFT and KCL Biomedical Research Centre, London, UK
  2. 2 Oxford Sleep Unit, Respiratory Department, Churchill Hospital, Oxford, UK
  3. 3 Medicine/Pulmonary & Crit Care, University of Chicago, Chicago, Illinois, USA
  4. 4 Laboratoire HP2, Hypoxie Physiopathologies, Université Joseph Fourier; INSERM U 1042, Grenoble Cedex 09, France
  5. 5 Respiratory Medicine, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia
  6. 6 Oxford Sleep unit, Oxford University Hospitals, Oxford, UK
  1. Correspondence to Dr Ari Manuel, Oxford Sleep Unit, Respiratory Department, Churchill Hospital, Oxford OX3 7LE, UK; ari.manuel{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

In response to the comments by Tulaimat and Littleton,1 we will clarify our original statement on ‘Obesity hypoventilation syndrome (OHS): does the current definition need revisiting?2 The two issues that these authors raise are curious and indeed re-enforce the statement we made previously, and we wholly appreciate this. We highlighted that the use of ‘calculated arterial standard bicarbonate (HCO3 ) level from a conventional blood gas machine, in the absence of another influence on metabolic acid-base status’ should be considered, and this is supported by Tulaimat and Littleton's comments. Additionally, we did not suggest removing obstructive sleep apnoea (OSA) from the definition of OHS, but rather, we wished to extend the definition, with a PaCO2 ≥45 mm  Hg (6 kPa) OR an arterial base excess >3 mmol/L OR a standard HCO3 >27 mmol/L (in the absence of another cause for a metabolic alkalosis). We agree that the phenotyping of such patients into OSA, combined OSA-OHS, and lone OHS, would be clinically useful and enhance the long-term management, but we did not necessarily address this in our original statement.3


View Abstract


  • Contributors All author contributed to the planning, conduct and reporting of the manuscript. JRS is responsible for the overall manuscript

  • Competing interests None.

  • Provenance and peer review Not commissioned; internally peer reviewed.

Linked Articles