ttp://www.bsava.

com PAPER

Comparison of initial treatment

with and without corticosteroids for
suspected acute pancreatitis in dogs
H. Okanishi*,†, T. Nagata†, S. Nakane† and T. Watari1,*

*Laboratory of Veterinary Internal Medicine, Department of Veterinary Medicine, Faculty of Bioresource Sciences,
Nihon University, Fujisawa, 252-0880, Japan
†
Nakane Animal Hospital, Tokyo, 115-0045, Japan
1
Corresponding author email: watari@brs.nihon-u.ac.jp

Objectives: To compare initial treatment with and without corticosteroids for acute pancreatitis in dogs
and investigate the therapeutic efficacy and prognosis.
Materials and Methods: Sixty-five dogs were included in this non-blinded, non-randomised clinical study.
Dogs with acute pancreatitis received treatment either with dose of 1 mg/kg/day prednisolone
(n=45) or without prednisolone (n=20). Response to treatment was based on changes in the
C-reactive protein concentration, improvement in clinical signs, duration of hospitalisation, mortality
and recurrence rate.
Results: From the third day of hospitalisation, C-reactive protein concentration was significantly lower
in the prednisolone group than that in the non-prednisolone group. The number of days required to
reach a C-reactive protein concentration of <2 mg/dL and clinical score of ≤2 was significantly lower
in the prednisolone group. The mortality rate 1 month after discharge was significantly lower in the
prednisolone group (11.3% versus 46.1%).
Clinical Significance: In dogs with acute pancreatitis, initial treatment with prednisolone resulted in
earlier reductions in C-reactive protein concentration and earlier improvement of clinical signs.

Journal of Small Animal Practice (2019)

DOI: 10.1111/jsap.12994
Accepted: 25 January 2019

INTRODUCTION the specific canine pancreatic lipase (Spec-cPL) and pancreatic

Acute pancreatitis (AP) is relatively common in dogs and may be
accompanied by variable involvement of other tissues or organ
systems (Kalli et al. 2009). Research suggests that the pathogen-
esis is associated with premature activation of digestive zymo-
gens within the acinar cells due to oxidative stress, hypotension,
changes in acinar pH and intra-cytoplasmic calcium ion shifts
(Rinderknecht 1986, Bhoomagoud et al. 2009). Dogs with AP
exhibit non-specific clinical signs such as abdominal pain, vomit-
ing and diarrhoea. Additional systemic clinical signs, such as car-
diovascular shock, are observed when severe inflammation results
in systemic inflammatory response syndrome (SIRS) (Mansfield
2012). Diagnosis of AP involves comprehensive evaluation of
clinical signs, haematological and biochemical profiles, abdomi-
nal imaging findings and histopathological examination (Mans-
field 2012, Haworth et al. 2014). New laboratory tests such as
elastase-1 test, and a new assay for serum lipase activity such as
canine lipase activity FUJI DRI-CHEM v-LIP-P (v-LIP) have
been recently developed for the diagnosis of AP (Steiner et al.
2003, Ishioka et al. 2011, Mansfield et al. 2011). Although a
number of management options are available for dogs with AP,
there are no specific treatments available for pancreatitis, and
these are generally limited to supportive care involving intrave-
nous fluid therapy, anti-emetics, analgesia and providing ade-
quate nutrition (Charles 2007).
In human patients with AP, it is critical to initiate manage-
ment care as soon as possible following diagnosis, because it
can profoundly influence prognosis (Banks et al. 2013, Tenner
et al. 2013, Isaji et al. 2015). A study in human patients with
AP reported that those with SIRS lasting for more than 48 hours
developed significantly higher rates of multiple organ dysfunc-
tion syndrome (MODS) and death than those with transient

Journal of Small Animal Practice • © 2019 British Small Animal Veterinary Association 1
 H. Okanishi et al.
SIRS lasting less than 48 hours (Mofidi et al. 2006). Further-
more, assessment of AP severity in humans based on prognostic
factors and CT findings within the first 48 hours is important for
ensuring that the appropriate initial treatment has been chosen
because even mild cases may progress rapidly during the early
stages (Isaji et al. 2015).
Glucocorticoids are known to counteract nearly all pathways
of inflammation. Research suggests that they play a key role in
enhancing apoptosis and increasing the production of pancreati-
tis-associated proteins, which confer a protective effect against
pancreatic inflammation (Zhang et al. 2004). Recent studies
have reported that glucocorticoids are effective for the treat-
ment of septic shock and SIRS (Annane et al. 1998, Marik et
al. 2008). The use of glucocorticoids has been avoided in dogs
with AP because these were previously considered a risk factor
for AP. Recently, glucocorticoids have been removed from the
list of drugs considered to cause pancreatitis in humans, and sev-
eral studies have indicated that they do not cause pancreatitis in
dogs (Parent 1982, Bang et al. 2008, Steiner et al. 2009). Several
research groups are currently investigating the potential benefits
of glucocorticoids in humans and animals with severe AP (Wan
et al. 2011, Yu et al. 2014, Dong et al. 2015). An experimental
study in dogs previously reported that glucocorticoid adminis-
tration was associated with improved survival and reduction in
severity of the pancreatic lesions in AP (Imahori et al. 1984).
However, no previous clinical study has investigated the efficacy
of glucocorticoids in dogs with AP.
The present study investigated the efficacy of prednisolone
(PDL) for the initial treatment of AP in dogs by comparing prog-
nosis in dogs treated with and without PDL.
MATERIALS AND METHODS
Dogs with AP treated at a primary care hospital from July 2011
to September 2016 were included in the present study. Dogs were
diagnosed with pancreatitis based on criteria established in previ-
ous studies (Ishioka et al. 2011, Chartier et al. 2014, Yuki et al.
2016) as follows: at least two clinical signs consistent with AP-
lethargy, weakness, loss of appetite, vomiting, diarrhoea, melaena,
haematochezia or abdominal pain (Annane et al. 1998); serum
Spec-cPL concentration >400 μg/L or plasma v-LIP >200 U/L
(Bang et al. 2008); ultrasonographic findings indicative of AP-
pancreatic enlargement, pancreatic hypoechogenicity, irregular
margins, hyperechoic mesenteric regions and/or changes in the
adjacent intestines (Banks et al. 2013). Furthermore, a plasma
Table 1. Scoring for clinical signs of acute pancreatitis in dogs
Clinical score 0 1
Weakness/lethargy Normal Mild
Appetite Normal Mildly Decreased
Vomiting None (≥ 50% as well as usual) 1 Time/day
Stool condition Normal Soft faeces
Abdominal pain None Discomfort on palpation
AP acute pancreatitis
2 Journal of Small Animal Practice
C-reactive protein (CRP; Laser CRP-2, [laser immunonephelom-
etry], Arrows Co., Ltd.) concentration of ≥1 mg/dL was added as
a criterion in the present study based on previous reports (Onishi
et al. 2000, Holm et al. 2004, Nakamura et al. 2008, Yuki et al.
2016). The diagnosis of AP in the present study was not based
on histological findings but on the sudden-onset severe clinical
signs consistent with AP. The following data were recorded for all
dogs: signalment, physical examination results, complete blood
count, serum/plasma biochemical profiles, and radiography and
ultrasonography findings. Furthermore, all dogs were given an
AP score of clinical signs based on five variables that are routinely
evaluated in affected dogs: weakness and lethargy, anorexia, vom-
iting, diarrhoea and abdominal pain (Table 1). The clinical score
on the first day of admission was assigned by the dog owner and a
clinician, and then by two clinicians during hospitalisation.
Dogs were treated either with PDL or without PDL (NPDL).
The cases in the early period of the study (from July 2011 to
December 2014) were included in the PDL group, and the cases
in later period (from January 2015 to September 2016) were
included in the NPDL group: Dogs with AP from July 2011 to
December 2014 were all treated with PDL with dose of 1 mg/kg/
day PDL (Prednisolone injection KS, Kyoritsu Seiyaku) subcuta-
neously (sc), and dogs with AP from January 2015 to September
2016 were treated without PDL. PDL was administered via sc
injections until the patients were discharged from the hospital.
Both groups also received the following treatment: intravenous
fluid (lactated Ringer’s solution, acetated Ringer’s solution, Ring-
er’s solution and saline solution), antiemetics [a dose of 1 mg/kg/
day maropitant citrate (Cerenia, Zoetis Japan), sc], gastric acid
suppression [a dose of 1 mg/kg/day famotidine (Gaster, Astellas
Pharma Inc.) sc], antibiotics [a dose of 5 mg/kg/day enrofloxa-
cin (Baytril, Bayer) sc], analgesia [a dose of 3 to 6 μg/kg/hour
fentanyl (Fentanyl injection, Daiichi Sankyo Co.) constant rate
infusion], and a multivitamin solution (Daivita-mix, Iwaki Sei-
yaku). Intravenous fluid therapy and fentanyl dose were adjusted
based on the individual dog’s electrolyte balance and pain level.
Dogs with underlying diseases or complications such as epi-
lepsy, cardiac disease (mitral or tricuspid regurgitation), prostatic
hyperplasia, tracheal collapse, biliary sludge, thickened gallblad-
der wall, gingivitis, and atopic dermatitis were included in the
present study. These cases did not have clinical signs of these
underlying diseases or related complications, and progression of
the diseases was not observed. Therefore, CRP concentrations on
the first day of admission were considered to be unrelated to these
underlying diseases. Cases of AP that were managed differently
from those described above were excluded from the present study.
2 3
Severe —
Moderately Decreased Severely Decreased
(<50% as well as usual) 2 Times/day (eat nothing) ≥ 3 Times/day
Watery diarrhoea Melaena and/or Hematochezia
Discomfort in Putting Abdomen on the Floor —
(“Prayer Position”)
• © 2019 British Small Animal Veterinary Association
 Corticosteroid therapy for canine pancreatitis
Response to treatment was assessed based on CRP concentra-
tion, improvements in clinical signs, duration of hospitalisation,
mortality, and recurrence rate. Changes in CRP concentration
during hospitalisation were recorded, along with the number
of days until CRP concentration had decreased to <2 mg/dL.
Improvements in clinical signs were evaluated based on the
number of days until the clinical score had decreased to ≤2. The
dogs that died or those discharged during hospitalisation were
excluded from these analyses (changes in CRP concentration,
the number of days until CRP concentrations had decreased
to <2 mg/dL, the number of days until the clinical score had
decreased to ≤2). Prognosis was evaluated based on rates of mor-
tality, and recurrence during hospitalisation and within 1 month
of diagnosis.
Follow-up information were obtained from the owners of the
dogs during the follow-up visit at the clinic.
Statistical analysis
Continuous data (age, bodyweight, duration of clinical signs
until the hospital visit, clinicopathologic data), CRP concentra-
tions, days until the CRP concentrations had reached <2 mg/
dL, clinical score, the number of days until the clinical score
had reached ≤2, and duration of hospitalisation were analysed
for normal distribution using the Shapiro-Wilk test. As the data
failed the normality test, non-parametric methods were used for
further analysis.
The data are reported as medians (ranges). The Fisher’s exact
test was used to analyse categorical data and data are reported
in proportions. The Mann-Whitney U test was used to compare
numerical data associated with signalment, blood examination,
CRP concentration, clinical score and the duration of hospitali-
sation between the PDL and NPDL groups. Stata (version 14 for
Windows, StataCorp) was used to examine the changes in CRP
concentration in the two groups over time (days). Survival curves
were generated using the Kaplan-Meier method, and survival
plots were compared using the log-rank test. Statistical analyses
apart from time series regression were performed using GraphPad
Prism.
Table 2. Median (range) or numeric values of baseline variables in dogs with acute pancreatitis treated with prednisolone
(PDL) or without PDL on day 1 of hospitalisation
PDL Group (n=45)
Median
Age (years) 11.8
Sex (Male, Female) 25 (14 M, 11 NM): 20 (8 F, 12 NF)
Breed DHM (9), Chihuahua (8), YT (7),
Papillon (3), Toy poodle (2), MINPN (2),
SHIH (1), MS (1), Kishu (1), ACS (1),
Samoyed (1), BT (1), MBT (1), Shiba (1),
FB (1), CKCS (1), BC (1), MB (3)
Weight (kg) 5.5
Clinical score (score) 6 3–11
Duration of clinical signs until 1 0–8
hospital visiting (days)
PDL prednisolone, NPDL non-prednisolone, F Sexually entire female, M sexually entire male, NF neutered female, NM neutered male, DHM Miniature dachshund, YT Yorkshire terrier, MINPN
miniature Pinscher, SHIH shih-tzu, MS Miniature schnauzer, ACS American cocker spaniel, BT Boston terrier, MBT miniature bull terrier, FB French bulldog, CKCS Cavalier King Charles spaniel,
BC border collie, MB mixed breed, SS Shetland sheepdog
Journal of Small Animal Practice • © 2019 British Small Animal Veterinary Association 3
RESULTS
Signalment and baseline data
Eighty-six dogs were hospitalised with a diagnosis of AP dur-
ing the study period; 65 of these met the inclusion criteria. The
following cases were excluded: three cases in which intravenous
dopamine hydrochloride solution was administered, one case in
which a blood transfusion was required, and five cases in which
low-molecular-weight heparin was administered. An additional
10 cases were excluded owing to complications (malignant lym-
phoma, n=4; hyperadrenocorticism, n=3; hypoadrenocorticism,
n=1; diabetes mellitus n=2) in order to avoid the potential influ-
ence of these conditions and associated treatments (e.g. chemo-
therapy, trilostane, fludrocortisone acetate, insulin) on PDL
outcomes. Two cases were also excluded because these required
surgical treatment for pyometra and gastrointestinal foreign
bodies. The PDL and NPDL groups included 45 and 20 dogs,
respectively. Baseline variables were similar between the groups
(Table 2, Table S1).
Baseline clinicopathologic data
White blood cell (WBC) count, packed cell volume (PCV),
platelet (PLT) count, blood urea nitrogen (BUN), creatinine
(CRE), alkaline phosphatase (ALP), alanine aminotransferase
(ALT), albumin (ALB), glucose (GLU), total bilirubin (TBIL),
calcium (Ca), v-LIP and Spec-cPL were evaluated on the first day
of admission. These baseline variables were similar between the
groups (Table 3, Table S2).
CRP concentration
Differences between groups became apparent on day 2 of admis-
sion: from day 3 onwards, CRP concentration remained signifi-
cantly lower in the PDL group than in the NPDL group (Table 4,
Table S3). Fifteen dogs in the PDL group and 13 dogs in the
NPDL group had CRP concentrations measured at all time
points. Analysis of CRP across time and group, while allowing
for baseline, revealed a strong effect of time (β=−2.21; 95%CI:
-2.58 to −1.85; P<0.001) and group (β=5.30; 95%CI: 3.03 to
NPDL Group (n=20)
Range Median Range
3.4 to 15.8 13.8 2.9 to 16.4
– 10 (4 M, 6 NM): 10 (2 F, 8 NF) –
– DHM (9), Toy poodle (4), Chihuahua (1), –
YT (1), Papillon (1), SHIH (1),
MS (1), Pomeranian (1), SS (1)
1.8–15.8 4.6 2.1–10.2
7 3–10
1 0–7
 H. Okanishi et al.

Table 3. Median (range) values of clinicopathologic variables on day 1 of hospitalisation in dogs with acute pancreatitis
treated with prednisolone or without prednisolone
Reference interval PDL group NPDL group
Median Range n Median Range n
WBC (/μL) 6000 to 17,000 18,200 7200 to 44,900 43 21,050 6000 to 68,800 18
PCV (%) 37 to 55 45.8 23.0 to 61.7 43 44.4 27.9 to 52.9 18
PLT (×103/μL) 200 to 500 354 85 to 1381 43 430 141 to 846 18
BUN (mg/dL) 9.2 to 29.2 18.7 7.6 to 231.5 45 27.2 7.2 to 190.8 20
CRE (mg/dL) 0.4 to 1.4 0.6 0.1 to 9.9 45 0.7 0.3 to 5.8 20
ALP (U/L) 47 to 254 420 41 to 3500 44 814 100 to 3500 18
ALT (U/L) 17 to 78 78 18 to 753 45 118 31 to 1000 19
ALB (g/dL) 2.6 to 4.0 3.3 1.4 to 4.3 41 3.2 1.5 to 4.2 20
GLU (mg/dL) 75 to 128 103 79 to 208 39 119 74 to 259 17
TBIL (mg/dL) 0.1 to 0.5 0.4 0.3 to 4.1 8 0.7 0.2 to 2.1 14
Ca (mg/dL) 9.3 to 12.1 10.3 8.1 to 11.7 29 9.6 7.3 to 11.6 10
CRP (mg/dL) 0.0 to 0.99 8.8 1.0 to 20 45 10 1.7 to 20 20
v-LIP (U/L) 10 to 160 967 210 to 1000 44 798 201 to 1000 18
Spec cPL (μg/L) ≤200 1000 1000 1 874 747 to 1000 2
PDL prednisolone, NPDL non-prednisolone, WBC white blood cell, PLT platelet, BUN blood urea nitrogen, CRE creatinine, ALP alkaline phosphatase, ALT alanine aminotransferase, ALB
albumin, GLU glucose, TBIL total bilirubin, Ca calcium, CRP C-reactive protein

Table 4. Median (range) CRP concentrations during

hospitalisation in dogs with acute pancreatitis treated
with prednisolone or without prednisolone
Day PDL group NPDL group P value
Median Range n Median Range N
1 8.8 1 to 20 45 10 1.7 to 20 20 0.85
2 11 1.5 to 20 45 18 3 to 20 17 0.15
3 4.2 0.3 to 20 43 8.6 0.9 to 20 17 0.048
4 2.5 0.3 to 20 36 9.5 2.1 to 20 15 <0.001
5 1.8 0.6 to 20 25 7.5 0.1 to 20 15 0.026
6 1 0.1 to 20 15 7 2.1 to 20 13 0.012
PDL prednisolone, NPDL non-prednisolone, CRP C-reactive protein

7.57; P<0.001) but no interaction between these variables (con-

FIG 1. Box-and-whisker plots of the number of days taken for the CRP
trast: χ2=6.37; P=0.17).
concentration to reach less than 2 mg/dL in the PDL and NPDL groups.
For the analysis of the number of days until the CRP con- Each box indicates the interquartile range, the horizontal line indicates
centration had reached <2 mg/dL, 43 dogs were included in the median, the whiskers indicate the 10th and 90th percentiles, and
circles indicate outliers
the PDL group, and 16 dogs in the NPDL group. The num-
ber of days until the CRP concentration had reached <2 mg/
dL was significantly lower in the PDL group than in the
NPDL group (PDL group, median: 4 days [range: 2 to 9] ver-
sus NPDL group, median: 8 days [range: 3 to 23]; P<0.001)
(Fig. 1, Table S4).

Clinical score
For the analysis of the number of days until the clinical score had
reached ≤2, 43 dogs were included in the PDL group, and 16
dogs in the NPDL group. The number of days until the clinical
score had reached ≤2 was significantly lower in the PDL group
than in the NPDL group (PDL group, median: 4 days [range
2 to 7] versus NPDL group, median: 7 days [range 3 to 23];
P<0.001) (Fig. 2, Table S4).

Duration of hospitalisation
For the analysis of the duration of hospitalisation, 45 dogs were
included in the PDL group, and 20 dogs were included in the
NPDL group. The duration of hospitalisation was significantly
FIG 2. Box-and-whisker plots of the number of days taken for the clinical
score to reach ≤2 in the PDL and NPDL groups. Each box indicates the
interquartile range, the horizontal line indicates the median, the whiskers
indicate the 10th and 90th percentiles, and circles indicate outliers

4 Journal of Small Animal Practice • © 2019 British Small Animal Veterinary Association
 Corticosteroid therapy for canine pancreatitis
shorter in the PDL group than in the NPDL group (PDL group,
median: 5 days [range: 2 to 10] versus NPDL group, median:
8 days [range: 1 to 23]; P=0.002) (Fig. 3, Table S4).
Prognosis
Rates of mortality, and recurrence within 1 month of diagno-
sis were investigated in both groups. One month after diagno-
sis, 38 dogs (88.7%) had survived in the PDL group, while 11
(57.9%) had survived in the NPDL group. The survival rate was
significantly higher in the PDL group than in the NPDL group
(P=0.005) (Fig. 4, Table S5). Two dogs were lost to follow-up
in the PDL group, while one dog was lost to follow-up in the
NPDL group; The data of these dogs were excluded from the
analyses of rates of mortality, and recurrence within 1 month of
diagnosis because these dogs were not brought for the follow-up
visit after discharge from the hospital.
During hospitalisation, two dogs in the PDL group and four
dogs in the NPDL group died or had been euthanased. All eight
FIG 3. Box-and-whisker plots showing the duration of hospitalisation in
the PDL and NPDL groups. Each box indicates the interquartile range, the
horizontal line indicates the median, the whiskers indicate the 10th and
90th percentiles, and circles indicate outliers
FIG 4. Kaplan-Meier survival curve at 1 month following diagnosis in dogs
with AP that were treated with or without PDL (PDL group: black line,
NPDL group: grey line)
Journal of Small Animal Practice • © 2019 British Small Animal Veterinary Association 5
dogs in the NPDL group had died or been euthanased during
the second week after diagnosis. Three dogs in the PDL group
and four dogs in the NPDL group had died or been euthanased
after discharge. Two of the three deceased dogs in the PDL group
were discharged with resolution of their symptoms and normal
CRP concentrations but, their symptoms deteriorated and they
subsequently died. The remaining dog in the PDL group was
discharged without response to treatment and later died. Four
dogs in the NPDL group were discharged without response to
treatment and later died or were euthanased.
One month following diagnosis, five dogs in the PDL group
and eight dogs in the NPDL group had died or been euthanased
due to unresponsiveness to treatment during hospitalisation or
after discharge from the hospital.
There was not a statistically significant difference in mortal-
ity during hospitalisation between the PDL and NPDL groups
[PDL group: 4.4% (two of 45) versus NPDL group: 20% (four
of 20), P=0.067]. However, at 1 month following diagnosis, the
mortality rate was significantly lower in the PDL group than in
the NPDL group [PDL group: 11.3% (five of 45) versus NPDL
group: 41.1% (eight of 20), P=0.007). Following discharge,
recurrence was observed in four of the 42 dogs in the PDL group
and one of the 10 dogs in the NPDL group. No significant dif-
ference in the rate of recurrence was observed between the two
groups (PDL group: 9.7%; NPDL group: 10.5%, P>0.05).
DISCUSSION
Results of this study suggest that administration of PDL may
improve the management of canine AP. In this respect, the ben-
efits of PDL treatment included a greater decrease in CRP con-
centration, shorter number of days until improvement of clinical
signs, shorter hospitalisation periods and better survival. How-
ever, because the study was not blinded or randomised, conclu-
sions must be made cautiously and further, objective, clinical
trials are needed to confirm the findings.
In many of the dogs, v-LIP activity was used as a factor for
diagnosis because the result could be obtained immediately in
our hospital and the v-LIP test had previously been shown to
be of use in canine pancreatitis (Yuki et al. 2016). However, the
v-LIP test is not a pancreatic lipase-specific test and may be infe-
rior to the Spec cPL test (Steiner et al. 2017). In future prospec-
tive studies that assess the effect of PDL on management of AP,
Spec-cPL should be considered instead of v-LIP as a diagnostic
marker for AP.
In humans with AP, treatment within 48 hours of diagnosis
is critical and can profoundly impact prognosis, because rapid
progression can occur even in mild cases (Otsuki et al. 2006). In
addition, the relationship between CRP concentration and prog-
nosis of dogs with pancreatitis has been examined, revealing that
the CRP concentration in samples obtained within 2 days of the
onset of clinical signs had a significant correlation with the out-
come (Mansfield et al. 2008). In the present study, differences in
CRP concentrations between the groups became apparent within
2 days, and the number of fatal cases in the first 2 days was sig-
 H. Okanishi et al.
nificantly lower in the PDL group than in the NPDL group.
Therefore, prompt initiation of treatment may be critical for
cases of AP in dogs.
A previous study of experimental AP in dogs reported that
the severity of lesions in pancreatic acinar cells in dogs treated
with glucocorticoids was significantly lower than in dogs without
glucocorticoid therapy and the survival time was longer (Imahori
et al. 1984). A study that investigated the effects and haemody-
namic changes brought about by glucocorticoids in experimental
pancreatitis in dogs reported that the treated groups showed an
increase in pancreatic arterial blood flow and had improved sur-
vival times (Studley & Schenk Jr. 1982). Another study on acute
experimental pancreatitis in rats reported that pro-inflammatory
cytokine interleukins (IL-1β, IL-6, IL-10) and phospholipase A2
in the group treated with glucocorticoid were significantly sup-
pressed compared with those in the untreated group, and that
glucocorticoid was effective in the treatment of early SIRS asso-
ciated with AP (Gloor et al. 2001). The present study assessed
the effect of PDL on the management of AP. Future studies on
the effectiveness of glucocorticoids in managing chronic pancre-
atitis should also be considered. They may be particularly use-
ful in treating chronic pancreatitis in the English cocker spaniel,
as this breed is thought to have autoimmune-mediated disease
(Watson et al. 2011). In the present study, CRP concentrations
in PDL-treated dogs were significantly lower than those of non-
glucocorticoid-treated dogs. CRP is an acute phase reactant that
is increased by inflammation, infection, and destruction of tissue
and is known not to be affected by glucocorticoids (Martínez-
Subiela et al. 2004). Therefore, PDL administration might con-
tribute to the suppression of tissue injury by improving pancreatic
arterial blood flow and decreasing the inflammatory reaction.
Alternatively, glucocorticoids may have been effective for dogs
with AP in the present study because these dogs were affected
by critical illness-related corticosteroid insufficiency (CIRCI).
CIRCI occurs when there is adrenal insufficiency due to a severe
pro-inflammatory state, resulting in hypotension and a poor
response to fluids or vasopressor therapy. Appropriate tests to
diagnose CIRCI are unknown, although the diagnosis in humans
is currently based on response to treatment with hydrocortisone
(Creedon 2015). Low-dose corticosteroids are recommended as
a therapy for humans with CIRCI (Sprung et al. 2008). A recent
study of AP in humans has reported that CIRCI is observed
in many patients with AP, and is associated with bacteraemia,
MODS, and increased mortality (Peng et al. 2009). Unfortu-
nately, it was unknown whether the dogs in the present study had
adrenal insufficiency. However, low-dose glucocorticoids may
enhance vascular activity/catecholamine reactivity and inhibit
inflammatory reactions in these dogs. Further studies are needed
to investigate the relationship between CIRCI and AP in dogs.
Ruaux & Atwell (1998) proposed a system for rating the clinical
severity of AP on a scale ranging from 0 to 4, indicating the number
of organs other than the pancreas exhibiting signs of compromise
or failure. In this system, the BUN, CRE, ALP, ALT, GLU and
WBC count are used to predict prognosis. Additional studies have
reported that elevated GLU, v-LIP, BUN, and/or CRE, decreased
PLT count, and marked elevation of Spec-cPL concentration can
6 Journal of Small Animal Practice
be used as prognostic factors for canine pancreatitis (Suzuki et al.
2013, Sato et al. 2017). In the present study, there were no appar-
ent differences in these factors between the two groups on the first
day of hospitalisation. Mansfield et al. (2008) proposed another
clinical severity scoring system based on the cardiac and respiratory
systems, vascular forces, intestinal integrity and acid-base balance.
Unfortunately, we were unable to utilise these scoring systems in
the present study, as not all of the relevant factors were evaluated in
the included dogs. Further studies are required to investigate that
effect of PDL on AP severity using these systems.
At 1 month following diagnosis, mortality was significantly
higher in the NPDL group than that in the PDL group. We
speculate that this discrepancy occurred because a greater num-
ber of dogs in the NPDL group were discharged due to a lack
of response to treatment. The reported mortality rate for AP in
dogs ranges from 27 to 58%, based on data obtained from vet-
erinary referral hospitals (Strombeck 1990, Cook et al. 1993,
Charles 2007, Zhang et al. 2008). In our study, mortality was
41.1% in the NPDL group (mortality during hospitalisation:
20%). Mansfield & Beths (2015) suggested that the mortality
rate may not reflect that observed in general veterinary practice,
as such reports originate from referral centres, and euthanasia for
non-medical (e.g. financial) reasons may also exert an influence.
Additionally, in the present study, cases in which dogs had been
euthanased or had died following discharge due to discontinua-
tion of hospital treatment were included in analyses of mortal-
ity. Further comprehensive studies are required to clarify the true
mortality rate of AP in dogs.
Our study has several additional limitations. First, it has a poten-
tial for bias because it was not blinded: the clinical scoring was
performed for each patient by the dog owners and two clinicians
involved the treatment. In the future, we will perform a blinded
clinical trial. Second, our study was not completely matched in
terms of dog breed between the two groups (in particular, min-
iature dachshunds were over-represented in the NPDL group).
In addition, the dogs in the NPDL group were comparatively
older than those in the PDL group. The grouping was unbalanced
because we divided the two groups based on the hospital visit dates.
Future studies should be randomised to avoid this problem. Third,
we used antibiotics in the dogs to prevent secondary bacterial infec-
tion of the inflamed pancreas. However, there is minimal evidence
that bacterial infection is of any significance in typical canine AP
and so prophylactic antibiotics should be avoided if possible.
In conclusion, for dogs with AP, initial treatment that included
PDL resulted in earlier reductions in CRP concentration and
improvements in the clinical signs compared the results seen in
dogs treated without PDL. Results of the present study suggest
that PDL might lead to an improvement in the prognosis of dogs
with AP over traditional management strategies. However, fur-
ther studies are required to investigate the effectiveness of gluco-
corticoid administration in dogs with AP.
Acknowledgements
The authors would like to thank the staff of the Nakane Animal
Hospital and the residents and interns of the Animal Medical Cen-
tre of Nihon University for their assistance with data collection.
• © 2019 British Small Animal Veterinary Association
 Corticosteroid therapy for canine pancreatitis
Conflict of interest
None of the authors of this article has a financial or personal
relationship with other people or organisations that could inap-
propriately influence or bias the content of the paper.
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Supporting Information
The following supporting information is available for this article:
Supplemental Table 1. Signalment and Baseline Data
Supplemental Table 2. Baseline Clinicopathologic Data
Supplemental Table 3. CRP Concentration
Supplemental Table 4. The data of days until the CRP con-
centrations had reached <2 mg/dL, clinical score, the number
of days until the clinical score had reached ≤2, and duration of
hospitalisation
Supplemental Table 5. The data of Kaplan–Meier survival
curve at 1 month following diagnosis in dogs with AP that were
treated with or without PDL (1=death, 0=censor)