2003, Number 4
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Cir Cir 2003; 71 (4)
Duodenogastroesophageal reflux -and esophagitis- induced disease
Nina-Virreira CO, Arenas-Osuna J, Quiroga-Via H
Language: Spanish
References: 40
Page: 286-295
PDF size: 86.73 Kb.
ABSTRACT
Objective: Our objective was to determine the relationship between
reflux of duodenogastric contents with different degrees of
esophagitis, and its levels and activity, with regard to the
severity of esophagitis-induced duodenogastroesophageal reflux
disease (DGERD).
Material and methods: Our study design was prospective,
transversal, descriptive, observational, and open. We took
samples of gastric and esophageal juices from patients with
a diagnosis of gastroesophageal reflux disease (GERD) and
esophagitis during the period from March to August 2002. Sample
material was placed in black rubber-covered assay tubes to prevent
bilirubin degradation. In our Unit’s central laboratory, these
samples were centrifuged for 30 min, the dissolved material
separated, and a reactive strip was introduced to measure the
amount of bile pigment. Endoscopic study reports were provided
by this Department on terminating the procedure. Univariate
analysis was used to obtain results.
Results: In 60% of cases, the esophageal liquid was positive for
total bilirubin; 40% presented stage II esophagitis, 27% chronic
esophagitis, and 27%, stage I esophagitis. Specific quantifications
of total bilirubin at different stages of esophagitis demonstrated
in stage II 50% with levels of 0.1-1, 33% with a level of 2-3, in
cases of chronic esophagitis 75% with levels of 0.1-1, and with
stage I esophagitis, 25% with levels of 2-3 mg/dl. Measurement of
gastric pH showed 18 (69%) < 3 and esophageal pH of 20 (67%) > 4,
with 10 (33%) referring occasional or asymptomatic dyspepsia.
We determined presence of duodenal elements in esophagus by means
of quantification of total bilirubin in 60% of patients, observing
greatest frequency of stage II esophagitis. Low but continuous
levels of duodenal, principally biliary, ele
ments continued in patients with DGERD, producing greatest damage in
esophageal mucosa.
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