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previously available laboratory tests for the diagnosis of pancreatitis (amylase,
lipase, and TLI) (McCord et al.
2007
).
Histological examination is the current definitive method of diagnosis, particu-
larly in cases of chronic pancreatitis, but multiple biopsies are necessary since
pathological lesions can be patchy in their distribution (Newman et al.
2004
).
However, pancreatic histology is difficult to perform in clinical practice because
of practical considerations such as the critical condition of the patient and expenses.
In this study, the diagnosis of pancreatitis was made on the basis of compatible
clinical and ultrasound signs and on the determination of Spec cPL values. The
results from the comparison of the mean values of Spec cPLI in sick patients at
T
0
,
at the beginning of treatment with MA, and at subsequent time points did not reveal
any significant differences (
P
0.05). However, the analysis of single values
showed an increase in Spec cPLI above the suggestive value for pancreatitis
(
>
g/L) in three out of 20 dogs at different times. In the first case, a cPLI
value of 1,000
400
>
m
g/L was detected at
T
9
with clinical symptoms (mild depression and
anorexia), and an ultrasound scan indicated pancreatic flogosis. In the second case,
a value of 652
m
g/L at
T
5
was also associated with mild depression and anorexia, but
there was no ultrasonographic evidence of pancreatitis. cPLI values of 493, 421,
584, and 468
m
g/L were detected in an asymptomatic dog without ultrasonographic
abnormalities on
T
5
,
T
6
,
T
7
, and
T
8
, respectively. A positive ultrasound scan for
pancreatitis and compatible clinical signs (vomiting, abdominal pain, and/or
depression) were associated with a cPLI value of 368
m
g/L in one case at
T
2
.
These data are in contrast with a recent survey where no clinical and biochemical
evidence of pancreatitis was found in 23 dogs treated for leishmaniasis (14 with MA
and nine with Allopurinol alone) (Xenoulis et al.
2010
).
In our study, the lack of significant differences between the mean values of cPLI
at
T
0
and subsequent time points could be due to the particular pharmacokinetics of
MA and the fact that the dosage used in this study (75 mg/kg subcutaneously every
12 h for 60 days) (Valladares et al.
1998
) did not lead to a cumulative and
progressive toxicity resulting in acute pancreatitis. The evaluation of serum-cPLI
was made in retrospect, so the presence of symptoms and alterations during
ultrasound scan was considered the priority during the weekly exams. Thus, in
the case with clinically evident pancreatitis (clinical and ultrasound signs), treat-
ment with MA was suspended, and MA treatments were not suspended in the case
that lacked clinical and ultrasonography signs, but had Spec cPL values greater than
the cutoff for pancreatitis at subsequent therapy time points (
T
5
-
T
8
). Mild
symptoms were revealed in two subjects where the ultrasound signs were compati-
ble with acute pancreatitis at
T
9
and one dog was given specific treatments. Analysis
of the odds-ratio values suggests that the probability that a dog being treated with
MA for leishmaniasis will develop pancreatitis as compared to that of a dog with
untreated leishmaniasis is not significantly greater.
The main limits of this study were the small number of subjects, the lack of a
control group, and the impossibility of histologically diagnosing all dogs at all
subsequent time points (
T
0
-
T
9
). In light of these limitations, it is the authors'
opinion that pancreatitis is probably underestimated due to the difficulty of
m
