Title

Subtitle

Cats with EPI

There is not a lot of information on how to manage cats with EPI ... supposedly it is rare for cats to develop EPI... unfortunately, we are seeing more and more cats being diagnosed with this condition.

 To best help serve the public and the veterinarian community, this page is divided into  sections....

  1. "Managing Cats with EPI" has personal stories of how some EPI cat owners manage their EPI cat on a day-to-day basis..... contact information is also included to help those in need of support.
  2. "EPI in Cats" is veterinarian peer-reviewed research information on this topic.
.......and of note is the latest CAT EPI research:

1. Published as of September 19, 2016 in "Journal of Veterinary Medicine" Volume 30, Issue 6, November 2016,  Feline Exocrine Pancreatic Insufficiency: A Retrospective Study of 150 Cases by Xenoulis PG1Zoran DL2Fosgate GT3Suchodolski JS1Steiner JM1.
 
2. Published as of November 28, 2012 in "Topics in Companion Animal Medicine" Volume 27, Number 3, Aug 2012  http://companimalmed.com/  has the 2nd most recent research on "Exocrine Pancreatic Insufficiency in the Cat" by Joerg M. Steiner, Vet, MD, PhD, Dipl. ACVIM, ECVIM-CA, AGAF of Texas A&M Gastroenterology Lab  
 
 
As of March 2014 ... a small EPI Kitty support yahoo-group was started by Soleil's mom, Carol.... but... has since grown so much that in lieu of the yahoo group we have now started a new "EPI In Cats" website with it's very own forum for support.
 
Please feel free to visit the new EPI in Cats website and join the EPI Cat forum: http://epiincats.webs.com/ 
 
or contact Carol at: [email protected] 
 

 

















  • This work was performed at the Gastrointestinal Laboratory, Department of Small Animal Clinical Sciences, Texas A&M University, College Station, TX.
  • Some of the results of this study were presented at the 2012 American College of Veterinary Internal Medicine Forum, New Orleans, LA.

Abstract

Background

Little information is available about the clinical presentation and response to treatment of cats with exocrine pancreatic insufficiency (EPI).

Objectives

To describe the signalment, clinical signs, concurrent diseases, and response to treatment of cats with EPI.

Animals

One hundred and fifty cats with EPI.

Methods

Retrospective case series.

Results

Questionnaires were sent to 261 veterinarians, and 150 (57%) were returned with data suitable for statistical analysis. The median age of the cats with EPI was 7.7 years. The median body condition score was 3 of 9. Ninety-two of 119 cats (77%) had hypocobalaminemia, and 56 of 119 cats (47%) had increased and 6 of 119 cats (5%) had decreased serum folate concentrations. Clinical signs included weight loss (91%), unformed feces (62%), poor hair coat (50%), anorexia (45%), increased appetite (42%), lethargy (40%), watery diarrhea (28%), and vomiting (19%). Eighty-seven cats (58%) had concurrent diseases. Treatment response was reported to be good in 60%, partial in 27%, and poor in 13% of 121 cats. Trypsin-like immunoreactivity <4 μg/L was associated with a positive response to treatment (OR, 3.2; 95% CI, 1.5–7.0; P = .004). Also, cobalamin supplementation improved the response to treatment (OR, 3.0; 95% CI, 1.4–6.6; P = .006).

Conclusions and Clinical Importance

Exocrine pancreatic insufficiency in cats often has a different clinical presentation than in dogs. The age range for EPI in cats is wide, and many cats can be ≤5 years of age. Most cats respond well to appropriate treatment for EPI, and cobalamin supplementation appears to be necessary for a good response.

Abbreviation

EPI

exocrine pancreatic insufficiency

BCS

body condition score

ERT

enzyme replacement treatment

fTLI

feline trypsin-like immunoreactivity

IQR

interquartile range

SIBO

small intestinal bacterial overgrowth

Exocrine pancreatic insufficiency (EPI) is characterized by inadequate production of pancreatic enzymes from pancreatic acinar cells and has been previously considered rare in the cat.[1] The related literature consists mainly of case reports of confirmed or suspected EPI cases in cats, with only 10 reports published between 1975 and 2009.[2-11] In addition, there have been only 2 small case series of EPI in cats that have been reported in the English peer-reviewed literature. The first of those studies evaluated the clinical utility of serum feline trypsin-like immunoreactivity (fTLI) concentration in 20 cats with a diagnosis of EPI.[12] The results of that study established serum fTLI concentration as the most useful test for the diagnosis of EPI in cats. In the second, more recent study, the aim was to describe the clinical and clinicopathologic findings in 16 cats with EPI.[11]

Since the introduction and validation of the fTLI test,[13] EPI in cats has been diagnosed more frequently.[1] However, many cases still may remain undiagnosed.[1] This suggestion is not surprising if one takes into consideration the fact that the clinical presentation, clinicopathologic findings, treatment options, and response to treatment of cats with EPI have not been well described. Therefore, the aim of our study was to describe the signalment, clinical signs, clinicopathologic abnormalities, concurrent diseases, and response to treatment in cats with EPI. In addition, data were analyzed to identify factors that may be associated with response to treatment.

Materials and Methods

Study Population and Data Collection

The database of the Gastrointestinal Laboratory, College of Veterinary Medicine and Biomedical Sciences at Texas A&M University, was searched for a period of 23 months (from March 2008 to January 2010) for cats with a serum trypsin-like immunoreactivity (fTLI) concentration diagnostic for EPI. The diagnostic criterion for EPI was a serum fTLI concentration ≤8 μg/L, which is the currently recommended cutoff value for the diagnosis of EPI in cats.[1, 12] A random subset (n = 261) of submitting veterinarians were contacted by phone (up to 3 times each) and asked to participate in this study by filling out a standardized questionnaire for each affected cat. Questions included age at diagnosis, breed, sex and neuter status, body weight and body condition score (BCS), medical history, clinical signs, concurrent medical problems, and treatment (including type of pancreatic enzyme replacement, dietary modifications, and adjunctive treatment). For each cat, the response to treatment was subjectively graded by the submitting veterinarian as good, partial, or poor. In general, a cat was considered to have a good response to treatment when no or only minimal clinical signs were present (eg, occasional soft feces), partial response when improvement was observed but clinical signs still were present (eg, less than ideal weight gain, diarrhea less severe than before), and poor when there was no or only minimal improvement. Where available, serum cobalamin and folate concentrations at the time of diagnosis were retrieved from the medical records. Cats for which it was reported by the veterinarians that the owners did not closely follow the recommended treatment were excluded from the study.

Assays

Serum fTLI concentrations were measured by a validated radioimmunoassay.[12, 13] The reference interval of the assay is 12–82 μg/L, and serum concentrations ≤8 μg/L are considered diagnostic for EPI.[12, 13] Serum cobalamin1 and folate2 concentrations were measured using commercially available chemiluminescent assays validated for use in cats. The reference intervals in cats are 290–1,500 ng/L for cobalamin and 9.7–21.6 μg/L for folate.

Statistical Analyses

The normality assumption was assessed for quantitative variables by plotting histograms, calculating descriptive statistics, and performing the Anderson–Darling test3 or the Kolmogorov–Smirnov test.4Categorical data were described using frequencies, proportions, and mid-P exact 95% confidence intervals.5 Quantitative data with a Gaussian distribution were reported as mean ± standard deviation (SD) and non-normal data using median and interquartile range (IQR). Data were compared among groups using Kruskal–Wallis and Mann–Whitney U-tests for 3 and 2 group comparisons, respectively. Associations between exposure variables and clinical response to enzyme replacement treatment (ERT) were estimated using binary logistic regression. Quantitative data were categorized before statistical analysis using reference intervals or medians of the distributions. Univariate screening models were fit, and all variables with P < .20 were selected for inclusion in a multivariable logistic regression model. The multivariable model was fit using a backward stepwise approach starting with all main effects identified in the screening models. Variables were removed one by one based on the largest Wald Pvalues and continued until all remaining variables were P < .05. Interaction terms were not evaluated, and the fit of the final multivariable model was assessed using the Hosmer–Lemeshow test. Statistical comparisons and modeling were performed with a commercially available software package6 and results interpreted at the 5% level of significance.

Results

Study Population

Serum from 46,529 cats was submitted for measurement of fTLI concentration during the study period. Of these, 1,095 (2.4%) cats had a fTLI concentration ≤8 μg/L. Questionnaires were sent to a random sample (n = 261) of the submitting veterinarians of these 1,095 cats. A total of 150 questionnaires (57%) were returned and contained sufficient information for inclusion in the study. Breeds included domestic short-haired (94 cats), domestic long-haired (15), domestic medium-haired (11), Maine Coon (7), British Shorthair (6), Siamese (6), Ragdoll (3), Abyssinian (1), Balinese (1), Himalayan (1), and Savannah (1), whereas 4 cats were of mixed breed. Sixty-one cats (41%) were female (all neutered), and 89 (59%) were male (86 neutered). The median (IQR) age of the cats was 7.7 (5.5, 11.4) years with an absolute range of 3 months to 18.8 years.

Clinical Signs

The most common clinical sign was weight loss, which was reported in 137 (91%) cats. In 8 cats (5.3%), weight loss was the only clinical sign reported. The median weight loss was 1.41 kg (range, 40 g to 6.8 kg). The median body condition score was 3 of 9 (range, 1 of 9 to 7 of 9). The median duration of weight loss was 6 months (range, 0.5 months to 4 years). Other clinical signs reported included unformed feces in 93 of 149 cats (62%; of these, 66% also had occasional watery diarrhea), poor hair coat in 73 of 145 cats (50%), increased appetite in 63 of 150 cats (42%), anorexia in 68 of 150 cats (42%), lethargy in 60 of 149 cats (40%), and vomiting in 29 of 150 cats (19%). Only 48 of 149 cats (32%) were presented with a combination of weight loss, unformed feces, and increased appetite, whereas 83 of 149 cats (56%) were presented with a combination of weight loss and unformed feces.

Serum Cobalamin and Folate Concentrations

Serum cobalamin and folate concentrations were measured in 119 cats. Of these 119 cats, 92 (77%) had serum cobalamin concentrations below the lower limit of the reference interval (median, 149 ng/L; range, 149–1,001 ng/L; Fig 1). Eighty-three cats (70%) had serum cobalamin concentrations below the detection limit of the assay (<150 ng/L). Serum fTLI concentrations in cats with hypocobalaminemia (median, 3.2 μg/L) were significantly lower than in cats with normal serum cobalamin concentrations (median, 5.5 μg/L; P = .0013; Fig 2). Fifty-six of 119 cats (47%) had increased and 6 cats (5%) had decreased serum folate concentrations (median, 21.1 μg/L; range, 3.9–121 μg/L; Fig 3). Forty-five cats (38%) had low serum cobalamin and high serum folate concentrations.


Figure 1.

Serum cobalamin concentrations in cats with exocrine pancreatic insufficiency. The dashed line represents the lower limit of the reference interval. The solid line represents the median. Note that the y-axis is split.

Figure 2.

Serum feline trypsin-like immunoreactivity concentrations in cats with normal serum cobalamin concentrations and cats with low serum cobalamin concentrations. The horizontal lines represent the median for each group. There was a statistically significant difference between the two groups (P = .0013).

Figure 3.

Serum folate concentrations in cats with exocrine pancreatic insufficiency. The dashed lines represent the reference interval. The solid line represents the median. Note that the y-axis is split.

Concurrent Medical Problems

Eighty-seven cats (58%) were reported to have concurrent medical problems. The most common were gastrointestinal problems (30 of 150 cats; 20%), endocrine disorders (21 of 150 cats, 14%; including 13 cats [9%] with diabetes mellitus), pancreatitis (11%), and hepatic lipidosis (6%).

Treatments

Accurate information regarding ERT was available for 121 cats. Products used included both enzyme powder and tablets, although the questions relating to enzyme treatment on the questionnaire did not require veterinarians to specify the exact type of product used in each case (ie, whether it was in powder or tablet form, whether it was enteric-coated or not). None of the cats received any form of raw pancreas as part of the ERT. Cats receiving ERT had lower BCS, more weight loss of longer duration, lower fTLI concentrations, and lower cobalamin concentrations (Table 1).

Table 1. Descriptive statistics and comparison of quantitative factors related to whether or not cats received ERT.

Antibiotics were used in 65 of 146 (45%) cats. The most commonly used antibiotic was metronidazole, which was used as the sole antibacterial in 39 cats (60% of cases treated with antibiotics or 27% of 146 cases). Other antibiotics, including enrofloxacin, amoxicillin, amoxicillin/clavulanic acid, tylosin, and clindamycin, were used in small numbers of cats (<5) each, whereas several cats were treated using different combinations of 2 or 3 antibiotics.

Cobalamin was given as part of EPI treatment in 72 of 147 cases (49%). None of the cats had received cobalamin before the diagnosis of EPI. Of the 72 cats that were supplemented with cobalamin, 18 (25%) had normal (10) or unknown (8) serum cobalamin concentrations.

Glucocorticoids were used in 34 of 146 cats (23%). Other treatments that were used in a small number of cases included probiotics (n = 11), H2-receptor antagonists (n = 7), antiparasitic drugs (n = 4), as well as medications to treat concurrent diseases.

The diet was changed in 64 of 124 cats (52%). Diets included elimination diets, hypoallergenic diets, gastrointestinal diets, and high fiber diets, whereas other cats were switched to homemade diets or regular commercial diets. Similarly, cats that were not switched to a specific diet also were on a variety of diets that included both prescription and commercial diets.

Response to Treatment

Fifty-seven percent (78 of 137) of cats were free of clinical signs at the time the questionnaire was completed. Of the 121 cats for which information was available, the response to treatment was reported to be good in 72 (60%), partial in 33 (27%), and poor in 16 (13%) cats.

Only serum fTLI concentration and cobalamin treatment were predictive of good clinical outcome (Table 2). Multivariable logistic regression suggested that the effects of these variables were independent because they were both significant in the final model (Table 3). Cats with a serum fTLI concentration <4 μg/L were 3.2 times more likely to have a good response to ERT (OR, 3.2; 95% CI, 1.5–7.0). Also, cats receiving cobalamin treatment were 3.0 times more likely to have a positive clinical response when adjusting for the initial fTLI concentration (OR, 3.0; 95% CI, 1.4–6.6). Interestingly, the presence of hypocobalaminemia before treatment did not affect the response to treatment.

Table 2. Univariate analysis to determine factors related to whether or not cats were reported as having a good response to ERT

Table 3. Multivariable logistic regression analysis to determine factors related to whether or not cats were reported as having a good response to ERT

Discussion

Ours is the largest case series of cats with EPI reported to date. One hundred and fifty cases of feline EPI were enrolled to describe the signalment, clinical signs, clinicopathologic abnormalities, concurrent diseases, response to treatment, and factors that may affect the response to treatment. This information can be used in clinical practice to more effectively identify cats that may have EPI and determine the best therapeutic plan and prognosis. To this end, a retrospective study design was employed and clinical information was gathered using a questionnaire. Diagnosis was based on the measurement of serum fTLI concentration, which is considered the current gold standard for the diagnosis of EPI in cats.[1, 12]

Domestic short-haired cats were most commonly affected by EPI in our study, which likely reflects the common occurrence of this breed in the general cat population. Males were slightly overrepresented. The median age of cats with EPI in the present study was 7.7 years, which is in agreement with previous studies.[11, 12] However, the age range was considerably wide, ranging from 3 months to almost 19 years. This finding is important because EPI has been traditionally considered a disease of middle-aged to older cats, although a previous study had reported similar findings with several cats with EPI being <1 year of age.[11, 12] The results of our study suggest that EPI should be considered in cats of any age. In addition, it has been suggested previously that EPI is a sequela of chronic pancreatitis in the cat in most cases.[14] The fact that several cats in our study were of young age might suggest that a different etiology exists in those cases. Alternatively, chronic pancreatitis may be able to destroy enough pancreatic tissue to produce EPI in a shorter period of time than previously assumed. Potential etiologies for EPI in younger cats could include pancreatic acinar atrophy, pancreatic hypoplasia or aplasia, and Eurytrema procyonis infestation.[1] Pancreatic acinar atrophy, the most common cause of EPI in dogs, has been reported in a very small number of cats with EPI in literature, but may be underdiagnosed in young cats.[1, 11] Additional studies are needed to investigate the spectrum and frequency of conditions that can lead to EPI in cats.

By far, the most common clinical sign in our cats with EPI was weight loss, which was present in >90% of cats and was the only clinical sign in 5% of them. This finding is similar to what has been reported in dogs with EPI.[15] Diarrhea (unformed feces) was present in only 62% of cats, which is much lower than what has been reported in dogs with EPI (95% in 1 study).[15] Interestingly, almost 33% of cats had watery diarrhea, at least occasionally, a characteristic that has been considered uncommon in dogs with EPI. However, this finding, along with other reported clinical signs (eg, anorexia, lethargy, vomiting), is more likely to be associated with concurrent diseases rather than EPI itself. Overall, the clinical presentation of many cats with EPI in our study did not closely resemble the typical presentation seen in dogs (ie, diarrhea, weight loss, polyphagia), and therefore, many cases might escape diagnosis. Therefore, EPI should be suspected in cats with unexplained weight loss or anorexia even when clinical signs that are considered classical for EPI in dogs (eg, diarrhea and polyphagia) are not present.

Serum cobalamin concentrations were decreased in most cats with EPI in our study (77%). This finding was not unexpected because the pancreas is the main source of intrinsic factor in cats, and in previous reports, almost all cats with EPI in which cobalamin had been measured were reported to have low serum cobalamin concentrations.[1, 11, 16] Cats with hypocobalaminemia were found to have significantly lower serum fTLI concentrations compared to cats with normal serum cobalamin concentrations. Because serum fTLI concentrations reflect the functional capacity of the exocrine pancreas, this observation suggests that normocobalaminemic cats with EPI have milder or early stage disease and thus might not have had enough time to develop hypocobalaminemia. Tissue cobalamin, however, is depleted before hypocobalaminemia develops, and therefore, normocobalaminemic cats in our study still could have had cobalamin deficiency at the cellular level.[17-19]

Despite the fact that hypocobalaminemia was diagnosed in 77% of cats with EPI in our study, cobalamin supplementation was instituted in only 49% of cats. Twenty-five percent of cats that received cobalamin supplementation had normal or unknown serum cobalamin concentrations. Cobalamin supplementation favorably affected response to treatment. This observation is not surprising because most cats were hypocobalaminemic, and cobalamin supplementation has been shown to be beneficial in hypocobalaminemic cats with gastrointestinal disease.[18] In dogs, hypocobalaminemia associated with certain gastrointestinal diseases has been shown to be a negative prognostic factor.[20] Also, severe hypocobalaminemia in dogs with EPI was found to be associated with shorter survival.[15] In our study, however, hypocobalaminemia before treatment was not associated with response to treatment. This finding in conjunction with the fact that cobalamin supplementation was also instituted in normocobalaminemic cats and was found to favorably affect outcome suggests that not only hypocobalaminemic but also normocobalaminemic cats with EPI could benefit from cobalamin supplementation. It is not clear why cobalamin supplementation may have a positive effect on hypocobalaminemic cats with EPI, but these cats may have depleted tissue cobalamin concentrations before hypocobalaminemia develops.[19, 21] Therefore, it may be helpful to supplement cats with EPI with cobalamin regardless of their serum cobalamin concentration. However, the benefit of cobalamin supplementation in normocobalaminemic cats with EPI warrants further investigation.

Serum folate concentrations were abnormal less commonly than serum cobalamin concentrations and more commonly were increased. A combination of increased serum folate and decreased serum cobalamin concentrations was identified in 38% of cases. Although this combination of findings has been used in dogs to diagnose small intestinal dysbiosis (previously called small intestinal bacterial overgrowth [SIBO]), controversy exists with regard to the usefulness of this diagnostic criterion.[22, 23] In cats, the value of identifying increased serum folate and decreased serum cobalamin concentrations is unknown. Multivariable analysis did not show that altered serum concentrations of cobalamin or folate affected response to treatment, although cobalamin supplementation was beneficial.

Another finding of our study was that cats with lower serum fTLI concentrations responded better to treatment. Although this might initially seem counterintuitive, it could mean that cats with more severe EPI (reflected in lower serum fTLI concentrations) would benefit more from treatment and therefore show a better response to treatment compared to cats with mild disease. However, it also could indicate that the specificity of the assay at <8 μg/L is <100% and that some of these cats may have been misclassified as having EPI.

Overall, response to treatment was considered good in 60% of affected cats, which is similar to what has been reported for dogs.[15] Only 13% of cats were reported to have a poor response to treatment, which is less than that reported for dogs.[15] The reason that some cats do not respond well to treatment for EPI is not clear. In the present study, cobalamin supplementation was found to affect response to treatment, and therefore, it can be assumed that partial or poor response to treatment could be associated, at least in part, with lack of cobalamin administration. Another factor that should be taken into consideration is that many of the cats enrolled in our study had concurrent diseases, and therefore, partial or poor response to EPI treatment could have been affected by these other conditions. Prospective clinical studies are needed to accurately determine the response to treatment of cats with EPI and identify factors associated with good response.

Antibiotics were used in approximately 50% cases in our study but their use was not found to affect outcome. In dogs, antibiotics often are used in the treatment of EPI to control concurrent intestinal dysbiosis, although no clear benefit has been shown in some studies.[15, 24] However, disturbances of the microbiota in cats with EPI have not been fully described or confirmed, and therefore, antibiotic use is of unknown benefit in these cases. Given the difficulty in identifying small intestinal dysbiosis in cats and dogs, a trial with antibiotics often is used in EPI patients that do not respond to enzyme and cobalamin supplementation. Additionally, cats with pancreatic disease commonly have concurrent intestinal and or hepatic inflammation, and antibiotic treatment often is used as part of the management of intestinal and hepatic disease.[25] Similarly, other treatments used in this group of cats, such as glucocorticoids, were likely used to treat concurrent inflammatory disease of the intestine, liver, or both.[25]

As with all retrospective and questionnaire-based studies, our study has limitations that should be taken into consideration. One of the limitations is related to the fact that the information was extracted retrospectively from medical records and based on referring veterinarians. However, all contacted veterinarians were asked to retrieve the information directly from the medical record of each cat and not answer questions based on memory alone. They also were asked to be as accurate and careful as possible in answering questions and to not answer questions if they were unsure about the answer. Unfortunately, it is not possible to determine how closely veterinarians followed these instructions. Another limitation is related to the assessment of response to treatment, which was subjectively scored as good, partial, or poor by the participating veterinarians. No validated scoring systems for response to treatment of cats or dogs with EPI have been reported, and the approach used in the present study also has been used in previous studies in dogs. In addition, an effort was made both during questionnaire design and data analysis to control for inaccuracies. For example, although there was a specific question on response to treatment, which was scored as good, partial, or poor, there was an additional question on whether the cat was free of clinical signs at the time of questionnaire completion. There was very good agreement between the answers to these 2 questions: 60% of cats were reported to have a good response to treatment and 57% of cats were reported to be free of clinical signs.

In conclusion, EPI in cats often has a different clinical presentation than that expected based on the typical presentation in dogs, and a portion of cases likely escapes diagnosis. Therefore, cats with unexplained weight loss, with or without diarrhea and regardless of the presence or absence of other clinical signs, should have EPI as a differential diagnosis. In addition, although most commonly seen in middle-aged to older cats, the age range for EPI in cats is very wide and many cats can be ≤5 years of age. Cobalamin supplementation had a positive impact on treatment response, potentially even in cases that had serum cobalamin concentrations within the reference interval. Antibiotic use was not found to affect response to treatment. Overall, most cats responded well to appropriate treatment for EPI.

Acknowledgments

The authors thank Dr. Penelope Woof for her help with data collection.

Conflict of Interest Declaration: Drs. Suchodolski and Steiner direct the Gastrointestinal Laboratory at Texas A&M University, which offers measurement of fTLI on a fee-for-service basis.

Off-label Antimicrobial Declaration: Authors declare no off-label use of antimicrobials.

Footnotes

  1. 1

Immulite 2000 Vitamin B12 solid-phase, competitive chemiluminescent enzyme immunoassay. Siemens Healthcare Diagnostics, Deerfield, IL

  1. 2

Immulite 2000 Folic Acid competitive immunoassay. Siemens Healthcare Diagnostics, Deerfield, IL

  1. 3

MINITAB Statistical Software, Release 13.32, Minitab Inc, State College, PA

  1. 4

Prism 5, GraphPad, San Diego, CA

  1. 5

Epi Info, version 6.04, CDC, Atlanta, GA

  1. 6

IBM SPSS Statistics Version 22, International Business Machines Corp., Armonk, NY

EPI article in August 2014   CAT FANCY  magazine

We are very pleased to announce that EPI was discussed in the August 2014 edition of the #1 cat magazine, "Cat Fancy"  written by Stephanie Bouchard  http://www.stephaniebouchard.net/portfolio/cats/

 

 

Managing Cats with EP - Soleil's story

"Soleil" the love of my life ..... was only five years old when she was diagnosed. 

 

Soleil started developing symptoms a little over a year ago with occasional vomiting and gagging.  They were treating her for hairballs.  They gave her a medication to increase her intestinal motility and it nearly killed her.  Following that, she received her yearly immunizations and she became very ill with fevers, lethargy, etc.  This had never happened before.  As an aside, I have decided not to give her immunizations anymore.  She is an inside cat and the last time was too scary.

 

Shortly after that, she started eating me out of house and home but  continued to lose weight.  She got down to 6 lbs. 2 oz. (her six month kitten weight).  She was so skinny . . .  fur and bones.    It made me cry just to look at her.  She would keep me up all night crying.  I would get up and pet her and try to console her, but I did not know what to do.  It was horrible!  Her bowel movements were very large and yellow in color.  Finally, my local vet sent me to a specialist.  They did an ultrasound which revealed thickened bowel and they told me they were pretty sure she had lymphoma.  I was devasted!   They did an endoscopy and biopsy of the affected area.  I was happy five days later to get a call telling me she did not have lymphoma but she had inflammatory bowel disease.  A few days later they called to tell me her lab results from blood tests were back and she had exocrine pancreatic insufficiency.  Wow!    They told me it was extremely rare in cats and they put her on 2.5 mg. of Prednisone every day for the inflammatory bowel disease and told me to mix Viokase with her food and she started a regimen of B12 injections.  That all seemed fine except Soleil would NOT eat any food with the enzymes in it.  For two months I syringe fed her with chicken baby food after adding Viokase and waiting 20 minutes.  It was horrible but it was the only way I could get the enzymes in her.  She started to gain some weight back which was good but she and I both hated the syringe feeding.  She would run and hide from me when I got home and although I got pretty good at it she would still freak out because they occasionally get choked by that method of feeding no matter how hard you tried not too.  She would fight me like crazy and I would stop and cry.  It was terrible!   

 

My next attempt at getting her the enzymes was to talk to a slaughter house in Lake Geneva, WI.  They would sell me raw bovine pancreas.  I cut it up and put it in a food processor and froze it in ice cube trays.   My vet said I could mix this in her food and if she ate it, this would give her the enzymes she needed.  My kitchen looked like a slaughter house by the time I was done with this process.  Raw pancreas is good for three months if you freeze it.   I tried feeding it to Soleil one evening and she threw up so bad I thought she was going to die.  I think she just over ate because she was so hungry, but after several attempts at feeding her raw pancreas I found that she did not like that either and I went back to the dreaded syringe feeding.

 

Shortly after that my local vet told me about Flavorx.  It is a company that sells materials to compound the Viokase to taste like chicken pot pie (or any flavor you want).  My vet would compound the enzymes which I would syringe drizzle over her food mix it up and she ate it!   I was so happy!   No more syringe feeding!    I asked my vet if I could do this myself at home.  I wanted to have control over all of it.  My vet wrote  a letter to the company "Flavorx" giving me the ability to order all the compounding products directly from them and he then showed me how to compound the enzymes and I am able to do this at home now.  

 

During all this, Soleil was receiving weekly, then bi-weekly B12 shots.  These were SO important for her.  Even after a long B12 therapy she was still low when tested.   A few months ago she was tested again and her levels are normal but they recommend monthly B12 shots and then she gets rechecked in February.  I will always continue to monitor this for her even though I hate when she gets the blood test because she has to fast for 12 hours prior.  Nothing worse than withholding food from an EPI animal.   I don't get much sleep.  LOL!   It is worth it though. 

 

At some point during all this craziness I talked to a holistic vet (a friend of someone else I met on line with a dog with EPI).   He suggested FortaFlora probiotics sprinkled on her food.  This was to help with the inflammatory bowel disease and digestion.   This seemed to help Soleil a lot and they smell like beef boullion and she seems to like the taste so I use about half packet of that on each of her two feedings daily.   I mix it with the food after I mix the compounded enzymes with the food. 

 

I did receive another tip for feeding cats enzymes from her specialist.  It did not work for Soleil but it might work for someone else.  You buy fish oil tablets and mix the liquid from the tablet with the Viokase (making a paste).  Some cats like this and will lap it up getting them their enzymes, but miss finicky did not care for it at all, but a good suggestion if it works, I guess.   It is a cheap way to compound the enzymes yourself if it works. 

 

Also during my research I found a product called "Cat Man Do" sprinkles.  These are dried bonitos fish flakes.  You sprinkle them over the food.  I sent some of these to my friend Melissa, mentioned above, and she said her cat loves them.  I bought some but never tried them with Soleil because I finally got the compounding flavored enzymes working well.  I would think these may help disguise the taste of the enzymes if the cat likes them.   You can order them on line.

 

Soleil is now on Prednisone, 2.5 mg. five days a week.  She needs this for her inflammatory bowel disease and it seems to keep her under great control.  I hate having to give her this, but when I cut back further she starts gagging again. 

 

I also purchased a pediatric scale for Soleil because it is hard to tell when a cat is gaining or losing weight and waiting between vet appointments to have her weighed was too stressful.  The scale cost about $70.00 and it was worth every penny.  I ordered it on line.   I can see immediately if there is any problem going on if she starts losing weight.  It weighs in ounces and pounds.

 

One other great item for those working cat mommies (such as myself) is the timed feeder from Petsmart.  My friend Melissa told me about this and it works great if you are going to be away from home for more than ten hours or so.  It has a slot under the trays that you can place an ice pack keeping the food and enzymes fresh.  As you know, you can't leave the enzymes out all day.   You set the timer and the door opens at the specified time.   Voila!  Dinner is served!   I rarely use this, but it has come in handy on a few occasions. 

 

I have the additional complication of having two cats.   Soleil's BIG sister weighs 13 1/2 lbs. They were not really litter mates, but I call them sisters anyway.   I have the challenge of getting Luna to lose weight and Soleil to gain weight.  The only good thing about Luna's additional weight is that she can no longer jump up on the counter tops.  This is where I have to feed Soleil so that Luna cannot get to her food.   Luna has to eat before I leave now because I cannot leave un-enzymed food down during the day or Soleil will eat that first.   

 

Soleil weighed in last night at 7 lbs. 6 oz.   This is a really good weight for her.  When she was two years old she weighed 7 lbs. 8 oz.  She has always been a small cat and was the runt of the litter when I adopted her.  She is a polydactyl kitty.  She has seven claws on her front paws and six claws on each back paw.  She has big mitten feet but they are so cute!  

 

Currently I am feeding Soleil Fancy Feast Chicken with some spinach in a broth (green can).  This is the food I mix the enzymes and probiotics in.  Then I top it off with Blue Buffalo dry food (Gluten free/grain free) chicken Freedom.  She loves that and seems to digest it very well.   I give her the Blue Buffalo for treats occasionally too, just not a lot without being in the enzymes.

 

If anyone goes the compounding route with the vet syrups and flavorings, they must NOT use the conventional syrup to compound the enzymes if their cat has diabetes.  Diabetes is somewhat common in cats with EPI.  I don't know about dogs.  However, there is another solution.  I believe it is called Versa Free (it contains no sugar).  This is what I believe you would use for a diabetic cat. Basically, if someone has a diabetic EPI cat they should definitely consult with their vet first.  I'm sure they would anyway, but just wanted to add this bit of info. 

 

Please feel free to join the the epi4dogs FORUM at http://www.epi4dogs.com/apps/forums/ and to start a discussion about your EPI cat, or feel free to contact Carol at:    [email protected]

Thanks for listening to my story, Carol. 

Managing Cats with EPI - Timothy's story

Timothy's EPI story began in the fall of 2011, when he abruptly began acting very sick.  My five year old Siamese mix, who had always been very playful and a great eater, suddenly refused his food and became extremely lethargic.  He had severe diarrhea and some vomiting, and waddled around the house as if it was very painful to move.  After a couple of vet visits and an ultrasound, he was diagnosed with acute pancreatitis and I took him home with subcutaneous fluids and injectable medications to support him as he recovered.  I had worked at a veterinary hospital for seven years back before I left to start a business of my own, so I was able to do all the necessary treatments without hospitalizing him, which was great as it was less stressful for him and less expensive for me.  Thankfully he pulled through the severe episode of pancreatitis, and a couple of less severe recurrences thereafter.
 
Even though he had survived the pancreatitis, Tim didn't really return to normal.
 
His stools remained soft, were a clay-like grey color rather than brown, and smelled truly horrible.  The stench was so intense that if he passed a stool at night, the smell would wake me up even though the litter box was located on another floor at the opposite end of the house from my bedroom!
 
Around February, I noticed that Timothy was behaving oddly.  He had always been extremely interested in food, but that interest began to morph into an absolute obsession with anything even remotely edible.  Nothing was safe in our house.  He would open the pantry and eat uncooked pasta and whole wheat bread.  He raided our fruit bowl for peaches and avocados. He also began to lose weight rapidly.  His pre-pancreatitis weight had been about eight pounds.  Between February and April, he went from seven pounds to just barely over five pounds.  As Tim's sixth birthday rolled around, I began seriously doubting that he would survive to see seven.
 
At some point, as I stood in the vet's office at yet another visit talking about awful things that it could be, one of us said, "Do cats get EPI?"  I can't remember which of us brought up the subject.  I had seen cases of EPI over the years in dogs, and so had the vet.  Neither of us had seen it in a cat, but the symptoms that Tim was exhibiting were uncannily familiar.  She left the room, and came back a few minutes later practically beaming as she declared that we would start him on enzymes right away.  I was so relieved to finally have something concrete to pursue, even if it was a condition that would require lifelong management.  I knew that EPI could be frustrating and expensive, but I also knew that it was treatable!
 
Tim's EPI is currently being managed with one teaspoon of EPI-Pro 6x enzyme powder mixed into each of his meals.  I had him on a probiotic for a while as well, but it didn’t seem to make much of a difference and he wasn’t especially pleased with his food when the probiotic was present, so we eventually discontinued it.
 
Finding a food that works for Tim has been a bit of a struggle.  He isn’t a fussy eater by any means, but it seemed as though I just could not get his diarrhea under control as long as he was on a normal canned diet, even if the canned diet was a very respectable brand like Innova EVO, Weruva, or Wellness.  For the last few months, I have been feeding The Honest Kitchen’s dehydrated “Prowl” diet, and that seems to be working very well.  He gets ¼ cup of the dehydrated food mixed with ½  cup of water and his enzymes twice per day.  The food looks kind of like a soup when made with that much water.  After mixing things up, I let everything sit for five minutes before feeding Tim.  So far, his stools have been pretty consistently firm on this diet plan.  It may be that the enzymes end up better mixed in his food now than they were previously, or that one of the ingredients in canned diets was not working well for Tim.  Whatever the cause of the improvement may be, I am glad for it.

 

I give him weekly subcutaneous injections of 250mcg of vitamin B12.  I noticed dramatic improvements in his energy level after beginning the B12 injections, and his stools seem to be approaching closer to normal as well.  The hope is that we may be able to reduce the frequency of the injections in the future, but we aren't to that point yet; every few months, I will try to space the injections out a little bit further, but doing so has so far resulted in a return to loose stools.  Tim is generally pretty good about his injections and allows me to give them without putting up much of a fight, though I do occasionally have to fall back on the "kitty burrito" method of wrapping the cat in a towel while giving the injection.  He loves his food, so if I give him the injection while he is eating, he often does not notice that I have done anything!


 
Since beginning treatment for EPI, Tim's weight has increased from five pounds to over eleven pounds. I have twice the cat I had before!  He is no longer constantly foraging for food around our house; he naps and plays like a normal cat.  His stools have returned to a normal color and no longer smell as foul, and are only rarely soft at all.
 
Timothy's doing great.  After coming so close to losing him over the last year, I almost feel like the EPI diagnosis was a blessing.  He's living with it-- living WELL with it!-- and I have my cat back 

I'm happy to talk to anyone who may need support or advice about working with their EPI cat. 
My email is [email protected].

 

MaryJo's "King Kitty"

  

Sadly MaryJo suddenly lost King Kitty to a respiratory illness in December 2012, but in honor of his legacy, MaryJo will gladly help anyone needing assistance with their EPI cat.

 

Please feel free to contact MaryJo at:    [email protected]

Nov 2014 "Skinny Old Cats" research by Dr. David A. Williams

 

The following EPI in Cats information is taken in it's entirety from the Mercola Pets website written by Dr. Karen Becker: 
http://healthypets.mercola.com/sites/healthypets/archive/2013/05/15/exocrine-pancreatic-insufficiency.aspx?e_cid=20130515_PetsNL_art_1&utm_source=petnl&utm_medium=email&utm_content=art1&utm_campaign=20130515

 

Exocrine Pancreatic Insufficiency: Can Cause Your Kitty to Starve to Death - Even While Eating Plenty

May 15, 2013 

By Dr. Becker    

 

Story at-a-glance

  • Exocrine pancreatic insufficiency (EPI) is thought to be rare in cats. But new research indicates that vets might need to take a closer look for evidence of the disorder in kitties with recurrent diarrhea and chronic weight loss.
  • The pancreas is involved not only with insulin production, but also with the production of digestive enzymes. Many people who understand the connection between the pancreas and diabetes are unaware this important organ can also play a role in digestive disease.
  • Exocrine pancreatic insufficiency means there is a decrease or lack of digestive enzymes being produced by the pancreas. As a result, proteins, starches and fats from the diet can’t get into the bloodstream to supply nourishment to the body’s tissues.
  • In the largest research study to date on feline EPI, it was revealed the disease may be more prevalent in cats than previously thought. Symptoms in cats vary significantly from those seen in dogs with the disease. For example, diarrhea isn’t consistently present in cats, nor is it as severe as it is in dogs. Also, about half the cats in the survey had a decrease rather than an increase in appetite.
  • In kitties with unexplained chronic weight loss with or without diarrhea, including diabetic cats, it may make sense to run fTLI, cobalamin and folate tests before considering more invasive, costly diagnostic procedures.

Exocrine pancreatic insufficiency (EPI), also called pancreatic insufficiency and maldigestion syndrome, is thought to be rare in cats. However, according to dvm360, new research suggests veterinarians should look more closely at EPI as a potential cause of diarrhea and chronic weight loss in kitties.

Exocrine Pancreatic Insufficiency

The pancreas has many functions. It produces not only insulin, but also various enzymes that provide for the digestion of food. Many people are aware the pancreas plays a role in insulin production and diabetes; relatively few people realize the role the pancreas can play in digestive diseases.

Pancreatic enzymes include amylase, which breaks down starches; lipase, which breaks down fats; and trypsin and chymotrypsin, which break down proteins.

The actions of these enzymes are crucial to the digestive process. They allow nutrients from the diet to be absorbed by the cells of the intestine, where they pass into the bloodstream and are transported throughout the body for use by tissues. When a cat eats, the pancreas gets a signal to release digestive enzymes, which travel into the small intestine via the pancreatic duct (“exocrine” glands secrete their products into ducts, whereas “endocrine” glands secrete their products directly into the bloodstream).

Once they reach the center of the intestine, the enzymes go to work breaking down food particles.

Exocrine pancreatic insufficiency means there is a decrease or lack of digestive enzymes being produced by the pancreas. In kitties with the disorder, proteins, starches and fats from the diet aren’t broken down sufficiently to be absorbed through the intestinal wall. This means nutrients can’t get into the bloodstream to supply nourishment to the body’s tissues. Much of the food that is eaten remains undigested in the GI tract and ultimately leaves the body in feces. If left untreated, a cat with EPI can literally starve to death despite how much food is consumed.

Causes, Symptoms and Diagnosis of EPI

Pancreatic insufficiency can have several potential causes, but the most common source in cats is chronic inflammation of the pancreas. Other causes are parasitic infestations, as well as cancer.

Signs a kitty may be dealing with EPI include weight loss; constant hunger; lots of watery, loose or semi-loose stools that may have a foul odor and contain large quantities of undigested fat; and poor coat condition. Cats with this disorder look and behave as though they are starving to death … because they are.

Occasionally, cats with EPI are also diabetic.

A test called the feline trypsin-like immunoreactivity (fTLI) assay is considered diagnostic for EPI. Prior to the availability of the fTLI, diagnosis was trickier and involved taking a symptom history and running repeated fecal digestion tests.

Results of Largest Feline EPI Study to Date

In 2010, the GI Laboratory at Texas A&M University received 775 samples from veterinarians of fTLI assay results that were consistent with a diagnosis of feline EPI.

Then in 2011, researchers from the GI Laboratory and Department of Clinical Sciences at Texas A&M conducted an EPI survey of veterinarians who submitted samples. One hundred-fifty surveys were returned. The average age of affected cats with the condition was eight years. Males represented 59 percent of the samples; females, 41 percent.

Average body condition of the kitties was poor. Of the cats for which cobalamin (vitamin B12) levels were measured, 77 percent were deficient and many had no detectable levels of B12 at all. For those that had folate concentrations tested, 47 percent showed an increase.

As for symptoms, in 91 percent of the cats, weight loss was the primary symptom. Weight loss varied from 1.4 ounces to 15 pounds, with an average of 3 pounds. Loose stools were seen in 62 percent of affected cats; poor haircoat in 50 percent; loss of appetite in 45 percent and increased appetite in 42 percent; and depression was present in 40 percent of the kitties. Almost 60 percent of the cats had coexisting diseases including inflammatory bowel disease (IBD), diabetes,pancreatitis and hepatic lipidosis.

Of the kitties with EPI, 68 percent were given pancreatic enzyme supplementation. Of those, 66 percent showed a good response, 24 percent had a partial response, and 10 percent had a poor response to the treatment.

What These Results Mean for Cat Owners and Vets

According to dvm360, the results of the survey are evidence that exocrine pancreatic insufficiency is not as uncommon in cats as previously thought. However, symptoms in cats vary noticeably from canine symptoms. In cases of feline EPI, diarrhea isn’t a consistent finding and isn’t as severe as it is in dogs dealing with the disease. Also in cats, excessive hunger is not consistently present, and in fact about half the cats in the survey showed a decrease in appetite.

Treatment with pancreatic enzyme supplementation appears to be successful in a large percentage of kitties with EPI. If there are also low cobalamin levels, subcutaneous (under the skin) supplementation for several weeks is often required to help resolve gastrointestinal symptoms.

Also, EPI can be associated with small intestinal dysbiosis (also called small intestinal bacterial overgrowth, or SIBO), especially when low B12 and high folate levels are present.

Cat owners and especially veterinarians should consider fTLI, cobalamin and folate tests for kitties with unexplained weight loss or chronic diarrhea, regardless of the pet’s age. These tests could conceivably eliminate the need for more expensive and invasive diagnostic procedures.

EPI should also be viewed as a possible concurrent condition in diabetic cats whose blood sugar levels are well controlled but who have weight loss and/or diarrhea. 

 in accordance with Mercola's copywrite permission, the following must be included when copying the article:

 

EPI in Cats (older research)

EPI in Cats

The following is from: http://www.ivis.org/advances/rcfeline/chap4part9/chapter.asp?LA=1

In:  Encyclopedia of Feline Clinical Nutrition, Pibot P., Biourge V. and Elliott D.A. (Eds.). International Veterinary Information Service, Ithaca NY (www.ivis.org), Last updated: 28-Apr-2009; A5106.0409

Nutritional Management of Hepatobiliary and Pancreatic Diseases

C. Rutgers1 and V. Biourge2

1Departement of Veterinary Clinical Sciences, The Royal Veterinary College, United Kingdom. 2Royal Canin Research Center, France.

Exocrine Pancreatic Insufficiency

Introduction

The exocrine pancreas plays a central role in the digestion and absorption of nutrients. Pancreatic acinar cells synthesize and secrete enzymes that digest proteins, fats and carbohydrates (protease, lipase and amylase). Pancreatic duct cells furthermore secrete bicarbonate to maintain an optimal pH for digestive and absorptive function, as well as intrinsic factor to facilitate cobalamin absorption.

Exocrine pancreatic insufficiency (EPI) results from deficient synthesis and secretion of pancreatic digestive enzymes. The lack of digestive enzymes in the duodenum leads to maldigestion and malabsorption of intestinal contents. The exocrine pancreas has a large functional reserve capacity and clinical signs of maldigestion do not occur until 90% of secretory capacity is lost.

Diagnosis
Overview

EPI is an uncommon cause of chronic diarrhea in cats; however, in the past it has been under diagnosed due to the lack of specific clinical and laboratory findings. Diagnostic accuracy has now been facilitated by the fTLI test, which is a species specific radioimmunoassay.

Clinical Signs

Clinical signs in affected cats are not specific for EPI: the most commonly reported clinical signs in cats with EPI are weight loss and soft voluminous feces (Steiner & Williams, 2005). Polyphagia despite weight loss is not as commonly seen as in dogs. Many cats also develop a greasy, unkempt hair coat, especially in the perianal and tail regions, resulting from the high fat content of their feces. Some cats have watery diarrhea secondary to intestinal disease. Affected cats may also have a previous history of recurring bouts of acute pancreatitis (e.g., anorexia, lethargy, vomiting) that resulted in chronic pancreatitis and EPI. Concurrent disease of the small intestine, hepatobiliary system and endocrine pancreas may be present.

Differential Diagnosis

The main differential diagnoses for a cat presented with diarrhea, weight loss and changes in appetite are hyperthyroidism, diabetes mellitus and chronic small intestinal disease (most commonly inflammatory bowel disease). Physical examination may help in differentiating these, e.g., by palpating a thyroid nodule or thickened intestinal loops. However, these diseases may be coexisting, especially in older cats, and laboratory testing and imaging (particularly ultrasound) are mandatory.

Laboratory Testing

Routine Laboratory Tests
Results of hematology and serum biochemistries are generally within normal limits or show nonspecific changes. Older cats may have evidence of concurrent renal disease, whereas cats with hyperthyroidism often have increased serum liver enzyme concentrations. Microscopic examination of feces will demonstrate steatorrhea and undigested fat, but this is not pathognomonic for EPI.

Serum concentrations of cobalamin and folate should also be determined in all cats with suspected EPI, because of the common occurrence of low levels (especially for cobalamin) (Steiner & Williams, 1999).

Pancreas-specific Tests
A feline-specific radioimmunoassay for trypsin-like immunoreactivity (fTLI) has now been developed and validated, it is sensitive and the test of choice to diagnose EPI in cats. Fasting serum fTLI concentrations less than 8 μg/L (reference range = 17 - 49 μg/L) are diagnostic for feline EPI (Steiner & Williams, 2000). When the fTLI concentration is between 8 - 17 μg/L, the test should be repeated ensuring adequate fasting; it is also possible the cat has partial EPI that in time may progress to complete EPI. The TLI test is a simple and reliable way of confirming the diagnosis of EPI; however; it is essential to use an assay specific for feline TLI since there is no cross reactivity between canine and feline TLI.

Diagnostic Imaging

Imaging findings are inconsistent; abdominal radiography and ultrasonography generally do not show any abnormalities.

Epidemiology
Risk Factors

Chronic pancreatitis is the most common cause of feline EPI (Figure 26), occurring mainly in mature and older cats. In most cases, it is idiopathic. Rare causes of feline EPI without chronic pancreatitis are pancreatic duct obstruction by liver flukes or pancreatic neoplasia (adenocarcinoma), leading to acinar atrophy. Fecal examination can help in the diagnosis of a fluke infestation, whereas abdominal ultrasonography is essential in detecting a pancreatic mass.

Pancreatic acinar atrophy (PAA) similar to the disease commonly observed in dogs has not been documented in cats. Chronic pancreatitis is the most common cause of EPI in cats. (© courtesy KW Simpson).

Breed and Sex Predisposition

There is no breed or sex predisposition for the development of EPI in cats.

Pathophysiology

Cats with EPI have an extensive and chronic disease, which is usually due to chronic and irreversible pancreatitis.

The typical signs of EPI (diarrhea, weight loss and polyphagia) are due to decreased intraduodenal concentrations of pancreatic digestive enzymes and bicarbonate with resultant malassimilation of fats, carbohydrates and proteins. This leads to malabsorption, osmotic diarrhea and steatorrhea, and malnutrition. In addition, there are secondary disturbances of intestinal mucosal growth and transport mechanisms that aggravate malabsorption. Cats normally have high numbers of anerobic organisms in their proximal small bowel (Johnston et al., 1993) and it is not known whether they develop changes in the nature and number of small intestinal flora, which is common in dogs with EPI.

Fat malabsorption may result in deficiencies of the fat-soluble vitamins (esp. vitamins K and E). Vitamin K-dependent coagulopathy has been reported in a cat with EPI (Perry et al., 1991) and may occur in other cases as well. Vitamin E deficiency could aggravate oxidative stress, but there are no reports documenting this in feline EPI.

EPI in cats is usually due to chronic pancreatitis, and many cats have concurrent diseases (inflammatory bowel disease, cholangiohepatitis, and diabetes mellitus) that may require additional treatment.

Many cats with EPI have low serum cobalamin concentrations, which impairs their response to treatment. Cobalamin is absorbed in the distal small intestine after it has formed a complex with intrinsic factor, a protein that in cats is exclusively secreted in the pancreatic juice (Fyfe, 1993). The lack of pancreatic intrinsic factor in EPI impacts severely the ability to absorb cobalamin. In addition, concurrent small intestinal disease (Weiss et al., 1996) may further impair cobalamin absorption in cats. Cats seem predisposed to develop markedly reduced serum cobalamin levels under those circumstances (Simpson et al., 2001). Uncorrected cobalamin deficiency may lead to villous atrophy, intestinal inflammation and worsening malabsorption, with resultant failure to respond to pancreatic enzymes alone.

Serum folate concentrations may be decreased in the case of concurrent small intestinal disease resulting in malabsorption of folate. This differs from the situation in canine EPI, where folate levels are often increased due to secondary small intestinal bacterial overgrowth. Cats have however normally high levels of bacteria in their small intestine and bacterial overgrowth is not a recognized syndrome in this species (Johnston et al., 1993; 2001).

Treatment
Enzyme Supplementation

Addition of exogenous pancreatic enzymes to the food is essential for resolution of clinical signs.

Synthetic dried pancreatic extracts are available in several forms.
Powdered pancreatic extracts are most commonly used due to their effectiveness and ease of use. Tablets, capsules and enteric-coated tablets are not recommended since they are usually less effective (Steiner & Williams, 2005). The powdered extract should be mixed within the food immediately prior to feeding (0.5 to 1 tsp per meal twice daily); pre-incubating the enzymes with the food or concurrent antacid therapy are unnecessary (Steiner & Williams, 1999). The amount should be adjusted based on its efficacy in resolving clinical signs; it is common practice to start with the higher dosage, after which it can be gradually decreased to the smallest dose that maintains remission.

Adequate management of cats with clinical EPI depends on long term enzyme replacement and dietary manipulation.

It is important that dietary management and enzyme supplementation are kept constant, since variation and especially the consumption of a non-supplemented meal can cause a return of the diarrhea.

Raw chopped pancreas (30 - 90 g per meal twice daily) may be used as an alternative and can be very effective. It can be stored frozen for at least three months, but is generally less convenient to use and has the potential for causing gastrointestinal infections (e.g., Salmonella, Campylobacter). Bovine pancreas is safest, since there is always a risk of transmitting Aujeszky’s disease when using porcine extracts. Raw chopped pancreas can however be a solution when the cat develops aversion to the powdered extract.

Vitamin Supplementation

Cats with EPI almost always have marked depletion of body cobalamin stores and severely decreased serum cobalamin concentrations. In addition, many cats with EPI have concurrent small intestinal disease which further impairs cobalamin absorption. Supplementation is by parenteral cobalamin (250 - 500 μg/kg subcutaneously every two or three weeks) to maintain normal serum concentrations of cobalamin (Ruaux et al., 2005).

Cats with EPI with or without concurrent small intestinal disease may also have low serum folate concentrations and should be treated with oral folate at 400 μg once daily for 2 - 4 weeks or longer, until serum levels have normalized.

Malabsorption of fat-soluble vitamins (vitamin A, D, E and K) may occur in EPI, although the clinical importance in cats is unknown. Cats with evidence of a coagulopathy should be supplemented with vitamin K. It may also be helpful to increase dietary vitamin E levels because of its antioxidant function, especially in cats that do not respond to enzymes and supportive management alone and especially in cats with concurrent diseases.

Management of Concurrent Diabetes Mellitus

Cats with chronic pancreatitis resulting in EPI as well as diabetes mellitus will need insulin treatment in addition to management of the EPI.

Nutritional Management (Table 10)

High digestibility is a mainstay of dietary management, since it requires less gastric, pancreatic, biliary and intestinal secretions for digestion, and thus facilitates absorption in the upper small intestine. Dietary modification may be required in cats that present with severe weight loss and protein-calorie malnutrition, and also in cats that do not respond adequately to this management.

Cats with EPI should be fed a highly digestible, good quality and energy dense diet, with an appropriate pancreatic enzyme supplement mixed into it

Cats with EPI should be fed a highly digestible, good quality and energy dense diet, with an appropriate pancreatic enzyme supplement mixed into it (Simpson, 2005). (© C. Hermeline).

Protein

The diet during early refeeding should contain higher protein levels, since many patients with EPI suffer from protein-calorie malnutrition. If response to treatment is poor, concurrent intestinal disease has to be investigated further, e.g., by a dietary trial with an antigen restricted diet. A diet based on rice and soy protein hydrolysate proved to be beneficial in the management of canine EPI (Biourge & Fontaine, 2004). This strategy remains to be validated in cats.

Fat

Fat malabsorption and steatorrhea are major signs in patients with EPI (Williams, 2005). However, fat restriction is of questionable benefit for cats, especially since this species needs a relatively high-fat diet. In addition, there is evidence that higher fat diets promote better digestibility (Suzuki et al., 1999). The cause is unclear, but it may be related to improved preservation of exogenous pancreatic enzymes, particularly lipase. Furthermore, a higher fat and thus more energy dense diet will help an animal in poor body condition to regain its optimal body weight faster. Dietary fat levels can therefore be within the normal range, but high digestibility is essential.

Fiber

Diets containing moderate amounts of fermentable fiber will help to improve GI health by its positive actions upon the mucosal barrier.

Carbohydrate

Cats are poorly adapted to handling carbohydrates, so excessive amounts should be avoided.

Trace Elements and Vitamins

The diet should contain high-normal concentrations of B-vitamins, since body stores are often depleted.

Treatment Failures
Reconfirm EPI
  • Make sure the diagnosis is correct, and resubmit an fTLI.
  • One should also ensure that serum cobalamin and folate concentrations are managed appropriately.
Inadequate Enzyme Supplementation

Ensure that the enzyme supplement being fed is appropriate (non-enteric coated powder), not outof- date, and fed at the right dose with each meal.

Small Intestinal Disease

Concurrent small intestinal disease may cause continued malabsorption despite adequate enzyme supplementation. Dietary modifications, e.g., to an antigen-restricted or protein hydrolysate diet, can help to evaluate for dietary intolerance/sensitivity. The diet should be fed exclusively, with added enzyme supplementation, for at least two to three weeks. If gastrointestinal signs resolve after the dietary trial, the cat should be challenged with components of its former diet in order to confirm a diagnosis of dietary intolerance/sensitivity.

If dietary modification is not effective, the cat should be investigated for structural intestinal disease (e.g., inflammatory bowel disease) with abdominal ultrasound and endoscopy with intestinal biopsy. Cats with concurrent inflammatory bowel disease usually can be successfully managed with oral prednisolone (Steiner & Williams, 2005).

Conclusion

Feline exocrine pancreatic disease, particularly acute pancreatitis, is more common than previously thought. It however requires a high level of clinical suspicion. Assay of serum fPLI combined with abdominal ultrasound is recommended for the diagnosis of pancreatitis, whereas a severely decreased serum fTLI concentration is diagnostic for EPI in the cat. In both pancreatitis and EPI, concurrent diseases should be assessed and addressed as necessary.

Provision of adequate calories and nutrients is essential in the management of cats with exocrine pancreatic disease. Supportive therapy is important to prevent complications and decrease mortality in acute pancreatitis, and early enteral feeding may be required in order to prevent secondary hepatic lipidosis. Cats with EPI will at least require dietary supplementation with pancreatic enzymes for resolution of clinical signs, and additional treatment with parenteral cobalamin is necessary in many cases.

References
  • 1. Akol KG, Washabau RJ, Saunders HM, et al. Acute pancreatitis in cats with hepatic lipidosis. J Vet Intern Med 1993; 7: 205-209.  - PubMed - 
  • 2. Bauer JE. Hepatic disease, nutritional therapy, and the metabolic environment. J Am Vet Med Assoc 1996; 209: 1850-1853.
  • 3. Beatty JA, Barrs VR, Martin PA, et al. Spontaneous hepatic rupture in six cats with systemic amyloidosis. J Small Anim Pract 2002; 43: 355-363.  - PubMed - 
  • 4. Biourge V. Clinical nutrition in liver disease, in Proceedings. 14th Annu ECVIM-CA Congress 2004; 63-65.
  • 5. Biourge V. Nutrition and liver disease. Semin Vet Med Surg 1997; 12: 34-44.  - PubMed - 
  • 6. Biourge V, Groff JM, Fisher C, et al. Nitrogen balance, plasma free amino acid concentrations and urinary orotic acid excretion during long-term fasting in cats. J Nutr 1994a; 124: 1094-1103.  - PubMed - 
  • 7. Biourge VC, Groff JM, Munn RJ, et al. Experimental induction of hepatic lipidosis in cats. Am J Vet Res 1994b; 55: 1291-1302.  - PubMed - 
  • 8. Biourge VC, Massat B, Groff JM, et al. Effect of protein, lipid, or carbohydrate supplementation on hepatic lipid accumulation during rapid weight loss in obese cats. Am J Vet Res 1994c; 55: 1406-1415. - PubMed - 
  • 9. Biourge VC, Fontaine J. Exocrine pancreatic insufficiency and adverse reaction to food in dogs: a positive response to a high-fat, soy isolate hydrolysate-based diet. J Nutr 2004, 134: 2166s-2168s.
  • 10. Blanchard G, Paragon BM, Milliat F, et al. Dietary L-carnitine supplementation in obese cats alters carnitine metabolism and decreases ketosis during fasting and induced hepatic lipidosis. J Nutr 2002; 132: 204-210. - PubMed - 
  • 11. Caney SMA, Gruffydd-Jones TJ. Feline inflammatory liver disease. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat. 6th edition. Philadelphia: WB Saunders Co, 2005; 1448-1453.
  • 12. Center SA. Chronic hepatitis, cirrhosis, breed-specific hepatopathies, copper storage hepatopathy, suppurative hepatitis, granulomatous hepatitis, and idiopathic hepatic fibrosis. In: Strombeck's Small Animal Gastroenterology. 3rd ed. Philadelphia: WB Saunders Co, 1996: 705.  - Available from amazon.com - 
  • 13. Center SA. Feline hepatic lipidosis. Vet Clin Small Anim 2005; 35: 225-269. - PubMed - 
  • 14. Center SA. Nutritional support of dogs and cats with hepatobiliary disease. J Nutr 1998; 128: 2733S-2746S. - PubMed - 
  • 15. Center SA. Pathophysiology of liver disease: Normal and abnormal function. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat. 5th edition. Philadelphia: WB Saunders Co, 2000a; 533-632. - Available from amazon.com - 
  • 16. Center SA, Elston TH, Rowland PH, et al. Fulminant hepatic failure associated with oral administration of diazepam in 11 cats. J Am Vet Med Assoc 1996; 209: 618-625. - PubMed - 
  • 17. Center SA, Randolph JF, Warner KL, et al. The effects of S-adenosylmethionine on clinical pathology and redox potential in the red blood cell, liver, and bile of clinically normal cats. J Vet Intern Med 2005; 19: 303-314. - PubMed - 
  • 18. Center SA, Warner K, Corbett J, et al. Proteins invoked by vitamin K absence and clotting times in clinically ill cats. J Vet Int Med 2000b; 14: 292-297. - PubMed - 
  • 19. Center SA, Warner KL, Erb HN. Liver glutathione concentrations in dogs and cats with naturally occurring liver disease. Am J Vet Res 2002; 63: 1187-1197. - PubMed - 
  • 20. d'Anjou MA, Penninck D, Cornejo L, et al. Ultrasonographic diagnosis of portosystemic shunting in dogs and cats. Vet Radiol Ultrasound 2004; 45: 424-437. - PubMed - 
  • 21. Day MJ. Immunohistochemical characterization of the lesions of feline progressive lymphocytic cholangitis/cholangiohepatitis. J Comp Pathol 1998; 119: 135-147. - PubMed - 
  • 22. De Cock HEV, Forman MA, Farver TB, et al. Prevalence and histopathologic characteristics of pancreatitis in cats. Vet Pathol 2007; 44: 39-49. - PubMed - 
  • 23. Delaney SJ. Management of anorexia in dogs and cats. Vet Clin North Am Small Anim Pract 2006; 36: 1243-1249.  - PubMed - 
  • 24. Feher J, Lengyel G, Blazovics A. Oxidative stress in the liver and biliary tract diseases. Scand J Gastroenterol Suppl 1998; 38-46.  - PubMed - 
  • 25. Ferreri JA, Hardam E, Kimmel SE, et al. Clinical differentiation of acute necrotizing from chronic nonsuppurative pancreatitis in cats: 63 cases (1996-2001). J Am Vet Med Assoc 2003; 223: 469-474. - PubMed - 
  • 26. Forman MA, Marks SL, De Cock HE, et al. Evaluation of serum feline pancreatic lipase immunoreactivity and helical computed tomography versus conventional testing for the diagnosis of feline pancreatitis. J Vet Intern Med 2004; 18: 807-815. - PubMed - 
  • 27. Fyfe JC. Feline intrinsic factor (IF) is pancreatic in origin and mediates ileal cobalamin (CBL) absorption. J Vet Intern Med 1993; 7: 133.
  • 28. Fuentealba IC, Aburto EM. Animal models of copper-associated liver disease. Comp Hepatol 2003; 2: 5  - PubMed - 
  • 29. Gagne JM, Armstrong PJ, Weiss DJ, et al. Clinical features of inflammatory liver disease in cats: 41 cases (1983-1993). J Am Vet Med Assoc 1999; 214: 513-516. - PubMed - 
  • 30. Gerhardt A, Steiner JM, Williams DA, et al. Comparison of the sensitivity of different diagnostic tests for pancreatitis in cats. J Vet Intern Med 2001; 15: 329-333.  - PubMed - 
  • 31. Gupta R, Patel K, Calder PC, et al. A randomised clinical trial to assess the effect of total enteral and total parenteral nutritional support on metabolic, inflammatory and oxidative markers in patients with predicted severe acute pancreatitis. Pancreatology 2003; 3: 406-413.  - PubMed - 
  • 32. Haney DR, Christiansen JS, Toll JD. Severe cholestatic liver disease secondary to liver fluke (Platynosomum concinnum) infection in three cats. J Am Anim Hosp Assoc 2006; 42: 234-237.  - PubMed - 
  • 33. Harkin KR, Cowan LA, Andrews GA, et al. Hepatotoxicity of stanozolol in cats. J Am Vet Med Assoc 2000; 217: 681-684.  - PubMed - 
  • 34. Haynes JS, Wade PR. Hepatopathy associated with excessive hepatic copper in a Siamese cat. Vet Pathol 1995; 32: 427 – 429. - PubMed - 
  • 35. Hecht S, Penninck DG, Keating JH. Imaging findings in pancreatic neoplasia and nodular hyperplasia in 19 cats. Vet Radiol Ultrasound 2007; 48: 45-50. - PubMed - 
  • 36. Hill RC, Van Winkle TJ. Acute necrotizing pancreatitis and acute suppurative pancreatitis in the cat. A retrospective study of 40 cases (1976-1989). J Vet Int Med 1993; 7: 25-33. - PubMed - 
  • 37. Holt DE, Schelling CG, Saunders HM, et al. Correlation of ultrasonographic findings with surgical, portographic, and necropsy findings in dogs and cats with portosystemic shunts: 63 cases (1987-1993). J Am Vet Med Assoc 1995; 207: 1190-1193. - PubMed - 
  • 38. Hooser SB. Hepatotoxins. In: Bonagura JD (ed). Kirk’s Current Veterinary Therapy XIII. Philadelphia: WB Saunders Co, 2000; 217-219. - Available from amazon.com - 
  • 39. Hunt GB, Kummeling A, Tisdall PL, et al. Outcomes of cellophane banding for congenital portosystemic shunts in 106 dogs and 5 cats. Vet Surg 2004; 33: 25-31. - PubMed - 
  • 40. Ibrahim WH, Bailey N, Sunvold GD, et al. Effects of carnitine and taurine on fatty acid metabolism and lipid accumulation in the liver of cats during weight gain and weight loss. Am J Vet Res 2003; 64: 1265-1277. - PubMed - 
  • 41. Jergens AE, Morrison JA, Miles KG, et al. Percutaneous endoscopic gastrojejunostomy tube placement in healthy dogs and cats. J Vet Intern Med 2007; 21: 18-24. - PubMed - 
  • 42. Johnson CD. Antioxidants in acute pancreatitis. Gut 2007; 56: 1344-1345.
  • 43. Johnston K, Lamport A, Batt RM. An unexpected bacterial flora in the proximal small intestine of normal cats. Vet Rec 1993; 132: 362-363.
  • 44. Johnston KL, Swift NC, Forster-van Hijfte M, et al. Comparison of the bacterial flora of the duodenum in healthy cats and cats with signs of gastrointestinal tract disease. J Am Vet Med Assoc. 2001 Jan 1; 218:48-51. - PubMed - 
  • 45. Kim SW, Rogers QR, Morris JG. Maillard reactions products in purified diets induce taurine depletion in cats which is reversed by antibiotics. J Nutr 1996; 126: 195-201. - PubMed - 
  • 46. Kimmel SA, Washabau RJ, Drobatz KJ. Incidence and prognostic value of low plasma ionized calcium concentration in cats with acute pancreatitis: 46 cases (1996-1998). J Am Vet Med Assoc 2001; 219: 1105-1109. - PubMed - 
  • 47. Krahenbuhl S, Reichen J. Carnitine metabolism in patients with chronic liver disease. Hepatology 1997; 25: 148-153. - PubMed - 
  • 48. Kyles AE, Hardie EM, Mehl M, et al. Evaluation of ameroid ring constrictors for the management of single extrahepatic portosystemic shunts in cats: 23 cases (1996 – 2001). J Am Vet Med Assoc 2002; 220: 1341 – 1347.  - PubMed - 
  • 49. Laflamme DP. Nutritional management of liver disease. In: Kirk’s Current Veterinary Therapy XIII, Bonagura JW (ed). WB Saunders Co, Philadephia, 2000: 277-293.
  • 50. Langdon P, Cohn LA, Kreeger JM, et al. Acquired portosystemic shunting in two cats. J Am Anim Hosp Assoc 2002; 38: 21-27. - PubMed - 
  • 51. Lasztity N, Hamvas J, Biro L, et al. Effect of enterally administered n-3 polyunsaturated fatty acids in acute pancreatitis - a prospective randomized clinical trial. Clin Nutr 2005; 24: 198-205. - PubMed - 
  • 52. Leveille R, Biller DS, Shiroma JT. Sonographic evaluation of the common bile duct in cats. J Vet Int Med 1996; 10: 296-299. - PubMed - 
  • 53. Levy JK, Bunch SE, Komtebedde J. Feline portosystemic vascular shunts. In: Bonagura J, ed. Kirk’s Current Veterinary Therapy Small Animal Practice XII. Philadelphia: WB Saunders Co, 1995; 743-749. - Available from amazon.com - 
  • 54. Lisciandro SC, Hohenhaus A, Brooks M. Coagulation abnormalities in 22 cats with naturally occurring liver disease. J Am Vet Med Assoc 1998; 12: 71-75. - PubMed - 
  • 55. Lucke VM, Davies JD. Progressive lymphocytic cholangitis in the cat. J Small Anim Pract 1984; 25: 247.
  • 56. Maddison JE. Newest insights into hepatic encephalopathy. Eur J Comp Gastroent 2000; 5: 17-21.
  • 57. Makola D, Krenitsky J, Parrish CR. Enteral feeding in acute and chronic pancreatitis. Gastrointest Endosc Clin N Am 2007; 17: 747-764. - PubMed - 
  • 58. Mansfield CS, Jones BR. Review of feline pancreatitis, part one: the normal feline pancreas, the pathophysiology, classification, prevalence and aetiologies of pancreatitis. J Feline Med Surg 2001a; 3: 117-124. - PubMed - 
  • 59. Mansfield CS, Jones BR. Review of feline pancreatitis, part two: clinical signs, diagnosis and treatment. J Feline Med Surg 2001b; 3: 125-132.  - PubMed - 
  • 60. Marchesini G, Fabbri A, Bianchi G, et al. Zinc-supplementation and amino-acid-nitrogen metabolism in patients with advanced cirrhosis. Hepatology 1996; 23: 1084-1092. - PubMed - 
  • 61. Marks SL, Rogers QR, Strombeck DR. Nutritional support in hepatic disease. Part I. Metabolic alterations and nutritional considerations in dogs and cats. Comp Cont Educ Pract Vet (Small Anim) 1994; 971-978.
  • 62. Marik PE, Zatoga GP. Meta-analysis of parenteral nutrition versus enteral nutrition in patients with acute pancreatitis. BMJ 2004; 328: 1407.  - PubMed - 
  • 63. Meertens NM, Bokhove CA, van den Ingh TS. Copper-associated chronic hepatitis and cirrhosis in a European Shorthair cat. Vet Pathol 2005; 42: 97-100. - PubMed - 
  • 64. Michel KE. Nutritional management of liver disease. Vet Clin North Am Small Anim Pract 1995; 25: 485-501. - PubMed - 
  • 65. Newell SM, Selcer BA, Girard E, et al. Correlations between ultrasonographic findings and specific hepatic diseases in cats: 72 cases (1985- 1997). J Am Vet Med Assoc 1998; 213: 94-98. - PubMed - 
  • 66. Nicholson BT, Center SA, Randolph JF, et al. Effects of oral ursodesoxycholic acid in healthy cats on clinicopathological parameters, serum bile acids and light microscopic and ultrastructural features of the liver. Res Vet Sci 1996; 61: 258-262. - PubMed - 
  • 67. Perry LA, Williams DA, Pidgeon G, et al. Exocrine pancreatic insufficiency with associated coagulopathy in a cat. J Am Anim Hosp Assoc 1991; 27: 109-114.
  • 68. Remillard RL, Saker KE. Nutritional management of hepatic conditions. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat. 6th edition. Philadelphia: WB Saunders Co, 2005; 574-577.
  • 69. Ruaux CG, Steiner JM, Williams DA. Early biochemical and clinical responses to cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia. J Vet Intern Med 2005; 19: 155–160. - PubMed - 
  • 70. Scherk M, Center SA. Toxic, metabolic, infectious, and neoplastic liver diseases. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat. 6th edition. Philadelphia: WB Saunders Co, 2005; 1464-1477.
  • 71. Schunk CM. Feline portosystemic shunts. Semin Vet Med Surg (Small Anim) 1997; 12: 45-50. - PubMed - 
  • 72. Seaman RL. Exocrine pancreatic neoplasia in the cat: a case series. J Am Anim Hosp Assoc 2004; 40: 238-245. - PubMed - 
  • 73. Simpson KW. Feline pancreatitis. Waltham Focus 2005; 15:13-19.
  • 74. Simpson KW, Fyfe J, Cornetta A, et al. Subnormal concentrations of serum cobalamin (Vitamin B12) in cats with gastrointestinal disease. J Vet Int Med 2001; 15: 26-32.  - PubMed - 
  • 75. Sokol RJ, Twedt DJ, McKim J, et al. Oxidant injury to hepatic mitochondria in patients with Wilson’s disease and Bedlington terriers with copper toxicosis. Gastroenterology 1994; 107: 1788-1798. - PubMed - 
  • 76. Sokol RJ. Fat-soluble vitamins and their importance in patients with cholestatic liver disease. Pediatr Gastroenterol 1994; 23: 673-705.  - PubMed - 
  • 77. Steiner JM. Diagnosis of pancreatitis. Vet Clin North Am Small Anim Pract 2003; 33: 1181-1195. - PubMed - 
  • 78. Steiner JM, Williams DA. Feline exocrine pancreatic disorders. Vet Clin North Am Sm Anim Pract 1999; 29: 551-574. - PubMed - 
  • 79. Steiner JM, Williams DA. Serum feline trypsin-like immunoreactivity in cats with exocrine pancreatic insufficiency. J Vet Intern Med 2000; 14: 627-629.  - PubMed - 
  • 80. Steiner JM, Williams DA. Feline exocrine pancreatic disease. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat. 6th edition. Philadelphia: WB Saunders Co, 2005; 1489-1495.
  • 81. Steiner JM, Wilson BG, Williams DA. Development and analytical validation of a radioimmunoassay for the measurement of feline pancreatic lipase immunoreactivity in serum. Can J Vet Res 2004; 68: 309-314.  - PubMed - 
  • 82. Suzuki A, Mizumoto A, Rerknimitz R, et al. Effect of bacterial or porcine lipase with low fat or high fat diets on nutrient absorption in pancreatic-insufficient dogs. Gastroenterology 1999; 116: 431-437.  - PubMed - 
  • 83. Swift NC, Marks SL, MacLachlan J, et al. Evaluation of serum feline trypsin-like immunoreactivity for the diagnosis of pancreatitis in cats. J Am Vet Med Assoc 2000; 217: 37-42. - PubMed - 
  • 84. Tillson DM, Winkler JT. Diagnosis and treatment of portosystemic shunts in the cat. Vet Clin North Am Small Anim Pract 2002; 32: 881-899.  - PubMed - 
  • 85. Trainor D, Center SA, Randolph F, et al. Urine sulfated and nonsulfated bile acids as a diagnostic test for liver disease in cats. J Vet Intern Med 2003; 17: 145-153.  - PubMed - 
  • 86. Van der Linde-Sipman JS, Niewold TA, Tooten PCJ, et al. Generalized AA-amyloidosis in Siamese and Oriental cats. Vet Immunol Immunopath 1997; 56: 1-10.  - PubMed - 
  • 87. Wang KY, Panciera DL, Al-Rukibat RK, et al. Accuracy of ultrasound-guided fine-needle aspiration of the liver and cytologic findings in dogs and cats: 97 cases (1990 – 2000). J Am Vet Med Assoc 2004; 224: 75-78. - PubMed - 
  • 88. Webster CRL. New insights into the cytoprotective action of ursodeoxycholate. In: Proceedings of the ACVIM Forum 2006; 639-641.
  • 89. Weiss DJ, Gagne J, Armstrong PJ. Inflammatory liver diseases in cats. Comp Cont Educ 2001; 23: 364-373.
  • 90. Weiss DJ, Gagne JM, Armstrong PJ. Relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis, and nephritis in cats. J Am Vet Med Assoc 1996; 209: 1114-1116. - PubMed - 
  • 91. Whittemore JC, Campbell VL. Canine and feline pancreatitis. Comp Cont Educ Pract Vet (Small Anim) 2005; 766-776.
  • 92. Williams DA. Diseases of the exocrine pancreas. BSAVA Manual of canine and feline gastroenterology. 2nd edition, 2005: 222-239.
  • 93. WSAVA Liver Standardization Group. Morphological classification of biliary disorders of the canine and feline liver. In: Rothuizen J, Bunch SE, Charles JA, eds. WSAVA Standards for Clinical and Histological Diagnosis of Canine and Feline Liver Disease. Philadelphia: WB Saunders Co, 2006. - Available from amazon.com - 
  • 94. Zoran DL. The carnivore connection to nutrition in cats. J Am Vet Med Assoc 2002; 221: 1559–1567.
  • 95. Zoran DL. Pancreatitis in cats: diagnosis and management of a challenging disease. J Am Anim Hosp Assoc 2006; 42: 1-9. - PubMed - 
  • 96. Schulz HU, Niederau C, Klonowski-Stumpe H, et al. Oxidative stress in acute pancreatitis. Hepatogastroenterology 1999; 46: 2736-2750. - PubMed - 

A great Cat Health website

http://www.felinecrf.org/index.htm

Although this cat website is designed to address Kidney Disease in Cats.... it is packed with great medical veterinarian information on understanding cat health issues.... and how to understand the CBC blood reports. I personally encourage cat and dog owners to check out this site and read much of the information as much of it also applies to dogs too!

 

Help spread the word about EPI !

AddThis Social Bookmark Button