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Critical Care
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 ResearchThe relationship between gastric emptying, plasma cholecystokinin, and peptide YY in critically ill patientsNam Q Nguyen1,2 , Robert J Fraser2,3 , Laura K Bryant3 , Marianne J Chapman4 , Judith Wishart2 , Richard H Holloway1,2 , Ross Butler5 and Michael Horowitz2  1
Department of Gastroenterology and Hepatology, Royal Adelaide Hospital, North Terrace, Adelaide, South Australia, 5000 2
Discipline of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, South Australia, 5000 3
Investigation and Procedures Unit, Repatriation General Hospital, Daw Road, Adelaide, South Australia, 5000 4
Department of Anaesthesia and Intensive Care, Royal Adelaide Hospital, Adelaide, South Australia, 5000 5
Centre for Paediatric and Adolescent Gastroenterology, Children, Youth and Women's Health Service, Adelaide, South Australia, 5000 author email corresponding author email
Critical Care 2007,
11:R132doi:10.1186/cc6205
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| Published: |
21 December 2007 |
Abstract
Background
Cholecystokinin (CCK) and peptide YY (PYY) are released in response to intestinal nutrients and play an important physiological role in regulation of gastric emptying (GE). Plasma CCK and PYY concentrations are elevated in critically ill patients, particularly in those with a history of feed intolerance. This study aimed to evaluate the relationship between CCK and PYY concentrations and GE in critical illness.
Methods
GE of 100 mL of Ensure® meal (106 kcal, 21% fat) was measured using a 13C-octanoate breath test in 39 mechanically ventilated, critically ill patients (24 males; 55.8 ± 2.7 years old). Breath samples for 13CO2 levels were collected over the course of 4 hours, and the GE coefficient (GEC) (normal = 3.2 to 3.8) was calculated. Measurements of plasma CCK, PYY, and glucose concentrations were obtained immediately before and at 60 and 120 minutes after administration of Ensure.
Results
GE was delayed in 64% (25/39) of the patients. Baseline plasma CCK (8.5 ± 1.0 versus 6.1 ± 0.4 pmol/L; P = 0.045) and PYY (22.8 ± 2.2 versus 15.6 ± 1.3 pmol/L; P = 0.03) concentrations were higher in patients with delayed GE and were inversely correlated with GEC (CCK: r = -0.33, P = 0.04, and PYY: r = -0.36, P = 0.02). After gastric Ensure, while both plasma CCK (P = 0.03) and PYY (P = 0.02) concentrations were higher in patients with delayed GE, there was a direct relationship between the rise in plasma CCK (r = 0.40, P = 0.01) and PYY (r = 0.42, P < 0.01) from baseline at 60 minutes after the meal and the GEC.
Conclusion
In critical illness, there is a complex interaction between plasma CCK, PYY, and GE. Whilst plasma CCK and PYY correlated moderately with impaired GE, the pathogenetic role of these gut hormones in delayed GE requires further evaluation with specific antagonists. |