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  • Title: The relationship between gastric emptying, plasma cholecystokinin, and peptide YY in critically ill patients.
    Author: Nguyen NQ, Fraser RJ, Bryant LK, Chapman MJ, Wishart J, Holloway RH, Butler R, Horowitz M.
    Journal: Crit Care; 2007; 11(6):R132. PubMed ID: 18154642.
    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.
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