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.     

Relationships between Low Serum Cobalamin Concentrations and Methlymalonic Acidemia in Cats

Background: Serum cobalamin concentrations below reference range are a common consequence of gastrointestinal disease in cats. Serum cobalamin ≤ 100 ng/L is associated with methylmalonic acidemia.
Objectives: To determine the prevalence of cobalamin deficiency, defined by elevated serum methylmalonic acid (MMA), in cats with serum cobalamin ≤ 290 ng/L, and the optimum serum cobalamin concentration to predict cobalamin deficiency in cats.
Sample Set: Residual serum samples (n = 206) from cats with serum cobalamin ≤ 290 ng/L.
Methods: Retrospective, observational study. Serum cobalamin and folate were measured with automated assays. Serum MMA was determined by gas chromatography-mass spectrometry. Cobalamin deficiency was defined as serum MMA > 867 nmol/L. Sensitivity and specificity of serum cobalamin concentrations ≤290 ng/L for detecting MMA > 867 nmol/L were analyzed using a receiver-operator characteristic curve.
Results: There was a negative correlation between serum cobalamin and MMA concentrations (Spearman's r =−0.74, P < 0.0001). The prevalence of MMA ≥ 867 nmol/L in cats with serum cobalamin ≤ 290 ng/L was 68.4%. Serum cobalamin ≤ 160 ng/L had a 74% sensitivity and 80% specificity for detecting MMA > 867 nmol/L. No significant difference in serum folate concentrations was detected between affected and unaffected cats.
Conclusions and Clinical Importance: Elevated MMA concentrations, suggesting cobalamin deficiency, are common in cats with serum cobalamin ≤ 290 ng/L. Cobalamin deficiency is clinically significant, and supplementation with parenteral cobalamin is recommended for cats with gastrointestinal disease and low serum cobalamin concentrations.     

Exocrine pancreatic insufficiency in the cat

While exocrine pancreatic insufficiency (EPI) is a well-documented functional disease of the pancreas in dogs, only a few reports characterize EPI in cats and no information is available on cats diagnosed with a function test from Europe. The present case series describes and discusses the clinicopathologic findings, diagnostics and therapy in 5 cats (18 months to 16 years) with EPI from Switzerland.     

Serum feline trypsin-like immunoreactivity in cats with exocrine pancreatic insufficiency

Exocrine pancreatic insufficiency is thought to occur rarely in cats. This assumption has been made based on the lack of a specific test for this disease in the cat. Clinical data from the 1st 20 cats with serum feline trypsin-like immunoreactivity (fTLI) concentrations < or = 8 microg/L are presented. In 17 of these 20 cats compelling evidence for a diagnosis of exocrine pancreatic insufficiency (EPI) was present and in the remaining 3 supportive evidence for a diagnosis of EPI was available. The conclusion was made that serum fTLI concentration is a specific test for EPI in the cat.     

Prognostic factors in canine exocrine pancreatic insufficiency: prolonged survival is likely if clinical remission is achieved

BACKGROUND: Response to therapy in canine exocrine pancreatic insufficiency (EPI) varies considerably, making it difficult to determine prognosis for individual patients. HYPOTHESIS: Response to initial treatment (RIT) and survival are affected by signalment, clinical variables, and therapeutic regimen employed. ANIMALS: Client-owned dogs diagnosed with EPI between 1990 and 2002 were included in this study. METHODS: The study comprised a retrospective, questionnaire-based review. RESULTS: One hundred seventy-eight completed questionnaires were returned. RIT was good in 60% of treated dogs, partial in 17%, and poor in 23%. On univariate analysis, dogs that received antibiotics (P = .037) or had high serum folate concentration (P = .037) had a poorer RIT. On multivariate analysis, there were no strong predictors of good RIT. Nineteen percent of treated dogs were euthanized within 1 year, but overall median survival time for treated dogs was 1919 days. No clear benefit of changing to a fat-restricted diet could be demonstrated, but marked hypocobalaminemia (< 100 ng/L) was associated with shorter survival (P = .012). Use of uncoated pancreatic enzyme supplements, antibacterials, or H2 antagonists was not associated with longer survival. Breed, sex, age at diagnosis ( < or = 4 years or > 4 years), and clinical signs at diagnosis also made no difference. CONCLUSIONS AND CLINICAL IMPORTANCE: Long-term prognosis in canine EPI is favorable for dogs that survive the initial treatment period. Although there are few predictors of good RIT or long-term survival, severe cobalamin deficiency is associated with shorter survival. Therefore, parenteral cobalamin supplementation should be considered when hypocobalaminemia is documented.     

Subnormal concentrations of serum cobalamin (vitamin B12) in cats with gastrointestinal disease

The present study sought to determine the spectrum of diseases associated with subnormal concentrations of serum cobalamin in cats undergoing investigation of suspected gastrointestinal problems. The solid-phase boil radioassay (RA) for cobalamin employed in the present study was immunologically specific, precise, and accurate, with a sensitivity of 15 pg/mL. The RA yielded results that strongly correlated with those obtained by bioassay (Spearmann rho = .805; P < .0001), although the absolute values were lower for the RA. Forty-nine of 80 serum samples submitted during the period of January 1996-January 1998 had cobalamin concentrations below the reference range for healthy cats (range 900-2,800 pg/mL; mean +/- SD, 1,775 +/- 535 pg/mL; n = 33). Cats with subnormal cobalamin concentrations (mean +/- SD; 384 +/- 272 pg/mL, range 3-883 pg/mL) were middle-aged or older and were presented for weight loss. diarrhea, vomiting, anorexia, and thickened intestines. Definitive diagnoses in 22 cats included inflammatory bowel disease (IBD), intestinal lymphoma, cholangiohepatitis or cholangits, and pancreatic inflammation. Serum concentrations of cobalamin were particularly low in cats with intestinal lymphoma, three-fifths of whom also had subnormal serum concentrations of folate (< 9 ng/mL). The simultaneous presence of disease in the intestines, pancreas, or hepatobiliary system in many cats made it difficult to determine the cause of subnormal cobalamin concentrations. The circulating half-life of parenteral cyanocobalamin was shorter in 2 cats with IBD (5 days) than in 4 healthy cats (12.75 days). The presence of subnormal serum concentrations of cobalamin in 49 of 80 cats evaluated suggests that the measurement of serum cobalamin may be a useful indirect indicator of enteric or pancreatic disease in cats. The rapid depletion of circulating cobalamin in cats suggests that cats may be highly susceptible to cobalamin deficiency. However, the relationship of subnormal serum cobalamin concentrations to cobalamin deficiency and the effect of cobalamin deficiency on cats remain to be determined.     

Early biochemical and clinical responses to cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia

Domestic cats with small intestinal disease may develop cobalamin deficiency because of reduced small intestinal uptake of this vitamin. This study assessed the impact of cobalamin deficiency on biochemical and clinical findings in cats with intestinal disease. Nineteen pet cats, all with severe hypocobalaminemia (< or =100 ng/L) and histories of gastrointestinal signs, were studied. Cats received cobalamin, 250 microg SC once weekly, for 4 weeks. Biochemical indices of cobalamin availability (e.g., serum methylmalonic acid, homocysteine, and cysteine concentrations), serum feline trypsinlike immunoreactivity (fTLI) and serum folate concentrations, and clinical findings were recorded at the start of the study and after 4 weeks of cobalamin therapy. Serum methylmalonic acid (MMA) concentrations (median; range) decreased after cobalamin supplementation (5373.0; 708.5-29,329.0 versus 423.5; 214.0-7219.0 nmol/L, P < .0001). Serum homocysteine concentrations were not significantly altered (mean +/- SD 8.2 +/- 2.9 versus 10.3 +/- 4.5 micromol/L, P = .1198), whereas cysteine concentrations increased significantly (122.3 +/- 38.8 versus 191.5 +/- 29.4 micromol/L, P < .0001). Mean body weight increased significantly after cobalamin therapy (3.8 +/- 1.1 versus 4.1 +/- 1 kg, P < .01), and the average body weight gain was 8.2%. Significant linear relationships were observed between alterations in serum MMA and fTLI concentrations and the percentage body weight change (P < .05 for both, Pearson r2 = 0.26 and 0.245, respectively). Mean serum folate concentration decreased significantly (mean +/- SD 19 +/- 5 microg/L versus 15.4 +/- 6.2 microg/L, P < .001). Reduced vomiting and diarrhea were observed in 7 of 9 and 5 of 13 cats, respectively. These results suggest that cobalamin supplementation in cats with small intestinal disease and severe hypocobalaminemia is associated with normalization of biochemical test results and improvements in clinical findings in most affected cats.     

Cobalamin, folate and inorganic phosphate abnormalities in ill cats

Hypocobalaminaemia in cats has previously been identified, but the incidence reported has varied, and the frequency of folate deficiency is unknown. The aims of this study were to evaluate the incidence of low cobalamin and folate levels in a population of cats that were suffering predominantly from diseases of the alimentary tract (including the liver and pancreas) and to ascertain whether severity of disease (as assessed by bodyweight and body condition score (BCS)) related to degree of deficiency. The study population comprised 103 cats, of which 16.5% had low cobalamin levels and 38.8% had low folate levels. A serendipitous finding was inorganic phosphate levels below the reference range in 48% of the cases. Significant associations were found between subnormal cobalamin levels and median BCS (P=0.049); combined low folate and low cobalamin and bodyweight (P=0.002), BCS (P=0.024) and inorganic phosphate levels (P=0.003). The finding of low levels of folate and cobalamin in clinical cases suggests that supplementation may be indicated more frequently than is currently recognised.     

Comparisons between cats with normal and increased fPLI concentrations in cats diagnosed with inflammatory bowel disease

Objectives : The aim of this study was to compare age, serum albumin and cobalamin concentrations, serum alanine amino transferase and alkaline phosphatase activities, feline inflammatory bowel disease clinical disease activity index, pancreatic ultrasound findings, intestinal histopathology scores, outcome, treatment and clinical response between cats diagnosed with inflammatory bowel disease with normal or increased serum feline pancreatic lipase immunoreactivity concentrations. Methods : Medical records for 23 cats diagnosed with inflammatory bowel disease and with serum feline pancreatic lipase immunoreactivity concentrations available were reviewed. Three groups were compared; cats with serum feline pancreatic lipase immunoreactivity concentrations 2·0 to 6·8 µg/l (group A), 6·9 to 11·9 µg/l (group B) and ≥12·0 µg/l (group C). Results : Sixteen of the 23 cats had increased serum feline pancreatic lipase immunoreactivity concentrations; 9 cats in group B and 7 cats in group C. The remaining seven cats were in group A. Cats with serum feline pancreatic lipase immunoreactivity concentrations ≥12·0 µg/l had significantly lower median serum albumin and cobalamin concentrations. No significant differences were identified between the three groups for age, serum alanine amino transferase and alkaline phosphatase activities, feline inflammatory bowel disease clinical disease activity index, pancreatic ultrasound findings, intestinal histopathology scores, clinical outcome, treatment or clinical response. Clinical Significance : Hypoalbuminaemia and hypocobalaminaemia were more frequently observed in cats with serum feline pancreatic lipase immunoreactivity concentrations ≥12·0 µg/l.     

Diagnosis and management of malabsorption in dogs

Malabsorption can result from interference with either the degradation or absorption phases in the handling of dietary constituents and represents an important cause of weight loss and diarrhoea in dogs. Effective treatment depends on identification and understanding of the underlying disease which could affect the functional capacity of the exocrine pancreas or small intestine. Exocrine pancreatic insufficiency (EPI) can be identified by a low concentration of trypsin-like immunoreactivity in serum and results in serious malabsorption due to interference with degradation of carbohydrate, protein and fat. Treatment with oral pancreatic extract complemented by a low fat, high quality protein diet, is effective in many cases. Refractory cases may need additional treatment with an oral antibiotic for small intestinal bacterial overgrowth (SIBO), and H₂-receptor blockers to help prevent denaturation of the pancreatic extract by stomach acid. The pancreas plays a key role in the normal absorption of cobalamin (vitamin B₁₂) in dogs and malabsorption of cobalamin in EPI may not resolve with treatment so that cobalamin may need to be given parenterally. Small intestinal disease may result in interference with the number or functioning of individual enterocytes, in some cases accompanied by cellular infiltration of the mucosa. Diagnosis depends on indirect assessment of intestinal damage, for example by assay of serum vitamins and determination of intestinal absorption and permeability, and in selected cases followed by endoscopic examination, intestinal biopsy and culture of duodenal juice. Treatment depends on the disease and may include oral antibiotic for SIBO and immunosuppressive drugs for infiltrative disease. Dietary management is also important, for example with a restricted fat diet containing highly digestible carbohydrate and high quality protein, and when a dietary sensitivity is suspected a restriction diet of a selected protein source may be needed.     

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.     

Metabolism of amino acids in cats with severe cobalamin deficiency.

OBJECTIVE: To validate an automated chemiluminescent immunoassay for measuring serum cobalamin concentration in cats, to establish and validate gas chromatography-mass spectrometry techniques for use in quantification of methylmalonic acid, homocysteine, cysteine, cystathionine, and methionine in sera from cats, and to investigate serum concentrations of methylmalonic acid, methionine, homocysteine, cystathionine, and cysteine as indicators of biochemical abnormalities accompanying severe cobalamin (vitamin B12) deficiency in cats. SAMPLE POPULATION: Serum samples of 40 cats with severe cobalamin deficiency (serum cobalamin concentration < 100 ng/L) and 24 control cats with serum cobalamin concentration within the reference range. PROCEDURE: Serum concentrations of cobalamin were measured, using a commercial automated chemiluminescent immunoassay. Serum concentrations of methylmalonic acid, methionine, homocysteine, cystathionine, and cysteine were measured, using gas chromatography-mass spectrometry, selected ion monitoring, stable-isotope dilution assays. RESULTS: Cats with cobalamin deficiency had significant increases in mean serum concentrations bf methylmalonic acid (9,607 nmol/L), compared with healthy cats (448 nmol/L). Affected cats also had substantial disturbances in amino acid metabolism, compared with healthy cats, with significantly increased serum concentrations of methionine (133.8 vs 101.1 micromol/L) and significantly decreased serum concentrations of cystathionine (449.6 vs 573.2 nmol/L) and cysteine (142.3 vs 163.9 micromol/L). There was not a significant difference in serum concentrations of homocysteine between the 2 groups. CONCLUSIONS AND CLINICAL RELEVANCE: Cats with gastrointestinal tract disease may have abnormalities in amino acid metabolism consistent with cobalamin deficiency. Parenteral administration of cobalamin may be necessary to correct these biochemical abnormalities.     

Effect of exocrine pancreatic insufficiency on cobalamin absorption in dogs

The possibility that the canine pancreas might have an important role in the physiologic absorption of cobalamin (vitamin B12) has been explored by determining the effect of exocrine pancreatic insufficiency on cobalamin absorption and by examining the subsequent influence of bovine pancreatic enzymes and canine pancreatic juice. Exocrine pancreatic insufficiency was induced by ligation of pancreatic ducts and confirmed by indirect assessment of exocrine pancreatic function. Cobalamin absorption was determined by oral administration of cyano[58Co]cobalamin and quantitation of radioactivity in blood, urine, and feces during 48 hours. Pancreatic duct ligation resulted in a significant (P less than 0.001) decrease in cobalamin absorption, which was not restored by oral administration of bovine pancreatic enzymes, despite considerable improvements in steatorrhea and in vivo proteolytic activities. In marked contrast, malabsorption of cobalamin was significantly (P less than 0.05) reversed by oral administration of canine pancreatic juice. These results indicate that pancreatic secretions have an important role in the normal absorption of cobalamin in the dog, a role that does not appear to be attributable to pancreatic enzymes, but is consistent with the existence of a pancreatic intrinsic factor in this species.     

Fat malassimilation in three cats

Three cats were thin despite eating well. Steatorrhoea was confirmed in each by 72-hour fat assimilation tests. Fat digestibility in all 3 increased twofold when the diet was supplemented with pancreatic enzymes, suggesting the possibility of exocrine pancreatic insufficiency. However, examination of stained faecal smears gave evidence of both maldigestion and malabsorption of fat, without maldigestion of starch, and only one case had indications of protein maldigestion. In the latter cat, fat digestibility normalised with pancreatic enzyme supplementation and exocrine pancreatic insufficiency was considered likely. However, at post-mortem examination enteropathy and pancreatitis, but not exocrine pancreatic insufficiency, were found. The cause of fat malassimilation in these cats was unknown. The evaluation of malassimilation in cats is difficult because investigative tests used in other species are either unsuitable or have not been evaluated in cats.     

Hypocobalaminaemia is uncommon in cats in the United Kingdom

Recent work has highlighted the importance of cobalamin deficiency in cats with a range of alimentary tract diseases. The primary aim of our study was to determine the incidence of subnormal cobalamin concentrations in sick cats with and without alimentary system disorders. Firstly, serum cobalamin concentrations were measured in a population of cats, with and without gastrointestinal (GI) disease, evaluated at a referral hospital. In the second part of the study, the incidence of cobalamin deficiency was assessed in samples submitted to a commercial laboratory specifically for cobalamin measurement. For both studies, a validated radioimmunoassay was used to measure serum cobalamin concentrations (reference range: > 150 pg/ml). In the first part of the study, 132 cats were included and none of these cats had subnormal cobalamin concentrations (median=1,172; range: 278 to >2,000). There were no differences in cobalamin concentrations between cats with alimentary system disorders, and those with diseases of other organs. In the second part, 682 samples were submitted for cobalamin assay over a period of 3 years, and only one cat had a result below the reference range (median=794; range: 147 to >2,000). Cobalamin deficiency was rare in the population tested and this may suggest that the incidence of this biochemical abnormality is less common than reported in the USA.     

Exocrine pancreatic insufficiency as an end stage of pancreatitis in four dogs

Chronic pancreatitis is a common cause of exocrine pancreatic insufficiency (EPI) in humans and cats but is rarely recognised in dogs in which pancreatic acinar atrophy (PAA) is reportedly more common. This paper describes four dogs which developed EPI secondary to pancreatitis. Two of the dogs also had diabetes mellitus which developed before EPI. One diabetic dog had concurrent hyperadrenocorticism and was euthanased five months after presentation; the other diabetic dog died 48 months after diagnosis. The remaining dogs were alive 78 and 57 months after diagnosis. The number of affected dogs was comparable to the number of cases of presumed PAA seen over the same time period in the same institution. Chronic pancreatitis may be a more common cause of EPI in dogs than previously assumed and may be under-recognised because of difficulties in diagnosis. The relative importance of chronic pancreatitis as a cause of canine diabetes mellitus remains to be ascertained.     

Serum cobalamin concentrations in healthy cats and cats with non-alimentary tract illness in Australia

Objective   To determine a reference range for serum cobalamin concentration in healthy cats in Australia using a chemiluminescent enzyme immunoassay and to prospectively investigate the prevalence of hypocobalaminaemia in cats with non-alimentary tract disease.
Design   Prospective study measuring serum cobalamin concentrations in clinically healthy cats and cats with non-alimentary tract illness.
Procedure   Blood was collected from 50 clinically healthy cats that were owned by staff and associates of Veterinary Specialist Services or were owned animals presented to Creek Road Cat Clinic for routine vaccination. Blood was collected from 47 cats with non-alimentary tract illness presented at either clinic. Serum cobalamin concentration was determined for each group using a chemiluminescent enzyme immunoassay.
Results   A reference range for Australian cats calculated using the central 95th percentile in the 50 clinically healthy cats was 345 to 3668 pg/mL. Median serum cobalamin concentration in 47 cats with non-alimentary tract illness (1186 pg/mL; range 117–3480) was not significantly different to the median serum cobalamin of the 50 healthy cats (1213 pg/mL, range 311–3688). Using the calculated reference range one sick cat with non-alimentary tract illness had a markedly low serum cobalamin concentration.
Conclusion   Although hypocobalaminaemia is uncommon in sick cats with non-alimentary tract illness in Australia, its occurrence in this study warrants further investigation.     

The prevalence of hypocobalaminaemia in cats with spontaneous hyperthyroidism

Objectives : To determine the prevalence of hypocobalaminaemia in cats with moderate to severe hyperthyroidism and to investigate the relationship between cobalamin status and selected haematologic parameters. Methods : Serum cobalamin concentrations were measured in 76 spontaneously hyperthyroid cats [serum thyroxine (T₄) concentration ≥100 nmol/L] and 100 geriatric euthyroid cats. Erythrocyte and neutrophil counts in hyperthyroid cats with hypocobalaminaemia were compared with those in hyperthyroid cats with adequate serum cobalamin concentrations (≥290 ng/L). Results : The median cobalamin concentration in hyperthyroid cats was lower than the control group (409 versus 672 ng/L; P=0·0040). In addition, 40·8% of hyperthyroid cats had subnormal serum cobalamin concentrations compared with 25% of controls (P=0·0336). Weak negative correlation (coefficient: –0·3281) was demonstrated between serum cobalamin and T₄ concentrations in the hyperthyroid population, and the median cobalamin concentration was lower in cats with T₄ above the median of 153 nmol/L compared with cats with T₄ below this value (P=0·0281). Hypocobalaminaemia was not associated with neutropenia or anaemia in hyperthyroid cats. Clinical Significance : This study indicates that a substantial proportion of cats with T₄≥100 nmol/L are hypocobalaminaemic and suggests that hyperthyroidism directly or indirectly affects cobalamin uptake, excretion or utilisation in this species.     

Exocrine Pancreatic Insufficiency in the Dog: Historical Background,Diagnosis, and Treatment

This overview summarizes research performed during the last decades that has had an impact on the diagnosis and management of exocrine pancreatic insufficiency (EPI) in dogs. Pancreatic acinar atrophy is by far the most common cause for the maldigestion signs of canine EPI. The ability to diagnose pancreatic acinar atrophy 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. Diagnosis of exocrine pancreatic dysfunction is based on typical findings in clinical histories and clinical signs and is confirmed with pancreatic function tests. In recent years, the measurement of serum canine trypsin-like immunoreactivity has become the most commonly used pancreatic function test to diagnose canine EPI. Serum trypsin-like immunoreactivity measurement is species- and pancreas-specific. When clinical maldigestion signs of EPI appear, enzyme replacement therapy is indicated. Despite accurate enzyme supplementation, only a small portion of orally administered enzymes are delivered functionally intact into the small intestine. In dogs, the highest enzyme activity in the duodenum has been obtained with nonenteric-coated supplements: raw chopped pancreas or powdered enzymes. Aside from dietary enzyme supplements, dietary changes are often made to improve clinical response, but sometimes weight gain and stool quality remain suboptimal. Other medications for treatment of gastrointestinal tract signs are often used in such dogs with EPI. Antibiotics are the most common adjunctive medication. Of the antibiotics administered, tylosin is used in Finland almost exclusively.     

Laboratory tests for diagnosis of gastrointestinal and pancreatic diseases

The panel of laboratory tests available for diagnosis of gastrointestinal (GI) diseases in dogs and cats is wide, and, recently, several new tests have been developed. This article will focus on advances in laboratory tests that are available for the general practitioner for diagnosis of GI diseases. Laboratory tests for diagnosis of gastric and intestinal infectious diseases include fecal parasite screening tests, enzyme-linked immunosorbent assays for parvoviral enteritis, and some specific bacterial tests like fluorescent in situ hybridization for identification of specific bacteria attached to the intestinal epithelial cells. Serum concentrations of folate and cobalamin are markers of intestinal absorption, but are also changed in exocrine pancreatic insufficiency and intestinal bacterial overgrowth. Hypocobalaminemia is common in GI and pancreatic disease. Decreased serum trypsin-like immunoreactivity is a very sensitive and specific test for the diagnosis of exocrine pancreatic insufficiency in dogs and cats. Serum pancreatic lipase is currently the most sensitive and specific test to identify pancreatic cell damage and acute pancreatitis. However, serum canine pancreas-specific lipase is less sensitive in canine chronic pancreatitis. Increased serum trypsin-like immunoreactivity is also specific for pancreatic damage but is less sensitive. It is very likely that further studies will help to better specify the role of these new tests in the diagnosis of canine and feline pancreatic diseases.