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Toxicosis with grapes or raisins causing acute kidney injury and neurological signs in dogs
September 11th, 2020
Several reports of dogs developing acute kidney injury (AKI) after ingestion of grapes, raisins, or currants have been published since 1998.1-8 The mechanism of toxicity is still unknown. Hypotheses include contamination of fruits with mycotoxins, heavy metals or pesticides, excess vitamin D, tannin intolerance or excessive ingestion of monosaccharides, hypovolemic shock, and renal ischemia. The exact amount of ingested fruits necessary to cause damage is unknown, and estimations are based on clinical cases. The lowest reported dosage to cause AKI is 19.6 g/kg body weight for grapes, and 2.8 g/kg for raisins.
Reported clinical signs typically include vomiting within 24 (81% of dogs) to 48 (100% of dogs) hours of ingestion, with vomitus or diarrhea fluid possibly containing grapes or swollen raisins. Other signs were compatible with acute uremia and included anorexia, lethargy, diarrhea, and abdominal pain, as well as oliguria or anuria in 49% of dogs. Azotemia developed rapidly within 2 days of ingestion. Less frequent signs reported include dehydration, edema, ptyalism, polyuria, polydipsia, hypothermia, hypertension, trembling, seizures, and ataxia in 23% of dogs. Median onset of ataxia was 2 (range, 0.6-6) days after ingestion of grapes or raisins. It was associated with a negative outcome, and in the only survivor affected, clinical signs of ataxia persisted for 6 days. A case report from Korea describes a Yorkshire Terrier with ataxia that began on the day after grape ingestion. However, the dog died on day 3, and detailed descriptions of neurological signs and associated neuropathology are lacking.
In contrast to previous reports, we observed severe neurological signs in the dogs presented to the Small Animal Clinic of the Vetsuisse Faculty Bern, Switzerland, for AKI after grape or raisin toxicosis (GRT), sometimes dominating the clinical picture and confusing the diagnostic evaluation. Our retrospective study had the following aims: First, to evaluate the clinical, laboratory, pathological, and outcome features of dogs diagnosed with GRT compared to dogs diagnosed with AKI of other origin, with emphasis on renal and neurological manifestations; and second, to investigate potential factors for development of neurological signs by comparing dogs with and without central nervous system deficits.
Background: The ingestion of grapes or raisins has been reported to cause acute kidney injury (AKI) in dogs, with a clinical picture dominated by early gastrointestinal signs and rapidly developing uremia. Ataxia is mentioned in a few reports, but not further characterized.
Objectives: To evaluate the clinical, laboratory, and pathological features of dogs diagnosed with grape or raisin toxicosis (GRT) with emphasis on renal and neurological manifestations, compared to a control group of dogs with AKI from other causes.
Animals: Fifteen client-owned dogs with GRT and 74 control dogs.
Methods: Retrospective study over 17 months.
Results: All dogs with GRT were presented with severe AKI (grade 4, n = 5; grade 5, n = 10). Eleven dogs (73%) had marked forebrain, cerebellar, or vestibular signs. These manifestations dominated the clinical picture in some dogs, but were not associated with the severity of azotemia or the presence of systemic hypertension. Eight dogs (53%) survived, and 5 dogs experienced a complete neurological recovery. Causes of death were unrelated to the neurological manifestations. Neuropathological examination of 4 dogs did not identify any structural central nervous system abnormality. Only 2 control dogs (3%) displayed neurological signs with seizures unrelated to the AKI; 42 control dogs (57%) survived.
Conclusions and Clinical Importance: Severe forebrain, cerebellar, or vestibular signs may be an important feature of GRT and dominate the early clinical picture. The described features suggest a reversible functional brain injury specific to GRT and unrelated to uremia.
Amyloidogenesis of feline amylin and plasma levels in cats with diabetes mellitus or pancreatitis
September 9th, 2020
Amylin is a pancreatic hormone co-secreted along with insulin and involved in pancreatic amyloidosis and b-cell apoptosis in diabetic cats and humans. Amylin is usually elevated in early stages of type 2 diabetes but recently was found to be increased in acute and chronic pancreatitis in humans. Currently, there are little data about feline amylin propensity to fibrillate and no information on circulating levels of this hormone during feline pancreatitis.
We compared 4 amylin analogues and found cat amylin to be more prone to amyloid fibrillation than human amylin, the triple-proline analogue pramlintide and rat amylin. We also measured plasma amylin levels in healthy lean cats, diabetic cats, and cats with pancreatitis. Plasma amylin was higher in diabetic cats compared with healthy lean cats (P < 0.001). Interestingly, amylin levels during pancreatitis were higher than those of both lean cats (P < 0.0001) and diabetic cats without pancreatitis (P < 0.005). These data support evidence of feline amylin being more prone to aggregation than human amylin in vitro, which may influence diabetes mellitus progression and b-cell failure in vivo. Furthermore, our data show an increase in amylin levels during feline pancreatitis and the need for future research on the role of this hormone in the pathogenesis of pancreatic inflammation associated to feline diabetes mellitus.
Pancreatitis and diabetes mellitus appear to occur concurrently in many species, including humans and cats. Although a causal association has not been proven yet in cats, the concurrence of these 2 diseases has clinical implications for case management and clinical control.
Recently, human pancreatitis has been associated with the decrease in b-cell function in a progression rate even higher than in type 2 diabetes mellitus. Previous studies in humans have shown that amylin is increased during acute and chronic pancreatitis. Currently, no study has determined if feline pancreatitis can also induce an increase in amylin levels.
Observational studies prospecting amyloid material in vivo have long suggested that proline residues modulate the propensity for amylin analogues to form amyloid aggregations. However, no comparative assays have been reported to date. In fact, the triple proline analogues rodent amylin and the triple-proline (25,28,29Pro) human amylin analogue pramlintide have long been assumed to be nonamyloidogenic and nontoxic in vitro and in vivo, until recent works revealed their propensity in forming amyloid material.
In the present study, we investigated the amyloid nature of cat amylin compared with other species, exploring the aggregation pattern of cat, human, and murine amylin as well as the amylin analogue pramlintide in vitro. Furthermore, we compared plasma amylin levels between healthy cats, diabetic cats, and cats with pancreatitis.
Prevalence and risk factors associated with systemic hypertension in dogs with spontaneous hyperadrenocorticism
Aug 31st, 2020
Systemic hypertension associated with hypercortisolism is common in people, affecting 70%-85% of the patients. The pathophysiological mechanisms for hypertension in HAC are incompletely understood, but in people a multifactorial model has been proposed with many pathways involved: the renin-angiotensin system, an increased mineralocorticoid activity, the sympathetic nervous system, the vasoregulatory system, metabolic factors, vascular remodeling and sleep apnea. In human medicine, risk factors for hypertension associated with hypercortisolism are reported. In pediatric patients there is a positive correlation between SH and high circulating cortisol concentrations. In addition, SH is more frequent in pediatric patients with ACTH-independent Cushing's syndrome (CS). In adults, this tendency has also been observed in patients with ACTH-independent CS, but the prevalence of SH is similar for ACTH-dependent and independent hypercortisolism. Furthermore, in adults with CS, age, body mass index and duration of hypercortisolism have been associated with the development of SH, but no correlation is observed with circulating cortisol concentrations. Hypertensive human patients with hypercortisolism tend to have lower potassium blood concentrations than normotensive patients, especially those with ectopic CS in which hypokalemia is frequent and strongly associated with hypertension.
Systemic hypertension is also recognized in dogs with HAC with a prevalence between 31% and 86%. Some pathophysiological mechanisms have also been proposed, such as increased mineralocorticoid activity, decreased nitric oxide concentrations or increased renal vascular resistance. There are few studies assessing the risk factors for SH in dogs with HAC; in previous studies, no difference in the prevalence or severity of SH is observed between dogs with PDH or ADH and there is no correlation between systolic blood pressure (SBP) and age, sex, reproductive status or results of the ACTH-stimulation tests. Previous studies have inconsistently identified a relationship between SBP and urinary protein to creatinine ratio (UPC) or baseline cortisol concentrations. A correlation between SBP and UPC but not with baseline cortisol concentrations has been described; however, other authors have found a correlation between SBP and baseline cortisol concentrations but not with UPC.
The objectives of our study were to determine the prevalence and severity of SH in dogs with naturally occurring HAC and to identify potential risks factors for SH in these dogs.
Background: Systemic hypertension (SH) is common in dogs with hyperadrenocorticism (HAC) however there are not many studies assessing its prevalence and risk factors.
Objectives: To determine the prevalence and severity of SH in dogs with HAC and its association with clinical and laboratory findings to identify potential risk factors.
Animals: Sixty-six client owned dogs with spontaneous HAC.
Methods: Retrospective cross-sectional study. Medical records of dogs with HAC were reviewed. Systolic blood pressure (SBP) was measured using Doppler ultrasonography. Clinical signs, physical examination findings and clinicopathologic data (CBC, serum biochemistry and electrolytes, urinalysis and urinary culture, and adrenal function tests) were reviewed for analysis.
Results: Prevalence of SH (≥150 mm Hg) was 82% (54/66) and prevalence of severe SH (≥180 mm Hg) was 46% (30/66). All dogs with thrombocytosis had SH (P = .002), and a platelet count ≥438 x 103/μL was 100% specific and 61.1% sensitive to predict SH (AUC = .802, P = .001). Median potassium levels were lower in hypertensive dogs (4.1 mEq/L, range 3.1-5.4 mEq/L) than in normotensive ones (4.5 mEq/L, range 4.0- 5.0 mEq/L) (P = .007). Dogs with UPC ≥ 0.5 had higher median SBP than those without proteinuria (P = .03). Dogs with concurrent diabetes mellitus seemed to have a reduced risk of SH (OR = .118, 95%CI = .022-.626, P = .02).
Conclusions and Clinical Importance: In conclusion, SH, which is frequently severe, is common in dogs with HAC and blood pressure should be routinely assessed in dogs with a suspicion of HAC. In those cases in which blood pressure cannot be routinely evaluated, the presence of thrombocytosis, low potassium concentrations and proteinuria should raise concerns about possible SH and the risk of TOD and might incite the clinician to perform this procedure. The association between SH and potassium concentrations might suggest a role of MR in the development of hypertension in these dogs; however further studies are needed to investigate the relationship between SH, aldosterone and 11β-HSD activity in dogs with HAC.
These findings might suggest that mineralocorticoid receptors (MR) could be involved in the development of SH in dogs with HAC. The MR has the same affinity to aldosterone and cortisol, but not to cortisone. The enzyme 11β-hydroxysteroid dehydrogenase (11β-HSD) converts cortisol into cortisone, and it is abundantly expressed in the classical mineralocorticoid target tissues (eg, renal cortex, vascular endothelium and smooth muscle cells), binding the selectivity of MR to aldosterone. Hypercortisolism saturates the 11β-HSD allowing cortisol to bind the MR and resulting in a cortisol induced apparent mineralocorticoid excess. In people with hypercortisolemia, this feature has been associated with sodium retention and potassium excretion, which could contribute to the development of SH.
Finally, dogs with concurrent DM and HAC seemed to have a reduced risk of development of SH; this finding should be further investigated.
Risk factors associated with progressive increases in serum creatinine concentrations in cats with cancer receiving doxorubicin
Aug 13th, 2020
In humans, doxorubicin is not associated with nephrotoxicosis, however, other chemotherapeutic agents, including cisplatin, mitomycin C, gemcitabine and ifosfamide, can be nephrotoxic. Several patient-related factors increase the risk and severity of drug-induced kidney injury. Risk factors nclude age and female sex as both are associated with decreased muscle mass and total body water and therefore likely an underrepresentation of pre-existing kidney dysfunction, as defined by serum creatinine concentration, before administration of chemotherapy. Intravascular volume depletion from vomiting, diarrhea and diuretics also increases the risk of drug-induced nephrotoxicosis.
Cancers such as multiple myeloma, lymphoma and leukemia and diabetes mellitus are associated with increased risk of nephrotoxicosis. While doxorubicin-induced nephrotoxicosis occurs in cats, risk factors for its development have not been thoroughly evaluated. In addition, previous studies have defined decreased kidney function by serum creatinine concentration outside of laboratory reference intervals, which identifies disease late in its course after considerable injury and function loss have occurred. The aims of this retrospective study were to determine the incidence of early loss of kidney function (as defined by ≥0.3 mg/dL increase in serum creatinine concentration) in cats with cancer receiving doxorubicin in single or multiagent chemotherapy protocols and to determine risk factors associated with these progressive elevations in serum creatinine concentration. We hypothesized that pre-existing chronic kidney disease, radiation therapy, recent anesthesia or surgery and cumulative dose of doxorubicin would be risk factors for increasing serum creatinine concentrations in cats receiving doxorubicin.
Background: Azotemia occurs in cats administered doxorubicin, but risk factors have not been explored.
Objective: To determine incidence of progressive increases in serum creatinine concentration in cats with cancer receiving doxorubicin in single or multiagent chemotherapy protocols and associated risk factors.
Animals: Seventy cats with cancer receiving doxorubicin.
Methods: A retrospective study (2007-2017) of cats with indices of kidney function recorded before and after doxorubicin administration was reviewed. Cats diagnosed with kidney injury because of known etiologies other than possible doxorubicin toxicosis were excluded. Variables were compared to identify risk factors.
Results: Mean age (±SD) was 10.9 years (±3.2). Cancer types included lymphoma (n = 36), sarcoma (n = 19) and carcinoma (n = 14). Chronic kidney disease was present in 29/70 (41%) cats before receiving doxorubicin. Of 70 cats, 24 (34%) developed an increase in serum creatinine concentration ≥0.3 mg/dL and 10 (14%) had an increase ≥50% from baseline. Mean time to increases in serum creatinine concentration ≥0.3 mg/dL from first administration of doxorubicin was 119.3 days (±89.7), with mean 2.8 (±1.2) doses administered. Neutropenia or anemia during chemotherapy and number of radiation therapy treatments under general anesthesia were risk factors for increases in serum creatinine concentration (P < .05). Cats receiving single agent doxorubicin had a higher likelihood of an increase in serum creatinine concentration ≥0.3 mg/dL from baseline than cats receiving CHOP-based chemotherapy
protocols (OR 20.0, 95% CI 2.9-100).
Conclusions and Clinical Importance: Progressive increases in serum creatinine concentration from baseline were common in cats receiving doxorubicin and associated risk factors were identified.
Utility of radiographic measurements to predict echocardiographic left heart enlargement in dogs with preclinical myxomatous mitral valve disease
July 20, 2020
Echocardiography is considered the gold standard for evaluating left atrial and left ventricular chamber size, however the skill and expertise required to perform and interpret echocardiographic examinations is often not available. In contrast, thoracic radiography is widely available and vertebral heart size (VHS) is a technique used to quantify cardiac size in dogs, including dogs with MMVD. There are parallel increases in VHS and echocardiographic left atrial and left ventricular dimensions before onset of congestive heart failure dogs with MMVD. Vertebral left atrial size (VLAS), a radiographic measurement specifically targeted to reflect left atrial size, is a useful and repeatable predictor of echocardiographically confirmed left atrial enlargement in dogs with MMVD.
The primary objective of this study was to evaluate the ability of VHS and VLAS to predict echocardiographic criteria for left heart enlargement (LHEECHO) in dogs with preclinical MMVD. We hypothesized that radiographic measurements would predict LHEECHO and would help determine severity of disease in dogs with preclinical MMVD. We aimed to identify clinically relevant values of VHS, VLAS, and sum of VHS + VLAS that predicted presence and absence of LHEECHO.
Background: Evaluation of left heart size helps determine disease severity in dogs with myxomatous mitral valve disease (MMVD).
Hypothesis/Objectives: Determine the ability of radiographic vertebral heart size (VHS) and vertebral left atrial size (VLAS) to predict LHEECHO in dogs with preclinical MMVD.
Animals: Seventy client-owned dogs with MMVD and no historical or present clinical or radiographic evidence of congestive heart failure (CHF).
Methods: Retrospective cross-sectional study of dogs with same-day echocardiography and thoracic radiography. Receiver-operating characteristic (ROC) curves were used to assess the ability of VHS, VLAS, and VHS + VLAS to discern dogs with and without LHEECHO, and clinically relevant cutpoints for these radiographic measurements were selected.
Results: The ability of VHS and VHS + VLAS to predict LHEECHO was moderate (area under the curve [AUC]VHS = 0.851; 95% CI, 0.762-0.941; AUCVHS + VLAS = 0.865; 0.783-0.947), and performance of VLAS and VHS + VLAS was not different from that of VHS alone. A VHS cutpoint of >10.8 had sensitivity = 91.1% (76.3%-98.1%) and specificity = 69.4% (51.9%-83.7%) for predicting LHEECHO. A cutpoint of >11.7 had sensitivity = 32.4% (17.4%-50.5%) and specificity = 97.2% (85.5%-99.9%) for predicting LHEECHO. Thirty (43%) of the 70 dogs had a VHS value of 10.9 to 11.7.
Conclusions and Clinical Importance: Vertebral heart size >11.7 identified dogs with LHEECHO and VHS ≤ 10.8 excluded dogs with LHEECHO.
In summary, the radiographic VHS is clinically useful in identifying LHEECHO in dogs with preclinical MMVD, but is limited by a substantial proportion of dogs with indeterminate VHS values. Radiographic measures of LA size such as VLAS possessed low correlation to echocardiographic LA size and did not significantly contribute to detection of LHEECHO in comparison to use of VHS alone in dogs with preclinical MMVD.
Prevalence and characterization of hypoadrenocorticism in dogs with signs of chronic gastrointestinal disease: A multicenter study
June 24th, 2020
Signs of gastrointestinal disease (SGD) secondary to a lack of glucocorticoids are indistinguishable from clinical signs caused by primary GI disorders. In the absence of electrolyte abnormalities, subtle laboratory abnormalities might lead to a suspicion of HA. These can include the lack of a stress leukogram, relative or absolute lymphocytosis, eosinophilia, prerenal azotemia, hypoalbuminemia, hypoglycemia or hypercalcemia. However, these changes are nonspecific, have a number of possible causes and do not help to discriminate primary GI disease from HA.
Hence, diagnosis of HA, especially GDH, is dependent on adrenal gland function testing, such as ACTH-stimulation test (ACTHST). This multicenter study was conducted in order to evaluate the necessity of performing this relatively expensive and time-consuming test in dogs with chronic SGD. The primary aim was to assess the prevalence of HA in dogs with chronic SGD. The secondary aim was to identify clinical and laboratory variables that might help to identify or exclude HA in this group of dogs before performing ACTHST, especially in comparison to other dogs with chronic SGD that do not have HA.
Background: Dogs with hypoadrenocorticism (HA) frequently show signs of gastrointestinal disease (SGD). The prevalence of dogs presented for chronic SGD with HA is unknown.
Objectives: The aims of this study were to determine the prevalence of HA in dogs with chronic SGD and to identify clinical and laboratory variables for HA in this population.
Animals: One hundred fifty-one dogs with chronic SGD.
Methods: In this multicentered prevalence study a standardized workup was performed in prospectively enrolled dogs with SGD > 3 weeks duration. Basal serum cortisol concentration was measured in every dog with ACTH stimulation test (ACTHST) if basal serum cortisol concentration was <3 μg/dL.
Results: Basal serum cortisol concentration was <3 μg/dL in 80/151 (53%) dogs, <2 μg/dL in 42/151 (28%) dogs, and < 1 μg/dL in 9/151 (6%) dogs. In 6/151 dogs HA was diagnosed based on ACTHST (stimulated serum cortisol concentration < 2 μg/ dL), a prevalence of 4%. There was no difference in history, physical examination, and laboratory variables between dogs with HA and those with other causes of chronic SGD. In 4/6 dogs with HA, there was melena or hematochezia indicating gastrointestinal blood loss. Hyperkalemia, hyponatremia, or both was not observed in any dog.
Conclusion and Clinical Importance: The prevalence of HA among dogs with chronic SGD is higher than in the general population. Based on these results, testing adrenal function should be performed as a standard screening test in dogs with chronic SGD to differentiate between HA and chronic enteropathies.
Application of therapeutic plasma exchange in dogs with immune-mediated thrombocytopenia
June 19th, 2020
Immune-mediated thrombocytopenia (IMT) is a disease in which antibodies bind to platelet surface epitopes and lead to platelet destruction. Resulting thrombocytopenia is severe and risk for spontaneous hemorrhage often develops when platelet counts are <50 000/μL. Immune-mediated hemolytic anemia (IMHA) is diagnosed concurrently in some cases, a condition known as Evan’s syndrome. Treatment for dogs with primary IMT consists of immunosuppression with corticosteroids, alone, or in combination with other immunosuppressive drugs including azathioprine, cyclosporine, and mycophenolate mofetil. Vincristine and human IV immunoglobulin (hIVIG) decrease the time required to restore platelet counts to ≥40 000/μL in affected dogs. Splenectomy also has been used in dogs with refractory IMT.
Therapeutic plasma exchange (TPE) is an extracorporeal treatment in which a patient’s plasma, containing pathogenic substances such as antibodies and antigen-antibody complexes, is removed and exchanged with replacement solutions. In dogs, TPE is emerging as an effective treatment for immune-mediated disorders, including IMHA and myasthenia gravis, but its application in dogs with IMT has not been described previously. With these case reports, we aimed to describe the techniques, complications, and outcomes of TPE in 4 dogs treated for IMT.
Abstract: Therapeutic plasma exchange (TPE) is an emerging treatment for dogs with immune mediated diseases, but reports for treatment of immune-mediated thrombocytopenia (IMT) are lacking. These case reports illustrate the application of centrifugal TPE in 4 dogs with IMT. All dogs presented with severe hemorrhage requiring ≥1 blood transfusions, were unresponsive to conventional treatment or both. Dogs were treated with 3 sequential centrifugal TPE sessions, totaling 4.0 to 4.9 total plasma volumes exchanged per dog. In 3 dogs, TPE was associated with improvement in clinical manifestations of bleeding and platelet count in combination with immunosuppressive drugs. One dog was euthanized after 3 treatments because of persistent severe thrombocytopenia and hemorrhage. Preliminary observations indicate that TPE is safe and may be a useful adjunct in the management of IMT that is severe or refractory to traditional treatment.
Retrospective study of the diagnostic utility of Spec fPL in the assessment of 274 sick cats
May 26th, 2020
Diagnosis of pancreatitis in cats usually involves a combination of clinical suspicion, evaluation of clinical pathology test results, ultrasonographic evidence of pancreatitis, and measurement of serum feline pancreatic lipase immunoreactivity (fPL). Because no gold standard diagnostic test is available, clinicians must assess test results critically in the context of the clinical presentation.
Lipase is secreted by several tissues and hence measuring the total serum activity of this enzyme is of no diagnostic value in the diagnosis of pancreatitis in cats. Pancreatic lipase, however, is exclusively secreted by the pancreas. This was demonstrated in dogs, because dogs with exocrine pancreatic insufficiency had no canine pancreatic lipase immunoreactivity (cPL) in their serum. However, no similar study has been reported in cats. Regardless, the amino acid sequence of feline pancreatic lipase should be different from that of lipase secreted by other tissues, which in turn should generate a specific immunologic response. The IDEXX laboratories developed the Spec fPL, a quantitative ELISA in 2008 for feline PL, as they had for the canine Spec cPL.
Clinical pathology results reported in cats with pancreatitis include hyperbilirubinemia, hypocalcemia, and hypoalbuminemia, but there are conflicting reports on whether or not clinically relevant differences in these variables occur in cats with pancreatitis.
Our aims were to evaluate the diagnostic utility of the Spec fPL test and selected biochemical tests in the diagnosis of pancreatitis in cats presented to a small animal referral teaching hospital in the United Kingdom. Because no gold standard to assess the diagnostic performance of Spec fPL is available, a combination of diagnostic findings (clinical signs and ultrasonography in all cats, histopathology and cytology in some cats) was used to reach a diagnosis of definite, probable, possible, or unlikely pancreatitis.
Background: Serum feline pancreatic lipase immunoreactivity (fPL) commonly is used in the assessment of sick cats suspected to have pancreatitis but its diagnostic utility is debated.
Objectives: To evaluate the diagnostic utility of the Spec fPL test and selected serum biochemistry tests in the diagnosis of pancreatitis in cats.
Animals: Two hundred seventy-four client-owned cats presented to a university teaching hospital in the United Kingdom, from April 2013 to May 2017, in which Spec fPL was measured.
Methods: Cats were classified into 1 of 4 groups based on clinical signs (all cats), ultrasonographic findings (all cats) and histopathological or cytological assessment of the pancreas where available (9 cats) regardless of Spec fPL concentration. The groups were (a) definite pancreatitis (n = 9), (b) probable pancreatitis (n = 49), (c) possible pancreatitis (n = 139), and (d) unlikely pancreatitis (n = 77). Spec fPL and selected serum biochemistry test results were compared among groups.
Results: Serum fPL concentrations >5.3 μg/L were classified as positive and concentrations <3.5 μg/L were classified as negative. There was a significantly (P = .03) lower proportion of false-positive results (cats unlikely to have pancreatitis, n = 77, with a positive fPL, n = 8, 10%) than false-negative results (cats with definite or probable pancreatitis, n = 58, with a negative fPL result, n = 14, 24%). None of the selected biochemical tests were helpful diagnostically.
Conclusion and Clinical Importance: A positive Spec fPL result indicates that pancreatitis is a probable diagnosis, but the test cannot be used to rule the diagnosis out.
In conclusion, our study supported the use of Spec fPL as part of the diagnostic evaluation of cats with suspected pancreatitis. However, our results must be interpreted with caution. A positive result increases the likelihood of the diagnosis, because in our study and others, the false-positive rate appears to be low. It cannot, however, be used to rule out pancreatitis as a diagnosis because the false negative rate is relatively high. Approximately 25% of the cases classified as definite or probable pancreatitis in our study would have been missed if Spec fPL was the only diagnostic test used. Pancreatitis in cats remains a challenge to diagnose, and results from multiple diagnostic modalities should be assessed when making the diagnosis.