Relationships between diet and malabsorption in dogs

Abnormalities affecting the pancreas or small intestine can result in malabsorption and diarrhoea by interfering with either the degradative or absorptive phases in the handling of one or more nutrients. Diet may be involved in the pathogenesis of certain disorders and can also influence the nature and severity of the clinical manifestations of gastrointestinal disease. Exocrine pancreatic insufficiency can have serious nutritional consequences as the pancreas plays a crucial role in the degradation of the main dietary constituents. Whereas gastrointestinal peptidases help compensate for pancreatic protease deficiencies, malabsorption of carbohydrate and fat occurs and can result in osmotic and secretory diarrhoea, respectively. Small intestinal disease can result in malabsorption by interference with either the number or functioning of individual enterocytes. Diarrhoea may be due to stimulated secretion and diminished absorption of fluid and electrolytes, and also to the osmotic effects of small molecules, particularly carbohydrates, that remain in the lumen. Specific therapy depends on the disease. Dietary management is also important, for example with a restricted fat diet containing highly digestible carbohydrate and a high quality protein source. Where a specific dietary sensitivity is suspected, such as gluten-enteropathy, a hypoallergenic diet may prove particularly valuable.     

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.     

Intestinal permeability and function in dogs with small intestinal bacterial overgrowth

Small intestinal bacterial overgrowth (SIBO) has been reported to occur commonly in dogs with signs of chronic intestinal disease. There are usually few intestinal histological changes, and it is uncertain to what extent bacteria cause mucosal damage. The aim of this study was to apply a differential sugar absorption test for intestinal permeability and function to the objective assessment of intestinal damage in dogs with SIBO. Studies were performed on 63 dogs with signs of chronic small and, or, large bowel disease, in which SIBO (greater than 10⁵ total or greater than 10⁴ anaerobic colony forming units/ml) was diagnosed by quantitative culture of duodenal juice obtained endoscopically. None of the dogs had evidence of intestinal pathogens, parasites, systemic disease or pancreatic insufficiency. Differential sugar absorption was performed by determining the ratios of urinary recoveries of lactulose/rhamnose (L/R ratio, which reflects permeability) and D-xylose/3-O-methylglucose (X/G ratio, which reflects intestinal absorptive function) following oral administration. Dogs with SIBO comprised 28 different breeds, including 18 German shepherd dogs. SIBO was aerobic in 18/63 dogs (29 per cent), and anaerobic in 45/63 (71 per cent). Histological examination of duode-nal biopsies showed no abnormalities in 75 per cent, and mild to moderate lymphocytic infiltrates in 25 per cent of the dogs. The L/R ratio was increased (greater than 0–12) in 52 per cent, and the X/G ratio reduced (less than 0–60) in 33 per cent of the dogs. Differential sugar absorption was repeated in 11 dogs after their four weeks of oral antibiotic therapy. The L/R ratio declined in all 11 dogs (mean ± SD pre: 0–24 ± 0–14; post: 0–16 ± 0–11; P<0–05), but changes in the X/G ratio were more variable. These findings show that SIBO is commonly associated with mucosal damage, not detected on histological examination of intestinal biopsies, and that changes in intestinal permeability following oral antibiotics may be used to monitor response to treatment.     

Experiments to optimize enzyme substitution therapy in pancreatic duct-ligated pigs

Ligation of the pancreatic duct in pigs leads to severe maldigestion and malabsorption of crude nutrients. Supplementation with 24 capsules of Creon (Solvay Pharmaceuticals GmbH, Hannover, Germany) per meal led to an increased digestibility of crude nutrients. With regard to optimization of the treatment of EPI no essential improvements can be achieved by adding omeprazol or lecithin to the diet. In pancreatic duct-ligated pigs the isolated addition of omeprazol led to an increase of the pre-caecal digestibility of crude fat and organic matter. With additional enzyme substitution, the application of omeprazol did not result in an improved fat digestibility. Isolated addition of lecithin to the diet resulted in a reduced total digestibility of crude fat. Offering the diet twice a day and using a higher frequency of enzyme applications (four or six instead of only two applications) had no effects on the digestibilty of crude fat or organic matter. According to the observations in pancreatic duct-ligated pigs, the addition of missing enzymes to the diet led to the best treatment results in EPI. Administration of omeprazol or a higher feeding frequency as well as the application of enzymes in small proportion of the whole meal or dosages given consecutively over the day showed no advantages. Furthermore, the present study suggests that the addition of lecithin cannot be recommended in EPI, when given diets with butter as the predominant fat source as in human dietetics.     

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.     

Exocrine Pancreatic Insufficiency in the Cat

Exocrine pancreatic insufficiency (EPI) is a syndrome caused by an insufficient amount of pancreatic digestive enzymes in the small intestine. Clinical signs most commonly reported in cats with EPI are weight loss, loose and voluminous stools, steatorrhea, polyphagia, and in some cases a greasy soiling of the hair coat in the perianal region. Serum feline trypsin-like immunoreactivity concentration is the diagnostic test of choice for the diagnosis of affected cats. Treatment of cats with EPI consists of enzyme supplementation with either a powdered pancreatic extract or raw pancreas. Most cats with EPI also have severely decreased serum cobalamin concentrations and may require lifelong parenteral cobalamin supplementation. Most cats respond well to therapy and can have a normal life expectancy and quality of life.     

Serum cobalamin, urine methylmalonic acid, and plasma total homocysteine concentrations in Border Collies and dogs of other breeds

Objective-To determine reference ranges for serum cobalamin (Cbl), urine methylmalonic acid (uMMA), and plasma total homocysteine (tHcys) concentrations and to compare values for healthy control dogs with values for Border Collies (BCs), a breed in which hereditary cobalamin deficiency has been identified. Animals-113 BCs, 35 healthy control dogs fed a typical diet, and 12 healthy dogs fed a bone and raw food diet exclusively. Procedures-Urine and blood samples were obtained from each dog and Cbl, uMMA, and tHcys concentrations were determined. Results-Reference ranges for Cbl (261 to 1,001 ng/L), uMMA (0 to 4.2 mmol/mol of creatinine), and tHcys (4.3 to 18.4 μmol/L) concentrations were determined. Four BCs had a Cbl concentration lower than the assay detection limit (150 ng/L); median uMMA and tHcys concentrations in these dogs were 4,064 mmol/mol of creatinine and 51.5 μmol/L, respectively. Clinical abnormalities included stunted growth, lethargy, anemia, and proteinuria. Abnormalities improved after administration of cobalamin. Of the 109 healthy BCs with Cbl and tHcys concentrations within reference ranges, 41 (37.6%) had a high uMMA concentration (range, 5 to 360 mmol/mol). Results for dogs fed raw food were similar to those for control dogs. Conclusions and Clinical Relevance-Hereditary cobalamin deficiency is a rare disease with various clinical signs. The finding of methylmalonic aciduria in healthy eucobalaminemic BCs and BCs with clinical signs of Cbl deficiency was surprising and indicated these dogs may have defects in intracellular processing of Cbl or intestinal Cbl malabsorption, respectively. Studies investigating Cbl absorption and metabolic pathways are warranted.     

Determination of fecal fat and trypsin output in the evaluation of chronic canine diarrhea.

Quantitative fat and trypsin analysis was done on the feces of dogs with chronic diarrhea. The results of clinical examination, quantitative fecal analysis, and other laboratory tests permitted assignment of the dogs into one of 4 groups: (1)pancreatic exocrine insufficiency,(2)small intestinal malabsorption,(3)colitis, and(4)other nonspecific or incompletely diagnosed diarrhea. The mean 24-hour fat output was significantly higher (p less than 0.01) in dogs with malabsorption or pancreatic insufficiency than in clinically normal dogs, dogs with colitis, or dogs with nonsteatorrheic diarrheas. The mean 24-hour trypsin output with pancreatic insufficiency was significantly (P less than 0.01) lower, and in dogs with malabsorption, significantly (P less than 0.05) higher than in clinically normal dogs. Normalization of the output data for body weight enhanced the value of fat and trypsin analyses in the differentiation of pancreatic insufficiency and intestinal malabsorption from other causes of chronic canine diarrhea.     

Use of pulmonary hydrogen gas excretion to detect carbohydrate malabsorption in dogs

Pulmonary H2 excretion was measured in 10 healthy dogs, in 6 dogs with pancreatic exocrine insufficiency, and in 6 dogs with chronic small intestinal disease. Concentration of expired H2 in fasted healthy dogs was 0.9 +/- 0.1 ppm (mean +/- SEM) and peak H2 concentration of 1.4 +/- 0.2 ppm was detected up to 8 hours after feeding. Dogs with pancreatic exocrine insufficiency had fasting expired H2 concentrations of 3.3 +/- 0.9 ppm, which increased to a mean peak H2 concentration of 28.8 +/- 2.0 ppm 6.5 hours after feeding. Following xylose administration, expired H2 concentrations increased from fasting concentrations of 3.6 +/- 0.9 ppm to peak at 19.0 +/- 2.0 ppm in 1.5 hours. Blood xylose concentrations were diagnostic for carbohydrate malabsorption in 4 of 6 dogs with pancreatic exocrine insufficiency. Plasma p-aminobenzoic acid concentration identified bentiromide maldigestion in all dogs with pancreatic exocrine insufficiency. In 3 pancreatic exocrine insufficient dogs tested, pancreatic enzyme replacement therapy partially corrected carbohydrate malabsorption. Fasting expired H2 concentration was 5.3 +/- 1.3 ppm in dogs with chronic small intestinal disease and increased to a peak H2 of 72.2 +/- 18.0 ppm 7 hours after feeding. Following administration of xylose to dogs with chronic small intestinal disease, fasting expired H2 concentration increased from 3.0 +/- 1.0 ppm to a peak of 35.5 +/- 7.2 ppm at 2 hours. Blood xylose concentration was abnormal in only 2 of 6 dogs with chronic small intestinal disease. Results of these studies indicate that expired H2 analysis can identify carbohydrate malabsorption in dogs with pancreatic exocrine insufficiency or chronic small intestinal disease, and that pulmonary H2 testing is more sensitive than xylose absorption testing for the identification of carbohydrate malabsorption.     

Transient glucose malabsorption in two horses fact or artefact?

Two horses, presented for investigation of chronic weight loss despite normal to increased feed intake, had flat oral glucose absorption curves, suggesting malabsorption. The cause of the apparent malabsorption was not evident grossly or on light microscopic examination of the intestinal tract. Both horses survived long term and at follow-up examination had regained weight and their capacity to absorb glucose. These cases illustrate that flat glucose absorption curves may occur in horses with no obvious intestinal lesions, that they may revert to normal and that the results of these tests should be interpreted with caution.     

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.     

Effect of intestinal inflammation on fecal elastase concentration in dogs

BACKGROUND: A commercially available ELISA kit for fecal elastase measurement can be used in the diagnosis of exocrine pancreatic insufficiency (EPI) in dogs. However, other causes of diarrhea also may affect fecal elastase concentration. OBJECTIVE: This study was undertaken to determine whether intestinal inflammation alters fecal elastase concentration in dogs. METHODS: Fecal elastase concentration was measured with an ELISA kit in the following groups of dogs: group 1 (n=16), control dogs, without gastrointestinal disease; group 2 (n=14), dogs with diarrhea and no histopathologic evidence of intestinal inflammation; and group 3 (n=12), dogs with diarrhea and histopathologic evidence of intestinal inflammation. Serum trypsin-like immunoreactivity (TLI) was determined in dogs with diarrhea to rule out EPI. RESULTS: All dogs in groups 2 and 3 had serum TLI concentrations >5 microg/L, ruling out EPI. No statistically significant difference was found in fecal elastase concentration among the 3 groups of dogs (P=.969). CONCLUSIONS: The results indicate that intestinal inflammation does not affect fecal elastase concentration, such that test results may be used to exclude a diagnosis of EPI even in animals with inflammatory bowel disease.     

Comparison of direct and indirect tests for small intestinal bacterial overgrowth and antibiotic-responsive diarrhea in dogs

Controversy exists over the diagnosis of idiopathic small intestinal bacterial overgrowth (SIBO) in dogs and some clinicians use the term antibiotic-responsive diarrhea (ARD) in preference. However, whether such terms are interchangeable is not clear. To examine the relationship between duodenal bacterial numbers and a clinical response to antibiotics, SIBO and ARD were defined by nonoverlapping criteria. Quantitative duodenal juice bacteriology and indirect serum biochemical tests were used to assess small intestinal bacterial populations in 30 dogs with gastrointestinal disorders, including 9 with ARD. Serum total unconjugated bile acid (TUBA) concentrations were measured in all dogs, serum folate and cobalamin concentrations were measured in 29 of 30 dogs, and quantitative culture of duodenal juice was performed in 22 of 30 dogs. Serum TUBA concentrations also were measured in samples from 38 control dogs. Twenty of 22 affected (clinical) dogs in which quantitative bacteriology was performed were classified as having SIBO (>10(5) colony-forming units of total bacteria per milliliter of duodenal juice), but bacterial numbers did not differ significantly between dogs with ARD and dogs with other disorders. Increased folate (19/29), decreased cobalamin (16/ 29), or a combination (9/29) were common, but increased TUBA concentrations were documented in only 5 of 30 clinical dogs. Again, no significant differences were observed between dogs with ARD and those with other disorders, and a similar proportion (5/38) of controls had abnormally high TUBA concentrations. Finally, no significant differences were noted when duodenal bacteriology and TUBA concentrations were assessed before and during antibiotic therapy. These results question the utility of quantitative duodenal juice bacteriology and indirect biochemical marker tests for SIBO in the investigation of canine gastrointestinal disorders.     

Failure to thrive and life-threatening complications due to inherited selective cobalamin malabsorption effectively managed in a juvenile Australian shepherd dog

A juvenile Australian shepherd dog exhibited failure to grow, inappetence, weakness, nonregenerative anemia, neutropenia, and cobalamin deficiency. DNA testing confirmed homozygosity of an amnionless mutation (AMN c.3G > A). Clinical signs resolved with supportive care and parenteral cobalamin supplementation. Inherited selective intestinal cobalamin malabsorption requiring lifelong parenteral supplementation should be considered in Australian shepherds, giant schnauzers, border collies, and beagles that fail to thrive.     

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.     

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.     

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.     

Intestinal permeability testing in dogs with diet-responsive intestinal disease

Fifteen dogs with signs of small and, or, large bowel disease that responded clinically to an exclusion diet were studied, using differential sugar absorption as an objective parameter of the mucosal response to the diet. Intestinal permeability and function were assessed by determining the urinary excretion ratios of lactulose/rhamnose and xylose/3-O-methylglucose, respectively, following oral administration of a mixture of these four sugars. Five dogs, all retrievers, were tentatively diagnosed as having dietary hypersensitivity, based upon resolution of clinical signs and normalisation of high intestinal permeability following an exclusion diet and recurrence of signs (in four of five dogs) upon challenge with the original diet. The fifth dog did not become symptomatic when challenged, but intestinal permeability increased. The remaining 10 dogs were diagnosed as having food intolerance, based upon clinical improvement on an exclusion diet, relapse on challenge with their original diet, but lack of improvement in intestinal permeability. These findings suggest that a differential sugar absorption test may be useful to determine the reasons for clinical response to exclusion diets. Demonstration of increased intestinal permeability with subsequent normalization following an exclusion diet may be useful in the diagnosis of dietary hypersensitivity, while persistent abnormalities in intestinal permeability are suggestive of underlying intestinal disease and food intolerance.     

Weight loss in cats which eat well

Four cats were investigated because they lost weight while eating well. One cat was found to have hypoinsulinaemic diabetes mellitus, and another had maldigestion caused by exocrine pancreatic atrophy. An enteropathy with presumed intestinal malabsorption was diagnosed in the third case. The fourth cat had hyperthyroidism and disseminated amyloidosis. The diabetic animal has been maintained satisfactorily on daily insulin injections for 2 ½ years, but treatment in the other three cases was either unsuccessful or not attempted. Weight loss is uncommon in cats which are eating well. In investigating this syndrome, it is suggested that initially urine should be tested for glucose and faeces examined for maldigestion or malabsorption. More specific tests for diabetes mellitus, pancreatic maldigestion, intestinal malabsorption or hyperthyroidism might then be indicated.     

Long term management of canine exocrine pancreatic insufficiency

Twenty dogs with exocrine pancreatic insufficiency (EPI) were managed for an initial four-month period on a low fat diet in conjunction with a non-enteric coated enzyme replacer. At the end of this initial period the clinical signs had been reversed in all the dogs and their body-weights had increased by an average of 24 per cent. Owners were subsequently encouraged to determine the most cost effective form of management; progress was followed up for between five and 39 months. Contact was maintained with 17 of the dogs of which 11 were progressing well (three had been euthanased because of unsatisfactory progress and three for unrelated reasons]. A range of dietary regimens were being implemented and in all cases the requirement for a daily enzyme replacer was less; in terms of absolute enzyme activity, between six and 58 per cent of the original requirement was being used at the follow-up. The low fat diet proved effective in the initial stabilisation of the dogs and was invaluable in their long term management.