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Plasma ghrelin and liquid gastric emptying in children with functional dyspepsia consistent with post‐prandial distress syndrome
Author(s) -
Hijaz N. M.,
Friesen C. A.,
Schurman J. V.,
Pearce R. E.,
AbdelRahman S. M.
Publication year - 2015
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/nmo.12591
Subject(s) - ghrelin , gastric emptying , medicine , endocrinology , ingestion , post prandial , meal , gastroenterology , irritable bowel syndrome , abdominal pain , chemistry , stomach , hormone , diabetes mellitus
Background Adult studies indicate a role for ghrelin in functional dyspepsia ( FD ) mediated through ghrelin's effect on gastric emptying ( GE ). This study examines the relationship between ghrelin, liquid GE , and pain in children with FD . Methods Thirteen FD patients reporting symptoms consistent with post‐prandial distress syndrome ( PDS ) and 17 healthy controls were enrolled. All participants received a liquid meal containing 13 C‐sodium acetate. Pain severity, liquid GE utilizing exhaled 13 CO 2 from the sodium acetate breath tests ( ABT ), plasma acyl ghrelin ( AG ), and des‐acyl ghrelin concentrations were measured at specific intervals over 240 min following ingestion. Key Results FD ‐ PDS patients demonstrated lower mean baseline AG (14.8 ± 9.7 vs 27.2 ± 14.0 fmol/mL; p = 0.013), AG C max (24.6 ± 8.2 vs 40.5 ± 16.8 fmol/mL; p = 0.007), and AG flux (18.2 ± 7.8 vs 32.7 ± 17.3 fmol/mL; p = 0.015) than controls. The time to reach maximum exhaled 13 CO 2 concentration (T max ) was longer in FD patients than controls (47.5 ± 18.5 vs 35.8 ± 11.8 min; p = 0.046). Significant relationships between ghrelin analyte ratios and ABT parameters were largely confined to control participants. Conclusions & Inferences FD ‐ PDS in children is associated with lower fasting and maximum AG concentrations, and dampened AG flux. These data suggest a possible role for altered ghrelin physiology in the pathogenesis of PDS .