Longitudinal Evaluation of Serum Pancreatic Enzymes and Ultrasonographic Findings in Diabetic Cats Without Clinically Relevant Pancreatitis at Diagnosis
Journal of Veterinary Internal Medicine
Abstract and Figures
Background
Cats with diabetes mellitus can have subclinical pancreatitis but prospective studies to confirm this are lacking. Metabolic control of diabetic cats with pancreatitis is difficult.HypothesisSubclinical pancreatitis occurs in diabetic cats at the time diabetes is diagnosed or might develop during the follow-up period, hampering diabetic remission.AnimalsThirty cats with newly diagnosed diabetes without clinical signs of pancreatitis on admission.Methods
Prospective study. On admission and 2 and 6 months later, serum Spec fPL and DGGR-lipase were measured and the pancreas underwent ultrasonographic examination. Pancreatitis was suspected if serum markers were increased or ≥2 ultrasonographic abnormalities were detected. Cats were treated with insulin glargine and diabetic remission was defined as euglycemia ≥4 weeks after discontinuation of insulin. Nonparametric statistical tests were used for analysis.ResultsSubclinical pancreatitis at the time of diagnosis was suspected in 33, 50, and 31% of cats based on Spec fPL, DGGR-lipase and ultrasonography, respectively; and in 60% when diagnostic criteria were combined. During the follow-up period, suspected pancreatitis developed in additional 17–30% cats. Only 1 cat had transient clinical signs compatible with pancreatitis. Seventeen of the 30 cats (57%) achieved remission. Frequency of abnormal Spec fPL and DGGR-lipase and abnormal ultrasonographic findings did not differ in cats achieving remission and those who did not. Cats achieving remission had significantly lower Spec fPL at 2 months (P < .001).Conclusions and Clinical ImportanceBased on laboratory and ultrasonographic measurements, many cats with diabetes might have pancreatitis, although without clinical signs. Cats with high Spec fPL might have a reduced chance of diabetic remission; however, this topic needs further studies in large cohorts of diabetic cats.
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... 15,16 in cats, it is fairly well established, both in clinical and histopathological investigations, that dM and pancreatitis often coexist. 17,18 in clinical studies, 31-83% of cats with dM were found to have clinical evidence of pancreatitis (based on feline pancreatic lipase immunoreactivity [fPLi; Spec fPL, idEXX] measurements and/or abdominal ultrasonography), although similar findings were also present in non-diabetic cats. 18,19 The majority of cats with pancreatitis were asymptomatic in these studies. ...
... 17,18 in clinical studies, 31-83% of cats with dM were found to have clinical evidence of pancreatitis (based on feline pancreatic lipase immunoreactivity [fPLi; Spec fPL, idEXX] measurements and/or abdominal ultrasonography), although similar findings were also present in non-diabetic cats. 18,19 The majority of cats with pancreatitis were asymptomatic in these studies. Results from necropsy studies are conflicting; histological evidence of pancreatitis was found in 51-57% of cats with dM in one study, 20 but, in another study, histological evidence of pancreatitis was not more common in diabetic cats compared with control cats; 21 although there were several limitations to the latter study. ...
... interest ingly, one study showed that 2 months after 30 cats were admitted with newly diagnosed dM and no clinical signs of pancreatitis, the serum Spec fPL concentrations were significantly higher in those that did not achieve remission than those that achieved remission. 18 These findings may suggest that cats with pancreatitis have a reduced chance of achieving diabetic remission; however, further studies are needed to support this hypothesis. ...
Practical relevance:
Diabetes mellitus (DM) is one of the most common feline endocrine disorders. It has been shown by several studies that DM in cats frequently coexists with pancreatitis.
Clinical challenges:
It has not been definitively established what the exact pathogenetic association between DM and pancreatitis is in the cat. However, the association between these two conditions is most likely bidirectional, with DM predisposing cats to pancreatitis and vice versa. Diagnosis of pancreatitis in cats with DM is crucial because concurrent pancreatitis commonly leads to difficulties in the management of DM. When pancreatitis is associated with diabetic ketoacidosis (DKA), therapeutic management is even more challenging.
Aims:
This review focuses on the concurrent presence of DM or DKA and pancreatitis in cats, mainly focusing on their clinical management.
Evidence base:
Information provided in this review is based on feline-specific clinical research when available. In addition, comparative and human research, as well as clinical experience, has been used to enrich knowledge in areas where feline-specific research is not yet available.
... Pancreatitis is also known to be a common comorbidity in cats with diabetes [11,27]. Subclinical chronic pancreatitis with the development of fibrosis is thought to be the main cause of diabetes in cats [27,28]. Pancreatitis was subclinical in almost all cats with newly diagnosed diabetes in one study, and its clinical relevance was questioned by the authors [28]. ...
... Subclinical chronic pancreatitis with the development of fibrosis is thought to be the main cause of diabetes in cats [27,28]. Pancreatitis was subclinical in almost all cats with newly diagnosed diabetes in one study, and its clinical relevance was questioned by the authors [28]. It is less clear whether preexisting diabetes can also trigger pancreatitis in cats. ...
Histological evidence of pancreatitis is commonly found in necropsy studies in cats. A clinical diagnosis of pancreatitis is challenging due to nonspecific clinical signs, a lack of diagnostic lipase cutoffs, and frequent presence of multiple diseases. It is still unknown how often pancreatitis alone is found in sick cats and how often clinicopathological evidence of pancreatitis in sick cats does not lead to a clinical diagnosis of pancreatitis. Our aims were to evaluate the extent of comorbidities
in cats with suspected pancreatitis, evaluate how often sick cats with hyperlipasemia are diagnosed only with non-pancreatic diseases, and compare their clinical findings. Medical records of 563 clientowned hospitalized cats with available lipase activity measurement (LIPC Roche) > 30 U/L (RI, 6–26) were searched and medical diagnoses recorded and grouped by organ system. Clinicopathological
findings were compared between cats with pancreatitis alone (PA), pancreatitis with concurrent disease (PD), and no suspected pancreatitis (NP). We found that PA was present in 33 (6%) cats, 159 cats (28%) were in the PD group, and 371 cats (66%) had no suspected pancreatitis (NP). Clinical, laboratory, and ultrasonographic findings did not differ between PA and PD cats. Lipase activities did not differ between the three groups. The most common disease categories in PD and NP cats
were gastrointestinal, hepatobiliary, renal/urinary, and endocrine, and renal/urinary, gastrointestinal, cardiac, and musculoskeletal, respectively. We conclude that cats are rarely hospitalized because of suspected pancreatitis alone, and PA cats did not differ clinically from PD cats. Hyperlipasemia in sick cats without a diagnosis of pancreatitis may be due to a reactive pancreatopathy or preexisting chronic pancreatitis.
... And dilatation or thickness of the bile duct were considered compatible with hepatopathy [25,26]. Irregular pancreatic contour, changes in parenchymal echogenicity, increased pancreatic duct size, and peripancreatic free fluid or hyperechoic mesentery were considered compatible with pancreatopathy [27]. ...
... Extraintestinal involvement has been assigned based on ultrasonography findings [39]. The collection of clinicopathological findings including liver enzymes, and fPLI would have resulted in a more accurate classification of cats, especially in terms of pancreatopathy [27]. However, it has been reported that ultrasonography findings and clinicopathological abnormalities are less able to correctly classify intestinal, hepatic, or pancreatic inflammation in cats with gastrointestinal signs when compared with tissue biopsy and histopathological evaluation [40]. ...
Few studies have investigated total protein (TP) and serum protein electrophoresis (SPE) in cats with chronic enteropathy (CE). Cats diagnosed with CE were evaluated to investigate the relationships between TP, SPE and endoscopy, histopathology, and extraintestinal involvement. Medical records were searched for cats with a history of chronic gastrointestinal signs and a final diagnosis of CE. Information on signalment, TP, SPE, endoscopic score, histopathological diagnosis and score, and concurrent hepatic or pancreatic ultrasonographic alterations was collected. Relationships between protein profiles and other variables were investigated. Ninety-nine cats were included in the study, 63 diagnosed with various degrees of bowel inflammation and 36 with small-cell alimentary lymphoma. The most common TP alteration was hypoproteinemia (24%). No significant differences were observed between protein profiles and endoscopic and histopathological severity scores. Forty-five cats showing concurrent pancreatic and/or hepatic ultrasonographic alterations, had significantly lower albumin, lower α-globulin, and higher γ-globulin levels than cats not showing concurrent alterations. Disease severity scores did not seem to influence the protein profile in cats with CE. Extraintestinal involvement may be suspected in cats with lower albumin and α-globulins and higher γ-globulins.
... In cats, it can be associated with loss of pancreatic cells by neoplasia or pancreatitis (adeno-carcinoma is reported in 8-19% of euthanized animals). More than 60% of the diabetic cats, pancreatitis may be present based on bio-chemical and imaging results (De Cock et al. 2007;Caney 2013;Zini et al. 2015). In literature, It is reported that pancreatitis alone does not only contribute severely to cause DM but also enhances the beta cell destruction and probability of DM remission (Zini et al. 2015). ...
... More than 60% of the diabetic cats, pancreatitis may be present based on bio-chemical and imaging results (De Cock et al. 2007;Caney 2013;Zini et al. 2015). In literature, It is reported that pancreatitis alone does not only contribute severely to cause DM but also enhances the beta cell destruction and probability of DM remission (Zini et al. 2015). The other specific types of DM may include increased insulin resistance in hyper-somatotrophism (acromegaly) and hyperadrenocorticism (Cushing syndrome) (Niessen 2010; American Diabetes Association 2021) in which the use of prescribed insulin doses are not enough to control the blood glucose level (Niessen 2013 Glucocorticoids Infection 8. ...
... Diabetes mellitus and exocrine pancreatic insufficiency (EPI) are believed to be possible sequelae to CP [10,12,[17][18][19]. Cats with DM often have increased serum feline pancreasspecific lipase (Spec fPL) concentrations (Idexx Laboratories, Kornwestheim, Germany) or chronic pancreatitis on histopathology and it is possible that CP may contribute to reduced glycemic control [19][20][21][22]. ...
... Chronic pancreatitis has been suggested as a possible reason for unstable DM in cats [19,22]. Monitoring of glycemic control varied significantly between the cats, making assessment of cyclosporine's effect on glycemic control difficult. ...
Chronic pancreatitis (CP) is a common disease in middle-aged to older cats. Cyclosporine has been suggested as an alternative treatment when other immunosuppressive treatments are insufficient or contraindicated. However, no published studies have investigated its efficacy on feline CP. The aim of this retrospective study was to evaluate the efficacy of cyclosporine on supranormal serum feline pancreas-specific lipase (Spec fPL) concentrations in cats with presumed CP. Inclusion criteria were history and clinical signs suggestive of CP, serum Spec fPL concentrations above 5.3 μg/L (reference range 0–3.5 μg/L, equivocal range 3.6–5.3 μg/L) on at least two occasions and treatment with cyclosporine for at least three weeks. Serum Spec fPL was analyzed at Idexx Laboratories, Kornwestheim, Germany. Nineteen cats, aged 6.9–17.5 years (median 11.6), were included. No pancreatic biopsies were available. Median (range) serum Spec fPL concentration was 14.2 μg/L (6.1–43.3) at baseline and 6.7 μg/L (0.9–23.6) at follow-up. Cyclosporine treatment (5.0–7.9 mg/kg orally SID) was associated with a significant reduction in serum Spec fPL concentrations (p < 0.001) at follow-up after 23–206 days (median 35). Body weight decreased significantly between inclusion and follow-up (p = 0.013). Significant improvement of clinical signs could not be measured (p = 0.781). This study has several limitations, including unstandardized treatment length and dose, no control group and lack of pancreatic biopsies. Despite the limitations, our results suggest that cyclosporine treatment reduces supranormal serum Spec fPL concentrations in cats with presumed CP
... 11 Currently, no strict clinical criteria distinguish between acute and chronic or chronic active pancreatitis. [2][3][4] Moreover, FP is commonly accompanied by other diseases such as cholangiohepatitis, inflammatory bowel disease, kidney disease or diabetes mellitus (DM), [12][13][14][15][16] which makes it difficult to determine the role of pancreatic inflammation in the overall clinical picture of the patient. Currently, FP is diagnosed on the basis of the history and clinical signs, along with the combination of an increased pancreatic lipase concentration quantified using ELISA (feline pancreatic lipase immunoreactivity, fPLI) or a colorimetric 1,2-odilauryl-rac-glycero-3-glutaric acid-(6 0 -methylresorufin) ester (DGGR) assay and abdominal ultrasonography. ...
Background
Feline pancreatic lipase immunoreactivity (fPLI) is commonly used to diagnose pancreatitis in cats (FP). Untargeted metabolomics has been extensively applied in human and veterinary medicine, but no metabolomic studies regarding FP have been conducted.
Objectives
To identify metabolites significantly associated with increased fPLI.
Animals
Forty‐nine client‐owned cats: 11 clinically healthy and 38 with various clinical conditions.
Methods
Analytical cross‐sectional study with convenience sampling. A panel of 630 metabolites belonging to 26 biochemical classes was quantified in plasma using a commercial metabolomic assay. The correlation between plasma metabolite concentrations and serum fPLI was evaluated using Spearman's rank correlation coefficient (Rs) with Bonferroni correction. Multivariable analysis then was performed to control for glomerular filtration rate, liver damage, and blood glucose concentration. The accuracy of selected metabolites in discriminating between cats with normal (≤3.5 μg/L) and increased (>5.3 μg/L) fPLI was estimated using the area under the receiver operating characteristic curve (AUROC).
Results
Four hundred and seven of 630 metabolites (64.6%) were quantified in all cats. When controlled for potential confounders only 3 sphingolipids were significantly positively correlated with fPLI: 2 cerebrosides: HexCer(d18:1/24:0); (Rs = .56), and HexCer(d18:1/24:1); (Rs = .58) and 1 sphingomyelin: SM C18:0 (Rs = .55). Their AUROCs in identifying cats with increased fPLI were 82% (95% confidence interval [CI 95%], 70%‐94%), 84% (CI 95%, 72%‐96%), and 78% (CI 95%, 65%‐92%), respectively.
Conclusions and Clinical Importance
Selected sphingolipids are moderately positively correlated with fPLI and appear to have fair to moderate diagnostic accuracy in discriminating between cats with normal and increased fPLI.
Une insulinorésistance peut conduire au développement d’un diabète sucré et en compliquer la prise en charge. D’autres facteurs d’échec au traitement sont cependant possibles et doivent être recherchés (erreurs techniques, cinétique ou dose d’insuline inadéquates, etc.). Les principales maladies associées à une insulinorésistance chez le chien (syndrome de Cushing, imprégnation en progestérone lors du diœstrus chez la chienne non stérilisée) et le chat (sécrétion excessive d’hormone de croissance par un adénome hypophysaire) sont présentées dans cet article.
En médecine vétérinaire, la possibilité de rémission diabétique constitue une spécificité du chat. Elle est définie par la résolution de l’hyperglycémie et des signes cliniques associés à la maladie pendant plus de quatre semaines consécutives, chez un animal ne recevant pas d’insuline exogène. Elle est rendue possible par le caractère souvent réversible des phénomènes de glucotoxicité et d’insulinorésistance : l’administration initiale d’insuline exogène conduit à une diminution de la glycémie moyenne, ayant pour résultat une reprise des capacités sécrétoires d’insuline endogène, et donc l’amélioration du tableau clinique.
L’entrée en rémission diabétique est le plus souvent favorisée par une gestion rigoureuse du diabète sucré, associant une prise en charge alimentaire (régime humide et pauvre en glucides), une perte de poids en cas d’obésité, et un contrôle glycémique rapproché. Cette approche peut être perçue comme lourde, et altérer la qualité de vie du propriétaire ou de l’animal.
Une rechute est attendue chez environ un tiers des chats entrant en phase de rémission diabétique. Elle peut survenir dans les mois ou années suivant cette dernière. La prévention de la rechute est difficile, mais repose sur l’éviction du phénomène de glucotoxicité, principalement permis par le maintien d’une alimentation pauvre en glucides. Des traitements médicamenteux adjuvants pourraient, à l’avenir, concourir à maintenir le statut de rémission au long terme.
Le diabète sucré (DS) est l’une des maladies hormonales les plus fréquemment diagnostiquées. Les pancréatites, principalement les formes chroniques, sont souvent retrouvées chez les animaux diabétiques. Pour autant, il n’est pas toujours établi quelle affection est primitive. Les pancréatites peuvent compliquer la gestion du diabète sucré à la fois en réduisant la sécrétion d’insuline et en induisant une insulinorésistance périphérique. Une surveillance rapprochée de la glycémie est nécessaire chez ces animaux. En cas de pancréatite aiguë concomitante au diagnostic de diabète sucré, la rémission après résolution de la pancréatite est possible chez le chat. Une hospitalisation est parfois nécessaire en cas d’altération marquée de l’état général et de pancréatite aiguë. En revanche, une gestion au domicile est préférable pour les animaux stables atteints de pancréatite chronique. L’insulinothérapie n’est pas toujours modifiée par le diagnostic de pancréatite. Il est parfois nécessaire de choisir temporairement une insuline rapide chez les animaux dysorexiques et/ou hospitalisés.
Diabetes mellitus (DM) has a heterogenous cause, and the exact pathogenesis differs between patients. Most diabetic cats have a cause similar to human type 2 DM but, in some, DM is associated with underlying conditions, such as hypersomatotropism, hyperadrenocorticism, or administration of diabetogenic drugs. Predisposing factors for feline DM include obesity, reduced physical activity, male sex, and increasing age. Gluco(lipo)toxicity and genetic predisposition also likely play roles in pathogenesis. Prediabetes cannot be accurately diagnosed in cats at the current time. Diabetic cats can enter remission, but relapses are common, as these cats might have ongoing, abnormal glucose homeostasis.
OBJECTIVE: To investigate agreement of a feline pancreas-specific lipase assay and a colorimetric lipase assay with a 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6'-methylresorufin) ester (DGGR) substrate with results of pancreatic ultrasonography in cats with suspicion of pancreatitis.
DESIGN: Retrospective case series.
ANIMALS: 161 client-owned cats with suspicion of pancreatitis.
PROCEDURES: Feline pancreas-specific lipase concentration and DGGR lipase activity were measured from the same blood sample in cats undergoing investigation for pancreatitis, with < 24 hours between ultrasonography and lipase determinations. Ultrasonographic variables evaluated were ultrasonographic diagnosis of pancreatitis, enlargement, margins, echogenicity, mesenteric echogenicity, peripancreatic free fluid, cysts, masses, and common bile and pancreatic duct dilation. Agreement was assessed by use of the Cohen κ coefficient.
RESULTS: Agreement between the lipase assays was substantial (κ = 0.703). An ultrasonographic diagnosis of pancreatitis had fair agreement with feline pancreas-specific lipase concentration > 5.4 μg/L (κ = 0.264) and DGGR lipase activity > 26 U/L (κ = 0.221). The greatest agreement between feline pancreas-specific lipase concentration > 5.4 μg/L and DGGR lipase activity > 26 U/L was found for a hypoechoic and mixed-echoic (κ = 0.270 and 0.266, respectively), hypoechoic (κ = 0.261 and 0.181, respectively), and enlarged (κ = 0.218 and 0.223, respectively) pancreas.
CONCLUSIONS AND CLINICAL RELEVANCE: Agreement between pancreatic ultrasonography and lipase assay results was only fair. It remains unknown whether lipase results or pancreatic ultrasonography constitutes the more accurate test for diagnosing pancreatitis; therefore, results of both tests need to be interpreted with caution.
Diabetes mellitus (DM) is common in the general population and it poses a heavy burden to society in the form of long-term disability, healthcare use and costs. The pancreas is a key player in glucose homeostasis, but the occurrence of newly diagnosed DM after acute pancreatitis (AP), the most frequent disease of the pancreas, has never been assessed systematically. The aim of this study was to conduct a systematic literature review to determine the prevalence and time course of DM and related conditions after the first attack of AP as well as the impact of covariates.
Relevant literature cited in three electronic databases (Scopus, EMBASE and MEDLINE) was reviewed independently by two authors. The main outcome measures studied were newly diagnosed prediabetes, DM, or DM treated with insulin. Pooled prevalence and 95% CIs were calculated for all outcomes.
A total of 24 prospective clinical studies, involving 1102 patients with first episode of AP, met all the eligibility criteria. Prediabetes and/or DM was observed in 37% (95% CI 30% to 45%) individuals after AP. The pooled prevalence of prediabetes, DM and treatment with insulin after AP was 16% (95% CI 9% to 24%), 23% (95% CI 16% to 31%), and 15% (95% CI 9% to 21%), respectively. Newly diagnosed DM developed in 15% of individuals within 12 months after first episode of AP and the risk increased significantly at 5 years (relative risk 2.7 (95% CI 1.9 to 3.8)). A similar trend was observed with regard to treatment with insulin. The severity of AP, its aetiology, individuals' age and gender had minimal effect on the studied outcomes.
Patients with AP often develop prediabetes and/or DM after discharge from hospital, and have a greater than twofold increased risk of DM over 5 years. Further studies are warranted to determine the optimal strategy for its detection and whether the risk of developing DM after AP can be reduced.
Background
Remission occurs in 10–50% of cats with diabetes mellitus (DM). It is assumed that intensive treatment improves β-cell function and increases remission rates.HypothesisInitial intravenous infusion of insulin that achieves tight glycemic control decreases subsequent insulin requirements and increases remission rate in diabetic cats.AnimalsThirty cats with newly diagnosed DM.Methods
Prospective study. Cats were randomly assigned to one of 2 groups. Cats in group 1 (n = 15) received intravenous infusion of insulin with the goal of maintaining blood glucose concentrations at 90–180 mg/dL, for 6 days. Cats in group 2 (n = 15) received subcutaneous injections of insulin glargine (cats ≤4 kg: 0.5–1.0 IU, q12h; >4 kg 1.5–2.0 IU, q12h), for 6 days. Thereafter, all cats were treated with subcutaneous injections of insulin glargine and followed up for 6 months. Cats were considered in remission when euglycemia occurred for ≥4 weeks without the administration of insulin. Nonparametric tests were used for statistical analysis.ResultsIn groups 1 and 2, remission was achieved in 10/15 and in 7/14 cats (P = .46), and good metabolic control was achieved in 3/5 and in 1/7 cats (P = .22), respectively. Overall, good metabolic control or remission occurred in 13/15 cats of group 1 and in 8/14 cats of group 2. In group 1, the median insulin dosage given during the 6-month follow-up was significantly lower than in group 2 (group 1: 0.32 IU/kg/day, group 2: 0.51 IU/kg/day; P = .013).Conclusions and Clinical ImportanceInitial intravenous infusion of insulin for tight glycemic control in cats with DM decreases insulin requirements during the subsequent 6 months.
Serum lipase activities measured by catalytic assays are claimed to be of limited utility for diagnosing pancreatitis in cats. The Spec fPL assay currently is believed the most sensitive test; however, studies comparing different lipase assays are lacking. 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6'-methylresorufin) ester (DGGR) assay for the determination of lipase activity has been evaluated in dogs, but no information is available in cats.
To investigate the agreement of DGGR-lipase activity and Spec fPL concentration in cats with clinical signs consistent with pancreatitis.
Two hundred fifty-one client-owned cats.
DGGR-lipase activity and Spec fPL concentration measured from the same blood sample in cats undergoing investigation for pancreatitis. The agreement between DGGR-lipase and Spec fPL at different cutoffs was assessed using Cohen's kappa coefficient (κ). Sensitivity and specificity were calculated for 31 cases where pancreatic histopathology was available.
DGGR-lipase (cutoff, 26 U/L) and Spec fPL (cutoff, >5.3 μg/L) had a κ of 0.68 (standard error [SE] 0.046). DGGR-lipase (cutoff, 26 U/L) and Spec fPL (cutoff, >3.5 μg/L) had a κ of 0.60 (SE, 0.05). The maximum κ at a Spec fPL cutoff >5.3 μg/L was found when the DGGR-lipase cutoff was set >34 U/L and calculated as 0.755 (SE, 0.042). Sensitivity and specificity were 48% and 63% for DGGR-lipase (cut-off, 26 U/L) and 57% and 63% for Spec fPL (>5.3 μg/L), respectively.
Both lipase assays agreed substantially. DGGR assay seems a useful and cost-efficient method compared to the Spec fPL test.
Pancreatitis is a common disease in cats that is difficult to diagnose.
To determine the sensitivity and specificity of ultrasonographic changes of the pancreas with serum feline pancreatic lipase immunoreactivity (fPLI) as the standard for diagnosis of pancreatitis.
35 cats with clinical signs consistent with pancreatitis with an abdominal ultrasound examination and serum fPLI concentration measured within 3 days of the ultrasound.
Retrospective study: Pancreatic thickness, pancreatic margination, pancreatic echogenicity, and peripancreatic fat echogenicity were evaluated. Sensitivity and specificity were calculated with an elevated serum fPLI concentration indicative of pancreatitis as the standard for diagnosis.
Serum fPLI was elevated and diagnostic for pancreatitis in 19 of 35 cats. The single ultrasound characteristic with the highest sensitivity was hyperechoic peripancreatic fat at 68% (95% confidence interval = 44–87%), indicating a moderate probability that cats with pancreatitis will have this abnormality on ultrasonographic examination. Specificity was >90% for each of increased pancreatic thickness, abnormal pancreatic margin, and hyperechoic peripancreatic fat. The sensitivity and specificity of ultrasound were 84% (95% confidence interval = 60–97%) and 75% (95% confidence interval = 48–93%), respectively, in cats with elevated serum fPLI indicative of pancreatitis.
The presence of a thick left limb of the pancreas, severely irregular pancreatic margins, and hyperechoic peripancreatic fat in cats with appropriate clinical signs and elevated serum fPLI are highly supportive of pancreatitis.
Objective:
To evaluate serum feline-specific pancreatic lipase immunoreactivity (fPLI) concentrations and abdominal ultrasonographic findings in cats with trauma resulting from high-rise syndrome.
Design:
Prospective case series. Animals-34 client-owned cats.
Procedures:
From cats evaluated because of high-rise syndrome between March and October 2009, a blood sample was obtained for measurement of serum fPLI concentration within 12 hours after the fall and at 24, 48, and 72 hours after the first blood collection. Pancreatitis was diagnosed in cats with an fPLI concentration > 5.4 μg/L. Each cat had abdominal ultrasonography performed twice 48 hours apart, and pancreatic trauma was assessed via detection of pancreatic enlargement, hypoechoic or heteroechoic pancreatic parenchyma, hyperechoic mesentery, and peritoneal effusion. Cats were assigned 1 point for each abnormality present, and a cumulative score ≥ 3 was considered suggestive of traumatic pancreatitis.
Results:
Traumatic pancreatitis was diagnosed in 9 and 8 cats on the basis of serum fPLI concentration and ultrasonographic findings, respectively. For cats with pancreatitis, fPLI concentration was significantly higher at 12 and 24 hours after the fall than at 48 and 72 hours after the fall, and serum fPLI concentration decreased as time after the fall increased. Significant agreement existed between the use of serum fPLI concentration and abdominal ultrasonography for the diagnosis of traumatic pancreatitis.
Conclusions and clinical relevance:
Cats with high-rise syndrome often had serum fPLI concentrations > 5.4 μg/L within 12 hours after the fall, and concurrent evaluation of those cats via abdominal ultrasonography twice, 48 hours apart, improved detection of traumatic pancreatitis.
Pancreatitis was considered a rare disease in the cat until a couple of decades ago when several retrospective studies of severe acute pancreatitis were published. It was apparent that few of the diagnostic tests of value in the dog were helpful in cats. With increasing clinical suspicion, availability of abdominal ultrasonography, and introduction of pancreas-specific blood tests of increasing utility, it is now accepted that acute pancreatitis is probably almost as common in cats as it is in dogs, although the etiology(s) remain more obscure. Pancreatitis in cats often co-exists with inflammatory bowel disease, less commonly with cholangitis, and sometimes with both. Additionally, pancreatitis may trigger hepatic lipidosis, while other diseases, such as diabetes mellitus, may be complicated by pancreatitis. Therapy is similar to that used in dogs, with added emphasis on early nutritional support to prevent hepatic lipidosis. Less is known about chronic pancreatitis than the acute form, but chronic pancreatitis is more common in cats than it is in dogs and may respond positively to treatment with corticosteroids.
OBJECTIVE- The objective of this study was to assess the risk of acute pancreatitis in patients with type 2 diabetes compared with that in patients without diabetes. We also examined the risk of biliary disease (defined as occurrence of cholelithiasis, acute cholecystitis, or cholecystectomy), which is a major cause of pancreatitis. RESEARCH DESIGN AND METHODS- We conducted a retrospective cohort study using a large, geographically diverse U.S. health care claims database. Eligible patients (≥18 years) were enrolled for at least 12 continuous months (1999-2005), with no incident events of pancreatitis or biliary disease during that 1 year baseline period. ICD-9 codes and prescription data were used to identify patients with type 2 diabetes; ICD-9 codes were also used to identify cases of pancreatitis and biliary disease. Overall, 337,067 patients with type 2 diabetes were matched on age and sex with 337,067 patients without diabetes. Incidence rates of disease and 95% CI were calculated per 100,000 person-years of exposure. RESULTS- The type 2 diabetic cohort had a 2.83-fold (95% CI 2.61-3.06) greater risk of pancreatitis and 1.91-fold (1.84-1.99) greater risk of biliary disease compared with the nondiabetic cohort. Relative to patients of corresponding age without diabetes, younger type 2 diabetic patients had the highest risk of pancreatitis (<45 years: incidence rate ratio [IRR] 5.26 [95% CI 4.31-6.42]; ≥45 years: 2.44 [2.23-2.66]). CONCLUSIONS- These data suggest that patients with type 2 diabetes may have an increased risk of acute pancreatitis and biliary disease.