Exocrine pancreatic insufficiency in dogs.

Pancreatic acinar atrophy (PAA) is by far the most common cause for the maldigestion signs of canine exocrine pancreatic insufficiency (EPI). The ability to diagnose PAA in the subclinical phase before the development of total acinar atrophy and manifestation of clinical signs has offered new possibilities to study the pathogenesis of the disease. Marked T-lymphocyte infiltration during the progression of acinar atrophy and the genetic susceptibility of the disease have been taken as a primary evidence of the autoimmune nature of the disease. The term autoimmune-mediated atrophic lymphocytic pancreatitis is preferred to describe pathologic findings. A single abnormally, low serum canine trypsin-like immunoreactivity (cTLI) concentration (< 2.5 mg/L), in dogs with typical maldigestion signs has been shown to be highly diagnostic for clinical EPI and is found in dogs with end-stage PAA. Repeatedly subnormal cTLI values (2.5-5.0 micrograms/L) in dogs with no clinical signs of EPI are valuable markers of subclinical EPI and highly suggestive for partial PAA. The primary treatment of EPI is supplementing each meal with pancreatic enzymes. The long-term treatment response for the nonenteric-coated enzyme supplements has been found to be good in half of these dogs, but the response varied considerably.     

Serum amylase and isoamylase values in dogs with pancreatic disease

Serum amylase and isoamylase values were determined in three groups of dogs. The first group contained control dogs while the other groups contained dogs with confirmed exocrine pancreatic insufficiency and diabetes mellitus respectively. The trypsin-like immunoreactivity test was also carried out on sera from dogs with exocrine pancreatic disease (EPI). A significant difference was detected in the serum amylase values between the three groups which may be of limited diagnostic value. Dogs with EPI had values lower than normal while those with diabetes mellitus had values higher than control dogs. No evidence of exocrine pancreatic insufficiency was found in dogs with diabetes mellitus.     

Autoantibodies to pancreatic islet cells in canine diabetes mellitus

Indirect immunofluorescence on normal canine pancreatic tissue fixed in Bouin's solution was used to detect islet cell antibodies in dogs with diabetes mellitus, other endocrine diseases, and pancreatitis. 18 of 25 dogs with diabetes mellitus alone, 2 of 8 dogs with diabetes mellitus and concurrent pancreatitis, and 2 of 2 dogs with diabetes mellitus and concurrent pancreatic exocrine insufficiency were positive for autoantibody. 2 of 12 dogs with hypoadrenocorticism, 3 of 6 dogs with hyperadrenocorticism, 6 of 28 dogs with hypothyroidism and one of 19 dogs with pancreatitis alone were also antibody positive. None of 20 healthy dogs or 20 dogs with disorders other than those of the pancreas or endocrine organs were antibody positive. Islet cell antibodies were demonstrated in dogs with diabetes mellitus and other endocrine disorders. The possibility of autoimmune involvement in the development of diabetes mellitus in the dog should be considered.     

Genetics of canine diabetes mellitus: Are the diabetes susceptibility genes identified in humans involved in breed susceptibility to diabetes mellitus in dogs?

Diabetes mellitus is a common endocrinopathy in companion animals, characterised by hyperglycaemia, glycosuria and weight loss, resulting from an absolute or relative deficiency in the pancreatic hormone insulin. There are breed differences in susceptibility to diabetes mellitus in dogs, with the Samoyed breed being overrepresented, while Boxers are relatively absent in the UK population of diabetic dogs, suggesting that genetic factors play an important role in determining susceptibility to the disease. A number of genes, linked with susceptibility to diabetes mellitus in humans, are associated with an increased risk of diabetes mellitus in dogs, some of which appear to be relatively breed-specific. Diabetes mellitus in dogs has been associated with major histocompatibility complex (MHC) class II genes (dog leucocyte antigen; DLA), with similar haplotypes and genotypes being identified in the most susceptible breeds. A region containing a variable number of tandem repeats (VNTR) and several polymorphisms have been identified in the canine insulin gene, with some alleles associated with susceptibility or resistance to diabetes mellitus in a breed-specific manner. Polymorphisms in the canine CTLA4 promoter and in other immune response genes are associated with susceptibility to diabetes mellitus in a number of pedigree breeds. Genome wide association studies are currently underway that should shed further light on the genetic factors responsible for the breed profile seen in the diabetic dog population.     

Cellular and humoral immune responses in atrophic lymphocytic pancreatitis in German shepherd dogs and rough-coated collies

The most common cause for the clinical signs of exocrine pancreatic insufficiency (EPI) in dogs is pancreatic acinar atrophy (PAA). In the subclinical phase of EPI, before total atrophy occurs, exocrine pancreas is affected by infiltrative lymphocytic inflammation, which gradually leads to selective destruction and atrophy of the acinar tissue.Here, we analyzed the role of cell-mediated and humoral immune mechanisms in the pathogenesis of atrophic lymphocytic pancreatitis in German shepherd dogs and rough-coated collies. Pancreas biopsies and serum samples were obtained from 12 dogs with subclinical EPI (SEPI), 13 dogs with clinical EPI and 13 healthy control dogs.Immunohistochemical analysis showed that, in the subclinical phase, the majority of the infiltrating lymphocytes were T-cells with an almost equal number of CD4+ 'T-helper' and CD8+ 'cytotoxic' T-lymphocytes. The distribution of the two lymphocyte subsets was different. Typically, the CD4+ cells were present in large cellular infiltrates in the affected parenchyma, and the scattered CD8+ cells had infiltrated both the affected and the normal parenchyma. In sections where destruction of acinar parenchyma was present, the CD8+ T-cells were predominant. In cases of marked T-cell infiltration, CD79+ B-lymphocytes and plasma cells, and lysozyme-positive macrophages were also detected. Lymphoid follicle germinal centers with a majority of cells staining positively for CD79 were found. The lymphocytic infiltration in the totally atrophic tissue of dogs with clinical EPI was less prominent. Indirect immunofluorescence staining showed serum antibodies reacting weakly with pancreatic acinar cells in five out of nine dogs with subclinical and three out of 10 dogs with clinical EPI, but not in the control dogs.The results suggest that the tissue destruction is largely T-cell-mediated, although the presence of numerous B-lymphocytes and pancreas-specific antibodies in the sera of some dogs indicate that humoral mechanisms are also involved. In conclusion, this study suggests that the atrophic lymphocytic pancreatitis in German shepherds and rough-coated collies is an autoimmune disease.     

Chronic Pancreatitis in Dogs

Chronic pancreatitis used to be considered uncommon in dogs, but recent pathological and clinical studies have confirmed that it is in fact a common and clinically significant disease. Clinical signs can vary from low-grade recurrent gastrointestinal signs to acute exacerbations that are indistinguishable from classical acute pancreatitis. Chronic pancreatitis is a significant cause of chronic pain in dogs, which must not be underestimated. It also results in progressive impairment of endocrine and exocrine function and the eventual development of diabetes mellitus or exocrine pancreatic insufficiency or both in some affected dogs at end stage. The etiology is unknown in most cases. Chronic pancreatitis shows an increased prevalence in certain breeds, and recent work in English Cocker Spaniels suggests it is part of a polysystemic immune-mediated disease in this breed. The histological and clinical appearance is different in different breeds, suggesting that etiologies may also be different. Diagnosis is challenging because the sensitivities of the available noninvasive tests are relatively low. However, with an increased index of suspicion, clinicians will recognize more cases that will allow them to institute supportive treatment to improve the quality of life of the patient.     

Protein-losing enteropathy in a dog with lymphangiectasia,lymphoplasmacytic enteritis and pancreatic exocrine insufficiency

This is a report of seven-year-old male Akita mixed dog, with protein-losing enteropathy (PLE). He had a history of chronic vomiting and diarrhea with anorexia/hyporexia. Previously he suffered acute abdomen about eight months prior to this visit. Our dog showed uncommon combination of diseases that could cause PLE since it was affected by inflammatory bowel disease (IBD), intestinal lymphangiectasia (IL), and exocrine pancreatic insufficiency (EPI). The dog had most of the abnormalities found in IL, as well as hypoalbuminemia, hyperglobulinemia, lymphopenia, hypocalcemia, and hypercholesterolemia. During endoscopy exam, we found changes characteristic of IL such as irregular small white spots. We took biopsies from stomach, duodenum, and cecum. These biopsies showed infiltration by lymphocytes and plasmatic cells in the lamina propria also, the duodenal biopsies showed moderate dilation of the lymphatic vessels. The patient had 2.1?µg/mL of TLI, this result was compatible with EPI. We assume that the first pathology in this animal was IBD, which caused chronic pancreatitis (CP) that in turn progressed to EPI. It is also possible that IL was secondary to IBD. We have reported for the first time the correlation of IBD and EPI in dogs. This should change our approach to treating chronic diarrhea in dogs. Therefore, we propose that dogs diagnosed with EPI should also be subjected to endoscopy and intestinal biopsy. Similarly, to rule out secondary EPI, TLI should be measured routinely in dogs with IBD.     

Bile duct obstruction secondary to chronic pancreatitis in seven dogs

Seven icteric dogs were determined to have bile duct obstruction secondary to chronic pancreatitis. All dogs had histories of intermittent vomiting and diarrhea. Alkaline phosphatase and alanine aminotransferase activities and total bilirubin concentrations were markedly elevated. Diagnosis was based on exploratory laparotomy and histological examination. Each dog had a 3 to 10 cm mass in the body of the pancreas and obstruction of the common bile duct. Three dogs treated with pancreatectomy, gastrojejunostomy, and cholecystojejunostomy died within five weeks. Three dogs treated with conservative surgical procedures were alive at 8, 16, and 26 months postoperatively. One dog was euthanized because of suspected neoplasia. Hepatic enzyme activity and bilirubin levels decreased markedly in the surviving dogs. Histological examination of the pancreatic masses indicated chronic pancreatitis. Hepatic biopsies revealed evidence of cholestasis. Chronic pancreatitis should be included in the differential diagnoses of icterus, bile duct obstruction, and masses in the pancreas.     

Morphologic and immunocytochemical study of young dogs with diabetes mellitus associated with pancreatic islet hypoplasia

In 11 dogs (7 males, 4 females; 10 purebred, 1 mixed breed), diagnosed as having diabetes mellitus before the age of 6 months, the pancreas was evaluated histologically; in 6, the pancreas also was examined by use of electron microscopy and/or immunocytochemical methods. Each dog was placed in 1 of 3 groups (A through C) on the basis of pancreatic histopathologic findings: Group A (n = 3)--no recognizable islets, but the pancreas in 2 dogs contained scattered endocrine cells detectable by use of immunoperoxidase staining or electron microscopy; Group B (n = 4)--no recognizable islets, but the pancreas had severe vacuolation of ducts and acini, as well as acinar atrophy; Group C (n = 4)--scant shrunken islets; 1 pancreas had reduced numbers of recognizable islets, hydropic beta-cell vacuolation attributable to glycogen deposition, and islet and nonislet endocrine cells in expected proportions. Insulitis was not observed in any pancreas, although scattered lymphocytes were seen in the pancreatic interstitial fibrous tissue of 3 dogs. Histologic pancreatic lesions in these young dogs were distinct from those of type-I (insulin-dependent) diabetes mellitus in human beings, as well as from those of diabetes mellitus in aged dogs, but were similar to those described in other young diabetic dogs. This uncommon syndrome is distinct from commonly recognized canine diabetes mellitus, on the basis of age of onset, predisposition for purebred dogs, lack of predisposing endocrinopathies or obesity, and pancreatic histologic features. The cause(s) is unknown, but is related to pancreatic endocrine hypoplasia and not to insulitis or to exocrine pancreatic inflammation. The term pancreatic islet hypoplasia is chosen as best describing this disorder.     

A pilot study evaluating changes in pancreatic lipase immunoreactivity concentrations in canines treated with L-asparaginase (ASNase), vincristine, or both for lymphoma

L-asparaginase (ASNase) is a common chemotherapy agent for the treatment of lymphoid malignancies. L-asparaginase has been reported to cause clinical pancreatitis in both humans and canines. Canine pancreatic lipase immunoreactivity (cPLI) is now a common diagnostic tool for evaluating pancreatitis in dogs. A total of 52 dogs were enrolled into this study. Canine pancreatic lipase immunoreactivity (cPLI) concentrations were evaluated before and after administration of ASNase, vincristine, or both. All dogs enrolled in the study were evaluated for signs compatible with clinical pancreatitis. No dogs receiving ASNase alone showed evidence of clinical pancreatitis after administration. Also, there was no statistically significant change in cPLI concentrations before or after treatment. Fourteen percent of dogs that received both vincristine and ASNase concurrently had elevated concentrations of cPLI after treatment. Of the 11 dogs with clinical signs compatible with pancreatitis after any chemotherapy treatment, no dog had a cPLI concentration > 400 μg/dL. In conclusion, ASNase did not cause clinical pancreatitis in this cohort of dogs but larger sample sizes are required to further validate this data.     

Pancreatic Pseudocysts in 4 Dogs and 2 Cats: Ultrasonographic and Clinicopathologic Findings

Pancreatic pseudocysts were diagnosed in 4 dogs and 2 cats based on ultrasonographic and clinicopathologic findings. All 6 animals had a clinical diagnosis of pancreatitis. Five of 6 pseudocysts were in the left pancreatic limb, and in 1 cat the pseudocyst was in the pancreatic body region. Cyst size ranged from 2 x 2 cm to 7 x 6 cm. All pseudocysts had anechoic regions that were aspirated using ultrasound guidance for diagnostic and therapeutic purposes. No morbidity was associated with the aspiration procedures. Cytologically the pseudocyst fluid was aseptic in all patients and had low numbers of inflammatory cells in 5 of 6 patients. All animals had high lipase activity in the pseudocyst fluid and in 2 dogs and 1 cat the lipase activity in the fluid was greater than in serum. Three of the 4 dogs were managed medically. In the 1 dog that had long-term follow-up ultrasound examination, the pseudocyst persisted for several days following aspiration and had disappeared 8 months after diagnosis. All 3 of these dogs were clinically normal 1.5-4 years after presentation. The 4th dog underwent surgical exploration and was euthanized shortly thereafter because of bronchopneumonia and chronic pancreatitis. The 2 cats died 10 days and 2 months, respectively, following initial diagnosis of the pseudocyst, but necropsies were not performed in either case. Ultrasound-guided fine-needle aspiration of pancreatic pseudocysts and clinicopathologic evaluation of cystic fluid are useful for diagnosis of pancreatic pseudocysts.     

COMBINED USE OF ULTRASONOGRAPHY AND CONTRAST ENHANCED COMPUTED TOMOGRAPHY TO EVALUATE ACUTE NECROTIZING PANCREATITIS IN TWO DOGS

The imaging findings in two miniature schnauzers with acute necrotizing pancreatitis are described. Both dogs were treated previously for diabetes mellitus and hyperlipidemia. Vomiting, anorexia, and lethargy were observed in both dogs at presentation. Laboratory evaluations supportive of pancreatitis included left shift, abnormally high serum amylase and lipase activities, hypocalcemia, and abnormally high serum activities of liver enzymes. Sonographically, both dogs had diffusely enlarged hypoechoic pancreatic tissue with anechoic foci compatible with necrosis, abscessation, phlegmon, and pseudocysts formation. Contrast-enhanced computed tomography (CT) findings in both dogs were compatible with pancreatic necrosis. Dog 1 was managed medically for 11 days. Follow-up CT scan in this dog disclosed decreased pancreatic size and increased contrast enhancement compatible with partial resolution of pancreatitis.     

Definition of diabetes mellitus

The nomenclature of human diabetes mellitus (DM) has been revised, and this classification has been accepted throughout the medical world and literature. The major categories of diabetes are: insulin-dependent DM, type I or IDDM; noninsulin-dependent DM, type II or NIDDM; secondary DM or type S; impaired glucose tolerance, IGT; gestational diabetes; and previous abnormality of glucose tolerance, PrevAGT. A review of the literature has shown that over half of the documented diabetic dogs, with a single medical diagnosis, appear to be type I, IDDM, with a substantial proportion being type S, and the remainder being type II, NIDDM. Obesity is frequently associated with IGT and NIDDM. Diabetic cats most commonly have pancreatic islet destruction associated with pancreatic amyloidosis; they are insulin deficient, IDDM. The commonest causes of secondary diabetes in dogs are pancreatic damage, hyperadrenocorticism and hypersomatotropism secondary to persistent progesterone influence. Progestogen therapy is the most frequently reported cause of secondary diabetes in cats. Diabetes in horses is type S, usually secondary to a functional pituitary tumor but occasionally following chronic pancreatitis. The blood glucose ranges for normal, IGT and diabetic animals, and the normal serum insulin values of various species is tabulated.     

A retrospective-cohort study on the development of cataracts in dogs with diabetes mellitus: 200 cases

The objective of the study was to determine the incidence and estimated median time to cataract formation in dogs with diabetes mellitus. The animals studied were 200 dogs with diabetes mellitus which were referred to a university teaching hospital between 1985 and 1995. Medical records from dogs with a diagnosis of diabetes mellitus were reviewed and, where necessary, further follow-up information was gathered from the referring veterinarian. Incidence rate and median time to diabetic cataract formation was calculated using survival-analysis techniques in a retrospective cohort study design. Among the 200 dogs in the study population, 23 had cataracts at the time of diabetes diagnosis that were presumed to be related to other disease processes. Of the remaining 177 dogs, 132 had documented cataract development with features suggestive as being secondary to diabetes. Twenty-three dogs did not have obvious cataracts at the time of their last examination while 22 dogs did not have cataracts at the time they were lost to follow-up. These 55 cases contributed to the statistical models as noncases of cataracts until the last date for which an examination was available. Half of the population had developed cataracts by the 170th day postdiagnosis of diabetes mellitus, while 75% and 80% of the population developed cataracts by 370 days and 470 days, respectively. The results of this study suggest that the majority of dogs with diabetes will develop cataracts within 5–6 months from the time of diagnosis of the disease, and that approximately 80% of dogs will develop cataracts within 16 months of diagnosis.     

Subclinical exocrine pancreatic insufficiency in dogs

OBJECTIVE: To study progression of autoimmune-mediated atrophic lymphocytic pancreatitis from the subclinical to the clinical phase (exocrine pancreatic insufficiency [EPI]) and determine whether progression of the disease could be halted by treatment with immunosuppressive drugs. DESIGN: Randomized controlled trial. ANIMALS: 20 dogs with subclinical EPI. PROCEDURE: Diagnosis of subclinical EPI was determined on the basis of repeatedly low serum trypsin like-immunoreactivity (TLI) in dogs with no signs of EPI. Laparotomy was performed on 12 dogs with partial acinar atrophy and atrophic lymphocytic pancreatitis. A treatment group (7 dogs) received an immunosuppressive drug (azathioprine) for 9 to 18 months, and a nontreatment group (13) received no medication. RESULTS: During the subclinical phase, serum TLI was repeatedly low (< 5.0 microg/L). Although a few dogs had nonspecific gastrointestinal tract signs, they did not need diet supplementation with enzymes. While receiving immunosuppressive medication, treated dogs had no clinical signs of EPI, but within 2 to 6 months after treatment was stopped, 2 dogs had signs of EPI, and diet supplementation with enzymes was started. Five of the 13 untreated dogs needed diet supplementation with enzymes within 6 to 46 months. During follow-up of 1 to 6 years, 3 of the 7 treated dogs and 8 of the 13 untreated dogs did not need continuous diet supplementation with enzymes. CONCLUSIONS AND CLINICAL RELEVANCE: Progression of atrophic lymphocytic pancreatitis varied widely. The subclinical phase may last for years and sometimes for life. The value of early treatment with an immunosuppressive drug was questionable and, because of the slow natural progression of the disease, cannot be recommended.     

Diagnosis of canine exocrine pancreatic insufficiency by the assay of serum trypsin-like immunoreactivity

A radioimmunoassay for canine serum trypsin-like immunoreactivity (TLI) has been developed and evaluated for use in the diagnosis of exocrine pancreatic insufficiency (EPI). The maximum fasting TLI concentration in 14 dogs with EPI was 1.8 μg/l, compared with a minimum value of 7.0 μg/l in a control group of 75 dogs. The measurement of serum TLI therefore provides a sensitive test for the diagnosis of EPI in the dog.     

Feline exocrine pancreatic disorders.

Despite the uncommon clinical diagnosis, cats frequently suffer from disorders of the exocrine pancreas. Pancreatitis is the most common feline exocrine pancreatic disorder. Pancreatitis can be acute or chronic and mild or severe. The etiology of most cases of feline pancreatitis is idiopathic. Some cases have been associated with severe abdominal trauma, infectious diseases, cholangiohepatitis, and organophosphate and other drug intoxication. The clinical presentation of cats with pancreatitis is nonspecific. Vomiting and signs of abdominal pain, which are the clinical signs most commonly observed in humans and dogs with pancreatitis, are only uncommonly observed in cats with pancreatitis. Routine laboratory findings are also nonspecific. Abdominal ultrasonography is a valuable diagnostic tool in feline patients with pancreatitis. Serum activities of lipase and amylase are rarely increased in cats with pancreatitis; however, these cats often have elevated serum fTLI concentrations. The goals of management are removal of the inciting cause, provision of supportive and symptomatic therapy, and careful monitoring for and aggressive treatment of systemic complications. Exocrine pancreatic insufficiency is a syndrome caused by insufficient synthesis of pancreatic digestive enzymes by the exocrine portion of the pancrease. The clinical signs most commonly reported are weight loss, loose and voluminous stools, and greasy soiling of the hair coat. Serum fTLI is subnormal in affected cats. Treatment of cats with EPI consists of enzyme supplementation with powdered pancreatic extracts or raw beef pancreas. Many cats with EPI have concurrent small intestinal disease. Most cats with EPI also have severely decreased serum cobalamin concentrations and may require parenteral cobalamin supplementation. Pancreatic adenocarcinoma is the most common neoplastic condition of the exocrine pancreas in the cat. At the time of diagnosis, the tumor has already metastasized in most cases, and the prognosis is poor. Pancreatic pseudocyst, pancreatic abscess, pancreatic parasites, pancreatic bladder, and nodular hyperplasia are other exocrine pancreatic disorders, that are less commonly seen in cats.     

Breed associations for canine exocrine pancreatic insufficiency

BACKGROUND: Knowledge of breed associations is valuable to clinicians and researchers investigating diseases with a genetic basis. HYPOTHESIS: Among symptomatic dogs tested for exocrine pancreatic insufficiency (EPI) by canine trypsin-like immunoreactivity (cTLI) assay, EPI is common in certain breeds and rare in others. Some breeds may be overrepresented or underrepresented in the population of dogs with EPI. Pathogenesis of EPI may be different among breeds. ANIMALS: Client-owned dogs with clinical signs, tested for EPI by radioimmunoassay of serum cTLI, were used. METHODS: In this retrospective study, results of 13,069 cTLI assays were reviewed. RESULTS: An association with EPI was found in Chows, Cavalier King Charles Spaniels (CKCS), Rough-Coated Collies (RCC), and German Shepherd Dogs (GSD) (all P < .001). Chows (median, 16 months) were younger at diagnosis than CKCS (median, 72 months, P < .001), but not significantly different from GSD (median, 36 months, P = .10) or RCC (median, 36 months, P = .16). GSD (P < .001) and RCC (P = .015) were younger at diagnosis than CKCS. Boxers (P < .001), Golden Retrievers (P < .001), Labrador Retrievers (P < .001), Rottweilers (P = .022), and Weimaraners (P = .002) were underrepresented in the population with EPI. CONCLUSIONS AND CLINICAL IMPLICATIONS: An association with EPI in Chows has not previously been reported. In breeds with early-onset EPI, immune-mediated mechanisms are possible or the disease may be congenital. When EPI manifests later, as in CKCS, pathogenesis is likely different (eg, secondary to chronic pancreatitis). Underrepresentation of certain breeds among dogs with EPI has not previously been recognized and may imply the existence of breed-specific mechanisms that protect pancreatic tissue from injury.     

Common bile duct obstruction secondary to chronic fibrosing pancreatitis: treatment by use of cholecystoduodenostomy in the dog

Six small to medium-sized, middle-aged, female dogs with histories of acute pancreatitis developed clinical signs of extrahepatic biliary obstruction. Clinical findings were similar in the 6 dogs and included icterus. Serum biochemical analyses indicated high concentrations of total bilirubin and cholesterol and high alkaline phosphatase and alanine transaminase activities. Exploratory abdominal surgery was performed in each dog. Each dog had a firm mass involving the body of the pancreas, with obstruction of the distal portion of the common bile duct, marked peripancreatic inflammation, and omental adhesions. Cholecystoduodenostomy, using an open mucosal appositional technique for biliary redirection, was performed in each dog. Clinically, results of surgery were good to excellent (ie, lack of postoperative icterus, anorexia, lethargy, or weight loss and absence or infrequency of vomiting). The mean postoperative evaluation period for the 6 dogs was 35 months (range, 20 to 48 months); 5 dogs were alive and healthy at the end of the study. Histologic examination of tissue specimens of the pancreatic mass indicated chronic active fibrosing pancreatitis in the 6 dogs.