Prevalence and Histopathologic Characteristics of Pancreatitis in Cats

42 De Cock, Forman, Farver, and Marks Vet Pathol 44:1, 2007Table 3. Histopathologic score for acute and chronic pancreatitis in the left and right limbs and body inapparently healthy cats, cats with gastrointestinal disease, and cats with extra-gastrointestinal disease.*DivisionNormal(n)Normal MeanMean Score (6SD)GI-Disease(n)GI-Disease MeanScore (6SD)Non-GI-Disease(n)Non-GI-DiseaseMean Score (6SD)LLAP 42 0.095 (60.484) 20 0.900 (61.774) 52 0.192 (60.627)LLCP 42 0.881 (61.418) 19 1.526 (62.270) 52 1.731 (62.223)BAP 41 0.024 (60.156) 20 0.600 (61.231) 52 0.192 (60.742)BCP 41 0.829 (61.263) 20 0.850 (61.348) 52 1.635 (61.868)RLAP 42 0.000 (60.000) 20 0.500 (61.000) 53 0.226 (60.724)RLCP 42 0.619 (61.011) 20 0.800 (61.361) 53 1.566 (61.995)* LLAP 5 left limb acute pancreatitis; LLCP 5 left limb chronic pancreatitis; BAP 5 body acute pancreatitis; BCP 5 bodychronic pancreatitis; RLAP 5 right limb acute pancreatitis; RLCP 5 right limb chronic pancreatitis.mean scores for AP and CP in the differentdivisions of the pancreas for the different clinicalgroups is given in Table 3. Healthy animals alwayshad the lowest score for AP and CP compared withanimals from group 2 or group 3. Animals withGI-disease (group 2) had higher scores of APcompared with animals in group 3, whereas thereverse occurred with CP. The highest scoresfor CP occurred in animals with extra GI-disease(group 3). In animals of group 3, the CP scoreswere comparable in all divisions of the pancreas,while in animals with GI-disease the left limb hada much higher CP score compared with the rightlimb and body.There was a statistically significant (P , .01)higher CP score in the left lobe compared with theright lobe in animals with GI-disease. There wasno statistically significant difference in AP or CPscore between the other clinical groups for theleft limb, right limb, and body when adjusted forage. There was a statistically significant correlation(P , .01) between the presence of CP andlocation in the pancreas. There was also a statisticallysignificant correlation (P , .01) between thepresence of AP and location in the pancreas. Astatistically significant correlation (P , .0005) wasfound between the age of the animal and thepresence of CP in the left limb, right limb, andbody unadjusted and when adjusted for other factors.There was no correlation between age andAP score in any location, both unadjusted andwhen adjusted for sex and breed. Sex and breedwere shown to be nonsignificant factors in allanalyses.HistopathologyIn general, the lesions of CP were multifocal.Only in the end-stage were the lesions confluent,although small nests of normal-appearing aciniwere always present. Lesions of AP were alsorandomly scattered throughout the pancreas andoften extended into the surrounding mesentericadipose tissue.Fibrosis. Fibrosis was a very prominent featureof CP. In the mild stages of CP, fibrosis usually wasminimal and composed of a thin layer of densefibrous tissue that surrounded 1 or several pancreaticlobules (Fig. 1). In the more severe CP, thefibrous tissue expanded uniformly around 1 ormore lobules and dissected into the lobule as thinstrands that separated the individual acini. In themost severe cases, the fibrosis was marked inthe interlobular and intralobular areas and oftenreplaced large areas of pancreatic exocrine parenchyma(Fig. 2). In all cats with severe CP, smalllobules with viable parenchyma were spared(Fig. 2). Occasionally fibrosis started within pancreaticlobules, individualizing the acinar structureswithout obvious interlobular fibrosis. The associatedacini in these cases often were atrophic, andinflammation was frequently more prominent.Fibrosis was not a feature of AP.Inflammation. A few scattered lymphocyteswithin the pancreatic parenchyma was considerednormal. Inflammation in CP was variable but oftenrather mild in comparison to the fibrous response.In the mild stages, only occasional inflammatorycells were scattered within the fibrous tissue(Fig. 1). As the amount of fibrous tissue increased,inflammation also became more prominent (Fig. 2)and more widely distributed within the lobules.Lymphocytes were always the major inflammatorycomponent in CP, but occasionally eosinophils andmacrophages were also present. Macrophages wereespecially prominent in the lumen of cystic acinarstructures that developed in the more chronicstages of pancreatitis (see cysts) (Fig. 3).In 29 pancreases (25%) there were nests oflymphocytes without associated signs of pancreatitis.The lymphocytes were small and monomorphous,closely arranged and located in small

44 De Cock, Forman, Farver, and Marks Vet Pathol 44:1, 2007Fig. 3. Pancreas; cat. Severe chronic pancreatitis;cystic acinar spaces with intraluminal macrophages(arrows). HE. Bar 5 200 mm.A striking feature found in 18 (15.7%) pancreaseswas prominent lobulation due to the interminglingof apparently normal looking lobules with prominentzymogen production and pale basophiliclobules with markedly less zymogen. (Fig. 5). Theacinar cells often looked slightly atrophic witha small, round, pale basophilic nucleus anda small amount of dark basophilic cytoplasm thatoften contained microvacuoles. However, theselobules occasionally also consisted of mildlydysplastic acinar cells with large, oval nuclei,increased nuclear:cytoplasmic ratio, pale basophiliccytoplasm, and scattered mitotic figures. Interlobularducts were not evident in these types oflobules. This feature appeared independently ofother changes in the pancreas.In addition, atypical pancreatic nodules werefound in 14 pancreases (12.2%). Two differenttypes could be distinguished. In the basophilic/vacuolated type, the cells contained a prominentamount of cytoplasm that was pale basophilic orvacuolated (Fig. 6A). The vacuolation in thesenodules was often more prominent in the antiluminalsite of the acinar cell. In the eosinophilicFig. 4. Pancreas; cat. Large cysts lined by acinarcells without significant chronic pancreatitis. The liningcells have normal zymogen granules. HE. Bar 5100 mm.type, the cytoplasm had a pale eosinophilic glassylookingcontent (Fig. 6B). Vacuolation of theacinar cells was not always confined to atypicalnodules. Scattered throughout the pancreas, smallareas with cytoplasmic vacuolation, was not uncommon.This type of vacuolation was distinctivelydifferent from the vacuolation seen in atypicalnodules, characterized by small well-demarcatedvacuolar spaces randomly distributed within a basophiliccytoplasm.Interlobular and intralobular ducts. In normalpancreases, the large intralobular ducts were oftendilated and the lumen was often filled with a paleeosinophilic, watery, amorphous mucoproteinousmaterial. The ducts were lined by a low columnarepithelium that often desquamated regionally. Thelatter was considered an artifact caused by manipulationof the tissues.Changes in the ducts were generally minimal andnot related to the extent of AP and CP in thesurrounding exocrine pancreas. The most commonchange in the small and larger interlobular ducts

Vet Pathol 44:1, 2007 Pancreatitis in Cats 45Fig. 5. Pancreas; cat. Prominent lobulation owingto the intermingling of apparently normal lookinglobules with prominent zymogen production and palebasophilic lobules with markedly less zymogen. Nopancreatitis is apparent. HE. Bar 5 100 mm.was mild to moderate dilation. The mucoproteinvaried in these ducts from pale eosinophilic todark eosinophilic often with a slight granular, oroccasionally more mucoid, pale basophilic appearance.Mineralization was rare and, if present,consisted of very small concrements. Pancreaticstones were not identified. The epithelium inmarkedly dilated interlobular ducts appeared lowcuboidal to flat. In 8 cases, the epithelium wasconvoluted forming small invaginations and intraluminalpapillary projections.Ductal inflammation was found in 12 cases. Inmost cases, the inflammatory infiltrate was verymild, lymphocytic, and mainly periductular. Insome cases, there was also a neutrophilic componentand intraluminal infiltration, rarely withaccompanying bacteria. Scattered epithelial cellswith changes consistent with apoptosis were occasionallyfound in association with ductal inflammation.A prominent ductal inflammation characterizedby a diffuse periductular lymphocyticinflammation with multifocal lymphoid follicleFig. 6. Pancreas; cat. Fig. 6a. Eosinophilic atypicalnodule. Fig. 6b. Basopilic atypical nodule in the felinepancreas. HE. Bar 5 25 mm.formation was found in 2 pancreases (Fig. 7). Theamount of inflammation in these ducts was farmore prominent than the inflammation of thesurrounding parenchyma.Islets. Amyloidosis was present in general in34 (29.6%) of the pancreases, varying from mild(,50% of the islets affected) (10.4%), to moderate(50–75% of the islets affected) (10.4%), to severe(75–100% of the islets affected) (8.7%).Vascular changes. Mild to severe arteriosclerosis,characterized by intimal fibrosis, was foundonly in 5 cats, either in the pancreatic-duodenalartery and gastroduodenal vein, or in the branchesthereof within the pancreas.DiscussionThis study confirms that CP is common in cats,with an overall study prevalence of 67%, including45% of apparently healthy cats. These figures areconsiderably higher than those previously reported,perhaps reflecting the high incidence of severe and

46 De Cock, Forman, Farver, and Marks Vet Pathol 44:1, 2007Fig. 7. Pancreas; cat. Significant periductular lymphocyticinflammation forming lymphoid follicles. HE.Bar 5 250 mm.complicated clinical conditions in the study population.11,26,30,38 In addition, the detailed examinationof the entire pancreas detected even very mildlesions as reflected by the low mean CP scoresfound in the pancreases of the healthy cats. Thefinding is also supported by the observations ofSteiner et al., who found a discrepancy betweenthe prevalence of pancreatitis in clinical and pathologicstudies from which they concluded thata significant number of cats have subclinicalpancreatitis. 38The high prevalence of CP in the cats with GIdiseaseis not surprising; however, cats withdisorders not involving the abdomen had a similaroccurrence of CP that was not attributable to agedifferences. This finding might suggests that thepancreas is very sensitive to drugs, stress, metabolicderangements, or ischemia associated witha wide variety of clinical conditions and potentiallyexplains why mild pancreatic lesions are commoneven in clinically healthy animals. Similarly, Stammfound an unexpectedly high incidence of pancreaticlesions such as lipomatosis, fibrosis, alterations ofducts and ductal epithelium, inflammatory infiltrates,focal necrosis, acinar dilation, and vascularchanges in his study of 112 human pancreasescollected from unselected autopsies of adult patientswith no known pancreatic disease. 36A significant correlation was found betweenage and CP in the cat. Previous studies also havereported that older cats are more likely to presentwith pancreatitis. 11,26 Mansfield and Jones notedthat Siamese cats were more likely to develop pancreatitiscompared with other breeds; however, wefound no correlation between breed and pancreatitisin our study. 26 A plausible reason for thisfinding is that most cats in the Mansfield and Jonesstudy were Domestic short hair (71%) and otherbreeds may have been under represented.The lesions of CP in cats partially resemble thechanges of CP in humans. As in humans, fibrosis ismore prominent than inflammation. 18,29 A majordifference between feline CP in this study andhuman CP is involvement of the pancreatic ducts,which is a prominent feature in human CP, and ismild in cats. 27 Common lesions that occur inhuman pancreatic ducts are intraluminal mucoproteinaccumulation and prominent mineralization/stone formation, ductular dilation, epithelial metaplasia,and ductal mucinous hyperplasia. 2,3,8,22,27,29Ductal mucinous hyperplasia, preneoplastic epithelialmetaplasia, and intraductal stone formationwere not identified in cat pancreases. Furthermore,ductular dilation, epithelial changes, mucoproteinaccumulation, and mineralization were remarkablymild in affected cats. This finding is in contrastwith the observations of Jubb et al., who describeCP as an extension from ductular inflammation. 20Zhao et al. also report ductular epithelial flattening,epithelial proliferation, and stenosis in experimentallyinduced pancreatitis in cats. 44 A possibleexplanation is that the technique used to inducepancreatitis in the cats in this study, namely,ductular damage is not representative for the waythe natural disease develops.Acinar cell metaplasia is common in humanCP. 9,14,33 The changes in the acinar cells as well asthe ductular epithelial changes are consideredpreneoplastic lesions, and a gradual progressionfrom mild to severe metaplasia and concurrentneoplasia has been well documented. 9,14,27,33 Whileatypical nodules and nodular atrophy with occasionaldysplasia (see below in discussion) wereoften present in the feline pancreases, transition tomore distinct preneoplastic or neoplastic changeswere not identified. The plausible reason for thisdifference is the different etiology of pancreatitis inhumans and cats. Alcohol abuse is responsible for70% of CP in humans, while the remaining 30% is

Vet Pathol 44:1, 2007 Pancreatitis in Cats 47autoimmune, dietary, genetic, idiopathic, or secondaryto pancreatic duct obstruction. 8,22,27,29 Thecause of pancreatitis in cats is still highly speculativeand, according to Steiner and Williams, 90% ofthe cases are idiopathic. 37 Correlations have beenfound between inflammatory bowel disease (IBD)and cholangiohepatitis and the presence of CP. 40Differentiation between the different etiologiesof CP based on histopathologic morphology wasnot possible in this study. This is similar to thefindings in humans, indicating that pancreaticdisease, independent of the underlying etiology,reaches a common immunologic stage beyondwhich it appears to progress as a single distinctiveentity. 34 An exception is the recently documentedautoimmune pancreatitis in humans characterizedby prominent periductular lymphoplasmacytic inflammationassociated with periductular sclerosis.23,28,31 A comparable severe lymphocytic inflammationwas observed in 2 feline pancreases(Fig. 7).Some histopathologic features found in feline CPmight be suggestive of a more specific etiology.Small lymphocytic infiltrates with no associatedparenchymal lesions were common in the examinedfeline pancreases. It appeared as a subjectiveobservation that these infiltrates were commonlyassociated with inflammatory bowel disease.In addition, the multilobular atrophy (Fig. 5)sometimes associated with dysplasia, but notassociated with inflammation found in 15.6% ofthe pancreases, is most likely associated witha specific insult to the pancreas. These lesions havebeen referred to in the literature as hyperplasticnodules. 20 However, it has never been investigatedwhether these lesions really are hyperplastic or not.In the pancreases examined for this project, thecells appeared rather atrophic based on the reducedamount of cytoplasm and lack of zymogen production.One possible reason for this is obstructionof smaller pancreatic ducts leading to atrophyof the associated lobule. Zhao et al. describedextensive exocrine and endocrine pancreatic atrophywithout fibrosis or inflammation in cases withcomplete obstruction of the pancreatic duct. 44However, Zhao et al. also found dilated ducts inthese particular cases, which was not present in themultilobular atrophy type of our study. 44 Moreresearch is warranted to determine the underlyingcause for this specific lesion.Some age-related changes described in thehuman pancreas were also frequently noticed infeline pancreases. This included acinar cell vacuolationand atypical eosinophilic and basophilicnodules. In addition, several pancreases had cysticstructures not related to CP. It was remarkablethat a high percentage of the cats with such cystswere of a long-haired breed. Since long-hairedbreeds have a predisposition for polycystic kidneydisease syndrome, the pancreatic cysts might berelated to this disease. 4–6,12 Similarly, in people withpolycystic kidney disease, pancreatic cysts are notuncommon. 1Pancreatic biopsy is still considered the goldstandard for the diagnosis of CP in humans andcats. 10,13,17,41,42 Even acute necrotizing pancreatitisand CP in cats cannot be distinguished from eachother solely on the basis of history, physicalexamination findings, results of clinicopathologictesting, radiographic abnormalities, or ultrasonographicabnormalities. 15 In humans, a highly significantcorrelation exists between direct functiontests and histopathology of the exocrine pancreas.17,18Surgical biopsy is facilitated by takinga biopsy of the most accessible part of the pancreas.An important observation in our study was thefinding of higher mean CP scores in the leftpancreatic limb in cats with GI-disease. The leftlimb is the most accessible portion of the pancreas,which should facilitate the diagnosis of CP in catswith GI-disease. In contrast, we did not find anydifferences in the severity of pancreatic scores inthe left limb, right limb, or body in cats with extra-GI disease. The reason for the differences in CPscores in the different divisions of the pancreas inanimals with abdominal disease is most likelyrelated to anatomic characteristics, blood supply,or both in relation to the rest of the GI tract. Theleft limb, which had higher scores of CP, was alsosignificantly bigger than the right limb. Therefore,it is assumed that differences in the size or morphologyof the ducts might influence invasion ofbacteria or regurgitation of bile from the GI tract.In contrast, in animals with generalized disease,the entire pancreas had comparable scores. It isthought that the lesions in these cases are related toblood-borne insults and therefore are more evenlydistributed lesions.Acute pancreatitis was relatively uncommon inthis study as was the prevalence of AP and CP inthe same pancreas. Forman et al. found a prevalenceof 44% of AP and CP in the same pancreas intheir study, which is significantly higher than the9.6% found in this study. 16 The most likely reasonfor this is the difference in selected animals for bothstudies.This study underscores the high prevalence of CPin cats. Histopathologic changes resemble thelesions found in human CP, although preneoplasticchanges were not noticed in cats. While determi-

48 De Cock, Forman, Farver, and Marks Vet Pathol 44:1, 2007nation of the underlying cause might not be possiblebased on histopathologic examination of thepancreas in most cases, very typical lesions werenoticed in feline pancreases that warrant furtherresearch to determine the underlying cause.AcknowledgementsSincere thanks are due to all the pathologists,clinicians, students, and technicians of University ofCalifornia, Davis, who helped collect cases for thisproject. Specifically, we would like to thank MonicaKratochvil for her excellent assistance. The authorsappreciate the critical review of this manuscript by Dr.James N. MacLachlan, Department of Pathology,Microbiology, and Immunology, University of California,Davis, School of Veterinary Medicine.References1 Al-Bhalal L, Akhtar M: Molecular basis of autosomaldominant polycystic kidney disease. Adv AnatPathol 12:126–133, 20052 Allen-Mersh TG: What is the significance ofpancreatic ductal mucinous hyperplasia? Gut 26(8):825–833, 19853 Allen-Mersh TG: Pancreatic ductal mucinous hyperplasia:distribution within the pancreas, andeffect of variation in ampullary and pancreatic ductanatomy. Gut 29(10): 1392–1396, 19884 Barrs VR, Gunew M, Foster SF, Beatty JA, MalikR: Prevalence of autosomal dominant polycystickidney disease in Persian cats and related breeds inSydney and Brisbane. Aust Vet J 79:257–259, 20015 Barthez PY, Rivier P, Begon D: Prevalence ofpolycystic kidney disease in Persian and Persianrelated cats in France. J Feline Med Surg 5:345–347,20036 Cannon MJ, MacKay AD, Barr FJ, Rudorf H,Bradley KJ, Gruffydd-Jones TJ: Prevalence of polycystickidney disease in Persian cats in the UnitedKingdom. Vet Rec 149:409–411, 20017 Chari ST, Singer MV: The problem of classificationand staging of chronic pancreatitis. Proposals basedon current knowledge of its natural history.Scand J Gastroenterol 29:949–960, 19948 Cruickshank AH: Noninfective chronic pancreatitis.In: Pathology of the Pancreas, ed. Cruickshank AHand Benhow EW, pp. 233–258. Springer, London,UK, 19959 Cylwik B, Nowak HF, Puchalski Z, Barczyk J:Epithelial anomalies in chronic pancreatitis as a riskfactor of pancreatic cancer. Hepatogastroenterology45:528–532, 199810 Dill-Macky E: Pancreatic diseases of cats. CompendContin Educ Pract Vet 15:589–598, 199311 Duffel SJ: Some aspects of pancreatic disease in thecat. J Small Anim Pract 16:365–374, 197512 Eaton KA, Biller DS, DiBartola SP, Radin MJ,Wellman M: Autosomal dominant polycystic kidneydisease in Persian and Persian-cross cats. Vet Pathol34:117–126, 199713 Etemad B, Whitcomb DC: Chronic pancreatitis:diagnosis, classification, and new genetic developments.Gastroenterology 120:682–707, 200114 Fang J, Hussong J, Roebuck BD, Talamonti MS,Rao MS: Atypical acinar cell foci in humanpancreas: morphological and morphometric analysis.Int J Pancreatol 22:127–130, 199715 Ferreri JA, Hardam E, Kimmel SE, Saunders HM,Van Winkle TJ, Drobatz KJ, Washabau RJ:Clinical differentiation of acute necrotizing fromchronic nonsuppurative pancreatitis in cats: 63 cases(1996–2001). J Am Vet Med Assoc 223:469–474,200316 Forman MA, Marks SL, De Cock HE, Hergesell EJ,Wisner ER, Baker TW, Kass PH, Steiner JM,Williams DA: Evaluation of serum feline pancreaticlipase immunoreactivity and helical computed tomographyversus conventional testing for the diagnosisof feline pancreatitis. J Vet Intern Med18:807–815, 200417 Hayakawa T, Kondo T, Shibata T, Noda A, SuzukiT, Nakano S: Relationship between pancreaticexocrine function and histological changes in chronicpancreatitis. Am J Gastroenterol 87:1170–1174, 199218 Heij HA, Obertop H, van Blankenstein M, ten KateFW, Westbroek DL: Relationship between functionaland histological changes in chronic pancreatitis.Dig Dis Sci 31:1009–1013, 198619 Hill RC, Van Winkle TJ: Acute necrotizing pancreatitisand acute suppurative pancreatitis in the cat. Aretrospective study of 40 cases (1976-1989). J VetIntern Med 7:25–33, 199320 Jubb KVF: The pancreas. In: Pathology of DomesticAnimals, ed. Jubb KVF, Kennedy PC, and PalmerN, pp. 407–424. Academic Press, San Diego, CA,199321 Kitchell BE, Strombeck DR, Cullen J, Harrold D:Clinical and pathologic changes in experimentallyinduced acute pancreatitis in cats. Am J Vet Res47:1170–1173, 198622 Klöppel G, Heitz, Ph: Exocrine pancreas. In:Pancreatic Pathology, ed. Klöppel G and Heitz,Ph, pp. 3–114. Churchill Livingstone, Edinburgh,UK, 198423 Klöppel G, Luttges J, Lohr M, Zamboni G, LongneckerD: Autoimmune pancreatitis: pathological,clinical, and immunological features. Pancreas27:14–19, 200324 Longnecker DS, Hashida Y, Shinozuka H: Relationshipof age to prevalence of focal acinar celldysplasia in the human pancreas. J Natl Cancer Inst65:63–66, 198025 Longnecker DS, Shinozuka H, Dekker A: Focalacinar cell dysplasia in human pancreas. Cancer45:534–540, 198026 Mansfield CS, Jones BR: Review of feline pancreatitispart two: clinical signs, diagnosis and treatment.J Feline Med Surg 3:125–132, 2001

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