Biology Reference
In-Depth Information
23.2 Material and Methods
Records of dogs in which IBD had been diagnosed at the Unit of Medicine and
Pharmacology, University of Messina (Italy) were retrospectively reviewed.
Criteria for inclusion in the study were persistent gastrointestinal clinical signs
(
3 weeks in duration), failure to respond to antibiotics and/or dietary therapies
carried out for at least 3 weeks, histopathological evidence of gastric, small
intestinal, or colonic inflammation, and failure to document other causes of
symptoms by thorough diagnostic evaluation (exocrine pancreatic insufficiency,
endoparasites, neoplasia, etc.). Calculation of the clinical assessment of disease
activity by CCECAI was scored 1-12. Hematological tests, serum biochemical
profiles (with folate, cobalamine, and trypsin-like immunoreactivity measurements),
and urinalysis were performed for all dogs. Repeated fecal flotation examination was
negative for parasitic ova and
Giardia
cysts. Endoscopy of the affected gastrointes-
tinal tract was performed. Multiple endoscopic biopsies were taken from the
gastrointestinal tract explored. The lesions revealed during endoscopic examination
were classified as normal mucosa [0]; slightly friable and edematous mucosa [1];
friable mucosa with superficial, whitish specks [2]; and friable mucosa easily
bleeding and poorly relaxing insufflation [3] (Jergens et al.
1992
). The
histopathological evaluation of biopsies, sectioned at 3-4
m
m and stained with EE
and PA, performed blind by a single veterinary pathologist, was based on architec-
ture of tissues and distribution of inflammatory cells. Severity of changes was
scored on a scale from 0 (normal), 1 (mild - inflammatory infiltration within
changes of architecture or mucosal epithelial immaturity), 2 (moderate - mucosal
epithelial immaturity and/or necrosis alone), or 3 (severe - inflammatory infiltration
with multifocal necrosis of epithelium or massive architectural distortion)
(Washabau et al.
2010
).
All dogs were fed a new protein commercial diet and had been given intermittent
antibiotic treatment with either transient or no clinical improvement. A monthly
follow-up was carried out for 6 months after the end of pharmacological treatment
by assessing the presence of clinical signs and the dietary management adopted.
Disease outcome at the time of follow-up was described as either “remission,”
“intermittent signs,” or “uncontrolled disease.” Dogs in remission were defined as
those free of clinical signs for the preceding 6 months. Those with “intermittent
clinical signs” were defined as experiencing clinical signs more frequently
than every 14 days. Dogs with “uncontrolled disease” were defined the subjects
symptomatic during the therapy. The Spearrman test was used to evaluate the
correlation between CCECAI, endoscopic scores, and histopathological scores.
The Mann-Whitney test was used to compare the CCECAI with endoscopic and
histopathological scores in hypoalbuminemic versus normoalbuminemic dogs with
inflammation of the small intestine. Statistical significance was associated with a
P
value less than 0.05.
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