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Background Diagnosis of pancreatitis is based on clinical signs, pancreatic lipase immunoreactivity (cPLI), and abdominal ultrasonography (AUS). Diagnostic discrepancies exist between test results which might be related to differences in the timeline for resolution of these abnormalities after pancreatic injury. Hypothesis/Objectives To evaluate disease severity, ultrasonographic findings, and serum biomarkers of pancreatitis in dogs over a period of 28‐days. Animals Sixteen client‐owned dogs with a clinical suspicion for acute pancreatitis based on history/physical examination, an abnormal SNAP cPLI, and ultrasonographic evidence of pancreatitis. Methods Prospective observational study. Clinical severity (modified clinical activity index [MCAI]), cPLI, C‐reactive protein (CRP), and AUS were evaluated at days 0, 2, 7, and 28. Owner assessed overall health (OH) was noted. Dogs were stratified into baseline cPLI ≥400 μg/L vs <400 μg/L groups for reporting. Results The median CRP, MCAI, and OH were 111.9 mg/L, 10, and 4/10 respectively in the cPLI ≥400 μg/L group. The median CRP, MCAI, and OH were 58.0 mg/L, 6, and 6/10 respectively in the cPLI <400 μg/L group. None of these variables were significantly different between groups. Most dogs (4/5) in the cPLI <400 μg/L group had a history of suspected pancreatitis (ie, suspect acute on chronic disease). cPLI and MCAI rapidly decreased in dogs with a baseline cPLI ≥400 μg/L, whereas sonographic evidence of pancreatitis persisted for a longer time period. Conclusions and Clinical Importance Ultrasonographic evidence of pancreatitis in the absence of overt clinical or biochemical abnormalities might represent a resolving injury rather than active disease.

Mesenchymal stem cells (MSCs) have significant anti-inflammatory properties and are beneficial in rodent models of pancreatitis. The safety and efficacy of MSCs is unknown in dogs with acute pancreatitis (AP). Dogs with AP who were treated with MSCs (n = 4) were identified prospectively for this pilot study from an academic hospital. Serum Spec cPL and C-reactive protein (CRP) concentrations were measured on the day of MSC administration and 2 days later. The clinical severity, via the Modified Clinical Activity Index (MCAI), was also calculated. Two dogs received MSCs shortly after AP diagnosis, while the remaining dogs received MSCs due to clinically refractory disease. Changes in Spec cPL, CRP, and MCAI in the MSC-treated dogs were compared to a control population (n = 7) receiving the standard-of-care treatment for AP. No significant differences were noted between the populations for changes in Spec cPL (p = 0.79), CRP (p = 0.67), or MCAI (p = 0.91). However, subjective clinical improvements were noted within 24 h of MSC infusion in the two dogs with previously refractory disease. MSC infusions appear safe in the management of AP in dogs and may be considered in refractory disease. However, given the nature of this pilot study and its limitations, larger randomized controlled clinical trials are needed to truly evaluate the efficacy of MSC infusions in dogs with AP.

While most cases of pancreatitis in dogs are thought to be idiopathic, potential risk factors are identified. In this article we provide a state‐of‐the‐art overview of suspected risk factors for pancreatitis in dogs, allowing for improved awareness and detection of potential dog‐specific risk factors, which might guide the development of disease prevention strategies. Additionally, we review important advances in our understanding of the pathophysiology of pancreatitis and potential areas for therapeutic manipulation based thereof. The outcome of pathophysiologic mechanisms and the development of clinical disease is dependent on the balance between stressors and protective mechanisms, which can be evaluated using the critical threshold theory.

In the last 20 years, the diagnosis of pancreatitis has become more frequent as a result of improved diagnostic modalities such as abdominal ultrasound examination, advanced imaging, and immunoassays for the measurement of pancreatic lipase. Our aim is to provide a state‐of‐the‐art overview of the clinical diagnosis of acute pancreatitis (AP) in dogs with a particular focus on pancreatic lipase assay validation and clinical performance, in addition to advanced imaging modalities. We also discuss the potential indications for cytology and histopathology in dogs with suspected AP.

Background A clinical diagnosis (CDx) of pancreatitis includes evaluation of clinical signs, abdominal ultrasound (AUS), and pancreatic lipase. However, practitioners are using AUS to diagnose pancreatitis and are using AUS severity to guide decisions. The validity of this is unknown. Objectives To determine whether (1) there is a correlation between AUS, specific canine pancreatic lipase (Spec cPL) assay, and CDx; (2) individual AUS abnormalities correlate more closely with CDx than others; (3) AUS severity mirrors clinical severity indices; (4) changes in AUS can be used as a marker for changes in Spec cPL or CDx; and (5) the sensitivity and specificity of AUS for pancreatitis. Animals One hundred fifty‐seven dogs. Methods In this retrospective case study, inclusion criteria were signs of gastrointestinal, pancreatic disease, or both, in addition to having a Spec cPL and AUS performed within 30 hours. Information extracted from the records included bloodwork, Spec cPL, AUS images/clips, and severity of ultrasonographic findings. Results AUS was weakly correlated with Spec cPL (rs = .0178, P = .03) and moderately correlated with CDx (rs = .379, P = <.001). Pancreatic size (rs = .285, P = <.001), echogenicity (rs = .365, P = <.001), and mesenteric echogenicity (rs = .343, P = <.001) were correlated with CDx. Change in AUS was not correlated with Spec cPL or CDx changes. When pancreatic enlargement, echogenicity, or altered mesenteric echogenicity were required for a diagnosis, the sensitivity and specificity were 89% (95% confidence interval [CI] 71.8, 97.7) and 43% (95% CI 34.0, 51.6). When all 3 criteria were required, the sensitivity and specificity were 43% (95% CI 24.5, 62.8) and 92% (95% CI 85.3, 95.7). Conclusions AUS should not be used in isolation to diagnose pancreatitis and is a poor indicator of severity.

ABSTRACT Background Inpatient management for pancreatitis might be costly. Hypothesis/Objectives Describe a standardized outpatient protocol for pancreatitis. Animals Nineteen client‐owned dogs. Methods Single‐arm prospective observational study. Inclusion criteria included ≥ 2 clinical signs of pancreatitis, an abnormal SNAP cPL, no evidence of mechanical obstruction, and no significant comorbidities. All dogs received: fuzapladib (0.4 mg/kg IV q24 h for 3 days), subcutaneous fluids (up to 20 mL/kg/d SQ), hydromorphone (0.01 mg/kg/h delivered by a wearable infusion device), anti‐emetics (maropitant citrate &/or ondansetron), and nutrition. Dogs were assessed every 24 h for 3 days via physical examination and calculation of modified clinical activity index (MCAI; indicator of severity) and Glasgow composite measure pain scale (GCMPS) scores (indicator of analgesic adequacy). Results Ten of 19 dogs had a Spec cPL ≥ 400 μg/L and were considered to have suspected pancreatitis. Nine dogs had an abnormal SNAP cPL but Spec cPL < 400 μg/L and were reported in the assessment of protocol complications only. In the suspected pancreatitis group, MCAI decreased from Day 0 to Day 2 (median: 6, IQR: 5, vs. median 3, IQR: 4.25). GCMPS decreased from Day 0 to Day 2 (median: 7.5, IQR: 7.75, vs. median 0, IQR: 2.75). 2/19 dogs were hospitalized, 1 dog due to relapsed clinical signs, and 1 dog at the owner's request. A cutaneous adverse reaction could not be ruled out in 1 dog. Conclusions and Clinical Importance In this non‐blinded study, most dogs were successfully treated on an outpatient basis. Mild to moderate cases of pancreatitis predominated.

ABSTRACT Background Acute pancreatitis (AP) in dogs has a broad clinical presentation and variable progression, making prognostication challenging. Hypothesis/Objectives (i) To compare predicted prognosis for death and for prolonged (≥ 5 days) hospitalization across scoring schemes for AP in dogs and (ii) to predict concordance of each scoring scheme with death and for prolonged hospitalization. Animals Five hundred four client‐owned dogs. Methods Multi‐institutional retrospective study. Data extracted from medical records included: signalment, history, physical examination findings, diagnostic results, length of hospitalization, and death. Five prognostic schemes (OS, CSI, APPLEfull, CAPS, MCAI) were calculated for each dog. Results Overall concordance was low. Only APPLEfull (p = 0.004) and MCAI (p = 0.01) scores were significantly different between survivors and non‐survivors. Overall, APPLEfull had the greatest concordance (0.632, 95% CI: 0.592–0.672) with length of hospitalization. Of the other more pancreatitis‐specific schemes, MCAI had the greatest concordance (0.576, 95% CI: 0.567–0.635) with length of hospitalization, while CSI had the lowest concordance with length of hospitalization (0.525, 95% CI: 0.494–0.556). Conclusions and Clinical Importance On a population level, APPLEfull and MCAI had the greatest predictive discrimination between dogs of normal and prolonged hospitalization. If an individual dog has any of the 5 prognostic score schemes above the proposed cut‐off for death, it should be interpreted with caution because of the low case fatality rate.

ABSTRACT Background The effects of vitamin D supplementation are unknown in dogs with protein‐losing enteropathy (PLE). Objective To evaluate the safety, efficacy, and clinical benefit of orally administered cholecalciferol in dogs with PLE and decreased serum concentrations of 25OHD. Animals Twenty‐eight dogs with PLE, decreased 25OHD, and serum ionized calcium (iCa) > 1.0 mmol/L (n = 15 treated with cholecalciferol, n = 13 treated with placebo). Methods Prospective, double‐blinded, randomized, controlled trial. Dogs randomized to receive 400 IU/kg cholecalciferol or placebo PO daily along with standard therapy for 6 weeks. Clinical and biochemical variables were measured at baseline (T0) and monitored at 2 (T1), 4 (T2), and 6 (T3) weeks postmedication initiation. Clinical and biochemical variables were also measured 6 weeks following discontinuation of study medication (T4). Variables were compared in dogs with PLE receiving cholecalciferol versus placebo at T0–T4 using Student's t test or Mann–Whitney U tests and a mixed‐effects model. Correlations between 25OHD and clinical and biochemical variables were also performed. Results Dogs with PLE treated with cholecalciferol had higher 25OHD concentrations at T2 compared to dogs treated with placebo (225 nmol/L, range 72–434 vs. 80 nmol/L, range 31–254 nmol/L; p = 0.004). Clinical and biochemical variables did not otherwise differ between dogs with PLE treated with cholecalciferol versus placebo at T0–T4. Serum albumin correlated with 25OHD at T0–T3(p < 0.005 for all comparisons). Hypervitaminosis D without ionized hypercalcemia occurred in five dogs (18%). Conclusions While PLE dogs treated with cholecalciferol had higher 25OHD concentrations at study timepoints, a clinical benefit of supplementation was not observed.

Background The prevalence and clinical importance of cardiac abnormalities in dogs with acute pancreatitis (AP) is unknown. Animals Twelve dogs with AP and 60 archived serum samples from dogs with suspected AP. Methods Two‐phase study. Phase I: Analysis of archived serum samples from dogs with clinical signs of AP and high Spec cPL concentrations. High sensitivity troponin I (TnIH) and N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP) concentrations were measured in achieved serum samples. Phase II: Prospective observational study. Dogs with AP underwent echocardiography and Holter monitoring. Serum cardiac troponin I (cTnI) and plasma NT‐proBNP concentrations were measured. Previously described disease severity indices were calculated for each dog. Results Phase I: 41 of 60 dogs suspected of having AP had abnormally high TnIH concentrations and 13 of 60 had abnormally high serum NT‐proBNP concentrations. Higher TnIH concentrations were observed in dogs with Spec cPL concentration >2000 μg/L as compared to those with concentrations of 1000‐2000 μg/L. Phase II: 11 of 12 dogs diagnosed with pancreatitis had abnormal cTnI concentrations (median: 0.384 ng/mL, range: 0.041‐2.966 ng/mL, RI: ≤0.06 ng/mL) and 7 of 12 dogs had plasma NT‐proBNP concentrations above the reference interval (median: 971 pmol/L, range: 250‐2215 pmol/L, RI: ≤900 pmol/L). Supraventricular and ventricular ectopic beats occurred in 3 dogs. Echocardiographic abnormalities were detected in 5 dogs. Cardiovascular variables were not associated with indices of disease severity. Conclusions and Clinical Importance Myocardial injury is common in dogs with AP, but clinical consequences appeared to be uncommon in our small cohort. Cardiac biomarkers should be interpreted with caution in dogs with AP.

Background Hypercalcemia has been associated with hypergastrinemia in humans. Hypergastrinemia could be responsible for gastrointestinal (GI) signs in dogs with primary hyperparathyroidism (PHPT). Hypothesis/Objectives (a) Determine whether hypergastrinemia occurs in dogs with PHPT, (b) assess for potential correlations among ionized calcium (iCa), parathyroid hormone (PTH), and serum gastrin concentrations, and (c) determine whether gastrin concentrations decrease after management of PHPT. Animals Phase 1: 151 client‐owned dogs at the time of PHPT diagnosis, Phase 2: 24 dogs that underwent treatment for PHPT. Methods Dogs with azotemia, concurrent disease, or those receiving acid suppressants were excluded. Twenty‐four treated dogs had baseline and repeat quantification of serum gastrin, PTH, and iCa concentrations 4 weeks after treatment. The effect of treatment on gastrin, iCa, and PTH concentrations was assessed using Wilcoxon signed rank sum tests. Fisher exact testing was used to compare the proportion of dogs with hypergastrinemia in dogs with and without GI signs. Results Twenty‐seven of 151 PHPT dogs (17.9%) had increased pre‐treatment serum gastrin concentrations (median, 45.0 ng/L; interquartile range [IQR], 20.0 ng/L). Gastrin concentrations were not correlated with iCa (P = .92) or PTH (P = .60). Treatment of PHPT decreased PTH (P < .001) and iCa concentrations (P < .001), but not gastrin concentrations (P = .15). The proportion of dogs with hypergastrinemia with and without GI signs did not differ (P = 1.00). Conclusions and Clinical Importance Mild increases in serum gastrin concentrations may be seen in dogs with PHPT, but this finding is independent of the presence of GI signs.