INTRAGASTRIC DISTRIBUTION AND GASTRIC-EMPTYING OF SOLIDS AND LIQUIDS IN FUNCTIONAL DYSPEPSIA - LACK OF INFLUENCE OF SYMPTOM SUBGROUPS AND H-PYLORI-ASSOCIATED GASTRITIS
Am. Scott et al., INTRAGASTRIC DISTRIBUTION AND GASTRIC-EMPTYING OF SOLIDS AND LIQUIDS IN FUNCTIONAL DYSPEPSIA - LACK OF INFLUENCE OF SYMPTOM SUBGROUPS AND H-PYLORI-ASSOCIATED GASTRITIS, Digestive diseases and sciences, 38(12), 1993, pp. 2247-2254
The relative contributions of altered gastric motor function and Helic
obacter pylori-associated active chronic gastritis to the pathogenesis
of functional dyspepsia are controversial. We therefore evaluated sci
ntigraphically the intragastric distribution and gastric emptying of a
mixed solid-liquid meal in 75 patients with functional dyspepsia; pat
ients were subdivided on the basis of both specific symptom clusters a
nd the presence or absence of H. pylori gastritis. Twenty-one (28%) pa
tients displayed abnormal solid and/or liquid gastric emptying, with p
rolonged solid lag time the most prominent alteration detected. The nu
mber of patients with abnormal scintigraphic patterns increased to 36
(48%) when intragastric distribution parameters (fundal half-emptying
time and antral maximal fraction) were examined. Although patients wit
h reflux-like dyspepsia (N = 36) demonstrated significantly slower rat
es of liquid emptying at 45 and 70 min and a higher prevalence of abno
rmal liquid intragastric distribution when compared to patients with m
otility-like dyspepsia (N = 39) or to controls (N = 34), the absolute
differences were small and unlikely to be of clinical significance. Pa
tients without H. pylori gastritis (N = 50) demonstrated a significant
ly more prolonged solid lag time when compared to those with H. pylori
gastritis (N = 25), but the difference was small and there were no ot
her differences between these two subgroups. We conclude that in patie
nts with functional dyspepsia: (1) abnormal solid gastric emptying is
present in less than one third; (2) assessment of parameters of intrag
astric distribution enables more subtle gastric motor dysfunction to b
e identified; and (3) neither dividing patients into symptom subgroups
nor accounting for the presence or absence of H. pylori gastritis has
a major influence on the prevalence or type of gastric motor dysfunct
ion.