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8/9/2015 Malabsorption Syndromes in Small Animals: Diseases of the Stomach and Intestines in Small Animals: Merck Veterinary Manual

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Malabsorption Syndromes in Small Animals

Malabsorption is the defective uptake of a dietary constituent resultingfrom interference with its digestion or absorption, due to eitherexocrine pancreatic insufficiency (EPI) or smallintestinal disease.Malabsorption typically results in diarrhea, altered appetite, and weightloss, but a number of animals (especially cats) will not have overtdiarrhea because of the ability of the colon to conserve water.

The primary function of the small intestine is digestion and absorptionof nutrients, and it occurs in sequential phases: intraluminal digestion,mucosal digestion and absorption, and delivery of nutrients to thebody. Many chronic, smallintestinal diseases cause malabsorption byinterfering with one or several of these processes. Malabsorptivesyndromes have been studied in most detail in dogs, but basicdiagnostic and therapeutic principles are relevant to other species.

PhysiologyThe normal digestive processes convert polymeric dietary nutrients

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into forms (mainly monomers) that can cross the luminal surface(brush border) of intestinal absorptive epithelial cells (ie, enterocytes).Most digestive enzymes are secreted by the pancreas; EPI is thus amajor cause of malabsorption. Terminal digestion before absorption isperformed by brush border enzymes, either at the brush bordersurface of the enterocyte in association with transport proteins for thespecific products, or when released into the intestinal lumen throughcleavage by pancreatic peptidases or through loss of senescententerocytes.

The main dietary carbohydrates are starch, glycogen, sucrose, andlactose. Starch and glycogen are first hydrolyzed by pancreaticamylase to the oligosaccharides maltose, maltotriose, and αlimitdextrins. These oligosaccharides and ingested disaccharides (sucrose,lactose) are further hydrolyzed to monosaccharides by enzymeslocated on the brush border of the enterocytes. Brush border lactaseactivity declines after weaning, especially in cats, and animals maybecome lactose intolerant, especially if the brush border has beendamaged by another disease. The final products of mucosal hydrolysis(glucose, galactose, and fructose) are actively transported into theenterocyte by sodiumlinked carriermediated processes, driven by asodiumpotassium ATPase. Once in the cell, glucose is not used bythe glycolytic pathway but is passed by facilitated diffusion via atransport protein on the basolateral enterocyte membrane down aconcentration gradient into the extracellular space, and then bydiffusion into the portal venous circulation.

Protein digestion and absorption follow a similar pattern. Proteolyticenzymes from the stomach and pancreas degrade protein into a



mixture of shortchain oligopeptides, dipeptides, and amino acids.Oligopeptides are further hydrolyzed by brushborder peptidases todipeptides and amino acids that cross the brushborder membrane onspecific carrier proteins.

Fatsoluble molecules do not need specific carriers to cross thephospholipid barrier of the brush border. However, intraluminaldegradation of large lipids is essential. Fat in the duodenum stimulatesrelease of cholecystokinin, which, in turn, stimulates secretion ofpancreatic lipase. After solubilization by bile salt micelles, triglyceridesare digested by pancreatic lipase to monoglycerides and free fattyacids. At the enterocyte membrane, the monoglycerides and free fattyacids disaggregate from the micelle and are passively absorbed intothe cell. Released bile acids remain within the lumen and are ultimatelyreabsorbed by the ileum and undergo enterohepatic recycling. Onceinside the cell, the monoglycerides and free fatty acids are reesterifiedto triglycerides and incorporated into chylomicrons, whichsubsequently enter the central lacteal of the villus, being delivered tothe venous circulation via the thoracic duct. Mediumchain triglycerides(C8–C10) may be absorbed directly into the portal blood, providing analternative route for fat uptake in case of lymphatic obstruction, butsome do normally enter the circulation via the thoracic duct.Consequently, they are no longer recommended in management oflymphangiectasia.

Etiology and PathophysiologyMalabsorption is a consequence of interference with mechanismsresponsible for either the degradation or absorption of dietary



constituents (see Table 1: Mechanisms of Malabsorption ).

Mechanisms of MalabsorptionLocation Disease Mechanism

Luminal Exocrine pancreaticinsufficiency

Lack of pancreaticenzymes(maldigestion)

Luminal Antibioticresponsivediarrhea, secondarysmallintestinalbacterial overgrowth

Bacterial activity: bilesalt deconjugation, fattyacid hydroxylation,competition forcobalamin andnutrients

Mucosal Inflammatory boweldisease, infectiousenteropathies, dietarysensitivities, neoplasticinfiltration

Mucosal damage:inflammation, brushborder defects,disturbed enterocytefunction, reduction ofsurface area

Mucosal Villous atrophy Reduction in surfacearea, immatureenterocytes due toincreased cell turnover

Mucosal Brush border enzymedeficiencies

Lactase deficiency,diffuse smallintestinaldisease

Postmucosal Lymphangiectasia Lymphatic obstructionimpairs delivery of

Table 1



chylomicrons

Postmucosal Vasculitis, portalhypertension

Impaired delivery

Diseases that disrupt the synthesis or secretion of digestive pancreaticenzymes cause maldigestion with subsequent malabsorption, so thatthe end result is the same. An important syndrome is EPI (see ExocrinePancreatic Insufficiency in Small Animals), which occurs if there is a loss of~85%–90% of exocrine pancreatic mass. EPI is characterized bysevere maldigestionmalabsorption of starch, protein, and mostnotably, fat. In dogs, EPI is most commonly due to acinar atrophy;chronic pancreatitis is less common and is seen in older animals, andpancreatic hypoplasia is a rare congenital cause. EPI in dogs is oftencomplicated by secondary antibioticresponsive diarrhea, which furtherdisrupts nutrient digestion and absorption. EPI is relatively uncommonin cats and is most frequently due to chronic pancreatitis.

Intraluminal effects of bacteria can also have important consequences.Bacterial deconjugation of bile salts interferes with micelle formation,which results in malabsorption of lipid. Deconjugated bile salts andhydroxy fatty acids exacerbate diarrhea by stimulating colonicsecretion. True smallintestinal bacterial overgrowth (SIBO) can besecondary to defective gastric acid secretion, interference with normalmotility or mechanical obstruction of the intestine, interference with thefunction of the ileocecal valve, and local immunodeficiency. In othercases, there is no evidence of overgrowth and no defined cause but alack of overt mucosal damage. However, a positive response toantibiotic therapy indicates that the malabsorption is related tobacteria, perhaps in how the innate immune system (tolllike receptors)

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respond to bacterial components. Originally called idiopathic SIBO, thissyndrome is better termed antibioticresponsive diarrhea (ARD).

Fat malabsorption may also be seen with a deficiency of intraluminalbile salts due to cholestatic liver disease, biliary obstruction, or ilealdisease resulting in defective absorption of conjugated bile salts.

Smallintestinal disease can cause malabsorption by reduction of thenumber or function of individual enterocytes. Diffuse diseases of themucosa can result in reduced activities of brush border enzymes,decreased carrierprotein function, decreased mucosal absorptivesurface area, and interference with final transport of nutrients into thecirculation. Weight loss may be compounded by reduced nutrientintake due to inappetence. In addition, malabsorbed nutrients exertstrong intraluminal osmotic effects that diminish intestinal and colonicabsorption of water and electrolytes, resulting in diarrhea. This may beexacerbated if mucosal damage is accompanied by intestinalinflammation, which can cause secretory and permeability diarrhea.

Potential causes of mucosal damage include idiopathic inflammatorybowel disease (IBD), enteric pathogens (eg, enteric viruses,pathogenic bacteria, Giardia, Histoplasma, Pythium), dietarysensitivity, ARD, and intestinal neoplasia (eg, lymphosarcoma).Histologic changes such as villous atrophy and infiltration withinflammatory cells indicate intestinal disease but do not identify theunderlying cause. For example, lymphocyticplasmacytic enteritis maybe a common response pattern of the intestinal mucosa to more thanone provocative agent, particularly microbial and dietary antigens.Definite associations with parasites, pathogenic bacteria, and dietarysensitivity have been demonstrated in dogs, but often the underlying



cause cannot be identified.

Mucosal damage may also occur without obvious changes under lightmicroscopy. This is typified by infection with enteropathogenicEscherichia coli (which specifically cause ultrastructural damage tomicrovilli in an attachingeffacing lesion) and by ARD in dogs, whichcan cause biochemical damage to the intestinal brush border,interfering with enterocyte function.

The main brush border enzyme deficiency reported is a relative lactasedeficiency, leading to milk intolerance in adult dogs and cats. Acquiredbrush border defects also may be seen in the course of generalizedsmallintestinal disease.

Postmucosal obstruction may be seen with lymphatic obstruction(especially lymphangiectasia) and vascular compromise (portalhypertension, vasculitis). Intestinal lymphangiectasia causes intestinalprotein loss as well as severe fat malabsorption.

Usually, in malabsorption a number of nutrients are affected andconsequently diarrhea occurs; malabsorption of a single ingredientwithout any GI signs is rare (eg, selective cobalamin malabsorption inGiant Schnauzers, Australian Shepherds, and Border Collies). Again, itshould be noted that the large absorptive capacity of the colon mayprevent overt diarrhea in some animals (especially cats) despitesignificant malabsorption and weight loss.

Clinical FindingsClinical signs of malabsorption are mainly the result of lack of nutrient



uptake and losses in the feces. The duration, severity, and primarycause determine the severity of signs, which typically include chronicdiarrhea, weight loss, and altered appetite (anorexia or polyphagia).The absence of diarrhea does not exclude the possibility of severe GIdisease. Weight loss may be substantial despite a ravenous appetite,sometimes characterized by coprophagia and pica. Typically, animalswith malabsorption are systemically well unless there is severeinflammation or neoplasia. Nonspecific signs may include dehydration,anemia, and ascites or edema in cases of hypoproteinemia. Thickenedbowel loops or enlarged mesenteric lymph nodes may be palpable,especially in cats.

DiagnosisChronic diarrhea and weight loss are nonspecific signs common to avariety of systemic and metabolic diseases, as well as malabsorption,although, typically, systemic diseases cause anorexia. A thoroughdiagnostic approach in dogs and cats with signs suggestive ofmalabsorption is therefore needed to help exclude association withpossible underlying systemic or metabolic disease. A precise diagnosisis also important to determine treatment and prognosis.

The history is particularly important, because it may suggest specificdietary intolerance, indiscretion, or sensitivity. Weight loss mayindicate malabsorption or proteinlosing enteropathy (PLE) but mayalso be due to anorexia, vomiting, or extraintestinal disease. Smalland largeintestinal diarrhea may be distinguished by a number offeatures (see Table 1: Differentiation of SmallIntestinal from LargeIntestinal Diarrhea ). This distinction is more helpful in dogs than incats, which rarely have exclusively largeintestinal disease. Suspected

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largeintestinal disease in dogs may be further evaluated bycolonoscopic biopsy of the large intestine. However, if signs of largeintestinal disease are accompanied by weight loss or large volumes offeces, then there is probably also concurrent smallintestinal disease.

A thorough physical examination should be performed. Abdominalpalpation is essential to identify abnormalities, and rectal examinationis required even when no largeintestinal disease is suspected, both toprovide a fecal sample and possibly to reveal previously unreportedmelena. In older cats, the thyroid should be palpated carefully andserum T4 assayed, because signs of hyperthyroidism can closelymimic those of malabsorption.

Initial evaluation should include a CBC, biochemical profile, urinalysis,fecal examination, abdominal ultrasonography and, when indicated byclinical signs or abnormal abdominal palpation, plain radiography.Hematologic correlates in smallintestinal diseases sometimes includeanemia of chronic blood loss (microcytic, hypochromic) or chronicinflammation (normocytic, normochromic); neutrophilia and/ormonocytosis associated with intestinal inflammation, infectiousenteropathies, or neoplasia; eosinophilia associated with parasitismand eosinophilic enteritis; and lymphopenia that may be associatedwith intestinal lymphangiectasia in dogs. Lymphocytosis in a dog withdiarrhea raises the suspicion of hypoadrenocorticism.

Biochemical tests and urinalysis help to exclude systemic diseasesthat cause chronic diarrhea, most notably hypoadrenocorticism,proteinlosing nephropathies, renal failure, and liver disease.Hypoproteinemia frequently is secondary to PLE and is seen more



commonly in dogs than cats. In most cases of PLE, serum albuminand globulin are both low, but a low albumin alone does not exclude it;inflammatory bowel disease (IBD) and neoplasia are rarely associatedwith hyperglobulinemia as well as hypoalbuminemia. Liver enzymes(ALT, AST) may be increased as a consequence of increasedintestinal permeability, allowing more antigens to reach the liver; insuch cases, a bile acid stimulation test as well as ultrasonographyshould be performed to exclude primary liver disease. However, in catsthere may be concurrent IBD and cholangitis. Hypocholesterolemiamay develop with fat malabsorption and is most notable inlymphangiectasia. Urinalysis is important to exclude renal causes ofhypoalbuminemia and/or renal disease. However, sometimes bothmay be seen together (eg, the familial PLE and nephropathy of Softcoated Wheaten Terriers). Hyperthyroidism in cats should be excludedby measuring serum T4 concentrations. Serologic tests for felineleukemia and feline immunodeficiency viruses should also beperformed, not only because both may be associated with secondary,chronic diarrhea but also because they are important prognosticfactors. Feline infectious peritonitis and toxoplasmosis have also beendescribed as occasional causes of chronic diarrhea in cats.

The presence of fat, undigested muscle fibers, or starch in feces mayprovide indirect evidence for malabsorption, but these are unreliable.Feces should be examined for parasites (especially hookworms andGiardia in dogs and Tritrichomonas and Giardia in cats) and potentiallypathogenic bacteria (including Salmonella and Campylobacter).Speciation of Campylobacter isolates by PCR allows distinction of thepathogenic C jejuni from the more common and probable commensalC upsaliensis. Pathogenic Escherichia coli are emerging as a



potentially important problem in dogs, but molecular techniques toidentify genes encoding pathogenicity determinants are required fordiagnosis. Giardia can be detected using serial zinc sulfate fecalflotations or a commercially available ELISA; the latter is easier toperform, and its sensitivity is better than fecal flotation performed byinexperienced personnel. Tritrichomonas typically causes colitis in catsrather than malabsorption and is best diagnosed by pouch culture orPCR. Detection of excessive leukocytes on fecal cytology may indicatechronic intestinal inflammation or the presence of enteric pathogens.Cytology of rectal scrapings may reveal Histoplasma organisms.

Abdominal radiography is more useful when vomiting is present orpalpable abnormalities are detected, but ultrasonography is animportant part of the investigation of most smallintestinal diseases. Itcan be used to measure intestinal wall thickness, layering, and luminaldiameter and to detect other intestinal lesions (eg, masses,intussusception), mesenteric lymphadenopathy (in neoplasia andinflammatory bowel disease), and abnormalities in other organs.Mucosal striations have been associated with lymphatic dilatation.

Once obvious dietary, systemic, parasitic, and infectious causes ofchronic smallintestinal diarrhea have been eliminated, the next step isdifferentiation of EPI from intestinal malabsorption; the diagnosis ofEPI is relatively straightforward, whereas that of smallintestinaldisease is more complex. Numerous tests have been used for dogsand cats with suspected EPI, but they are too inaccurate or impracticalto be recommended. Assay of serum trypsinlike immunoreactivity(TLI) is a highly sensitive and specific test and should be used fordiagnosis of EPI. This assay measures trypsinogen, some of which



normally leaks from the pancreas into the blood, thereby providing anindirect assessment of functional pancreatic tissue. In EPI, functionalexocrine tissue is severely depleted and serum TLI concentrations areextremely low, clearly distinguishing EPI from other causes ofmalabsorption. This test requires a fasted serum sample. Speciesspecific canine and feline TLI tests are available.

The diagnosis of smallintestinal disease is difficult because oflimitations of routine screening procedures, the need for biopsy, andfrequently the absence of diagnostic histologic changes. Bacteriologicculture of duodenal fluid obtained endoscopically or at laparotomy hasbeen used to confirm a diagnosis of ARD. However, the exact cutoffpoint at which smallintestinal bacterial numbers are consideredexcessive is a matter of debate, because numbers >105 total or >104

obligate anaerobic colonyforming units (CFU)/mL may be found inapparently clinically healthy dogs, depending on circumstances,including environment, diet, scavenging, and coprophagia.

The assay of serum folate and cobalamin (vitamin B12) concentrationscan be a helpful initial test in assessment of smallintestinal disease.Folate is absorbed primarily by the proximal small intestine (jejunum),whereas cobalamin is absorbed by the distal small intestine (ileum). Asa result, serum folate concentrations can be decreased in proximalsmallintestinal diseases, serum cobalamin concentrations can bedecreased in distal diseases, and both can be decreased in diffuseenteropathies. Other factors such as the severity, extent, and durationof a mucosal abnormality; dietary intake; and vitamin supplementationalso influence these concentrations. In addition, EPI can affect serumfolate and cobalamin concentrations, and changes in serum folate and



cobalamin concentrations are unreliable for the diagnosis of ARD andsecondary antibioticresponsive diarrhea. The validity of serum folateand cobalamin concentrations as markers of smallintestinal disease incats is less clear, but low serum cobalamin concentrations may befound with both smallintestinal disease and EPI. Hypocobalaminemiais particularly associated with IBD and alimentary lymphoma andresults in metabolic changes, including methylmalonic acidemia, thatcan lead to anorexia; low cobalamin concentrations are an indicationfor parenteral supplementation.

A further indirect approach to detect smallintestinal disease isassessment of intestinal function and permeability by oraladministration of test substances that are subsequently measured inblood or urine samples. Historically, the xylose absorption test wasused to assess intestinal function, but it was insensitive, especially incats, and is no longer used. Measurements of the differentialabsorption of Dxylose/3OmethylDglucose and of intestinalpermeability have not been shown to be clinically useful. Hydrogenbreath testing after oral administration of individual sugars wasconsidered a simple test to detect malabsorption and to assess transittime, but it has also fallen out of favor. Attempts to diagnose ARD bybreath hydrogen or measurement of serum unconjugated bile acidswere unreliable, because bacterial numbers may not actually beincreased in ARD.

IV administration of 51Crlabeled albumin (or 51CrCl3 to labelendogenous albumin) has been used historically to document PLE indogs. Measurement of 3day fecal excretion of this radioactive markerprovides an estimation of labeled albumin and hence protein loss into



the intestinal lumen. However, its use is very limited because of theuse of radioactive markers. An alternative approach is themeasurement of α1 protease inhibitor in the feces. This plasmaprotein is lost into the intestinal lumen together with albumin, but unlikealbumin it is an antiprotease and is excreted in the feces essentiallyintact. Speciesspecific assays have been developed. Three freshfecal samples passed by spontaneous evacuation are required; any GIbleeding invalidates the result.

Definitive diagnosis of chronic smallintestinal disease typicallyincludes histologic examination of intestinal biopsies taken byendoscopy or at laparotomy. Endoscopy is minimally invasive andallows visualization of the mucosa and targeted biopsy sampling.However, endoscopic mucosal biopsies may not always give anadequate representation of deeper disease and are limited to the partsof the small intestine (duodenum and sometimes proximal jejunum andileum) that can be visualized via colonoscopy. Endoscopic biopsy ispreferred initially because the risk of intestinal surgical wounddehiscence can exceed 10% in debilitated, malnourished, orhypoproteinemic animals. However, surgery is the preferred optionwhen there is a concern about deeper or extraintestinal disease or afocal lesion. If a laparotomy is performed, multiple elliptical,longitudinal biopsy samples should be collected from the duodenum,jejunum, and ileum; mesenteric lymph nodes should be biopsied andother organs examined.

Histologic examination of intestinal biopsy specimens can identifymorphologic changes in intestinal inflammation (including lymphocyticplasmacytic enteritis and eosinophilic enteritis), intestinal



lymphangiectasia, villous atrophy, and intestinal neoplasia. Thedescription of morphologic abnormalities can provide a baseline toevaluate response to treatment if sequential smallintestinal biopsiesare possible. Morphologic abnormalities may also provide prognosticinformation, because more severe enteropathies tend to be moredifficult to manage. However, there may be minimal or no obviousabnormalities in certain disorders (eg, ARD) despite considerableinterference with intestinal function. Histologic descriptions aloneprovide little information on possible etiology or underlyingmechanisms of damage, which would clearly assist effectivemanagement. Furthermore, inconsistencies in histologic descriptionsbetween pathologists is a recognized problem. However, the WorldSmall Animal Veterinary Association GI Standardization Group haspublished a descriptive template as a basis for concordance.

TreatmentTreatment of malabsorption involves treatment of the primary cause (ifidentified), dietary therapy, and management of complications.Management of EPI in dogs is relatively straightforward (see ExocrinePancreatic Insufficiency in Small Animals) and includes feeding a lowfiberdiet that contains moderate levels of fat or highly digestible fat, verydigestible carbohydrate, and highquality protein. Specific treatmentinvolves lifelong supplementation of each meal with pancreatic extract.Powdered extracts (1 tsp/10 kg body wt) are preferable to tablets,capsules, and most entericcoated preparations. Fresh or frozenpancreas can be used as an alternative (100 g/meal for an adultGerman Shepherd). If the response to pancreatic replacement therapyis poor, secondary antibioticresponsive diarrhea may be suspected,and the animal should be treated concurrently with oral antibiotics for

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≥1 mo (see below). Acid suppressants (eg, H2receptor blockers, suchas cimetidine or ranitidine; proton pump inhibitors, such asomeprazole) may be given 20 min before a meal to inhibit acidsecretion and to minimize acid degradation of enzymes in thepancreatic extract, but they are expensive and their value isquestionable. Oral multivitamin supplementation should be consideredas supportive therapy, but cobalamin (500–1,000 mcg/wk untilnormalized) should be given parenterally. Dietary requirements of catswith EPI can generally be met by conventional commercial diets, butpancreatic replacement therapy is still needed, as well as parenteralcobalamin supplementation in cats with low serum cobalaminconcentrations.

Effective treatment of smallintestinal disease depends on the natureof the disorder, but therapy may be empirical when a specific diagnosiscannot be made. In dogs with ARD, a lowfat diet may help byminimizing secretory diarrhea due to bacterial metabolism of fattyacids and bile salts. Oral broadspectrum antibiotic therapy withoxytetracycline (10–20 mg/kg, tid for 28 days) has been successful.Metronidazole (10–20 mg/kg, bid) and tylosin (20 mg/kg, tid) areeffective alternatives; there is rarely a need to use other antibiotics,and the nontargeted use of fluoroquinolones should be avoided.Repeated or longterm treatment may be necessary in dogs withidiopathic ARD. Vitamin supplementation may be helpful, particularlyfor animals with cobalamin deficiency. Secondary antibioticresponsivediarrhea usually resolves with appropriate management of theunderlying disease, but idiopathic ARD can be difficult to control,especially in young German Shepherds, which are predisposed todeveloping the condition.



Dietary modification is an important aspect of the management ofsmallintestinal disease in both dogs and cats. Diets generally containmoderate levels of limited protein sources and highly digestiblecarbohydrates (to reduce protein antigenicity, reduce osmolar effects,and improve nutrient availability) and low to moderate levels of fat. Inaddition, they are lactose and gluten free; may be fiberrestricted; andmay contain increased levels of antioxidants, prebiotics (eg, fructooligosaccharides), or omega3 fatty acids. These additives are thoughtto modulate the inflammatory response and increase the health of thebacterial gut flora and enterocytes. Treatment with an exclusion dietconsisting of a single novel protein source or a hydrolyzed proteinshould be used as trial therapy when dietary sensitivity is suspected.Intestinal inflammation is sometimes a manifestation of dietarysensitivity, and an initial exclusion food trial is indicated in mild casesof IBD before other treatments. Boiled white rice and potato aresuitable carbohydrate sources, while fish, lamb, or chicken are oftenused as a protein source, depending on the dietary history. Cottagecheese, horsemeat, rabbit, or venison may be acceptable alternatives.Commercial exclusion diets are not necessary to diagnose foodhypersensitivity; however, they are preferred for maintenance toreduce potential dietary imbalances. Protein hydrolysates may be themost effective diets to detect dietary sensitivity. The response to anexclusion diet is often rapid, but the diet must be fed for at least 3 and,in a few cases, up to 10 wk before being considered a failure. Oralprednisolone (1 mg/kg, bid for 2–4 wk, followed by a reducing dose) incombination with an exclusion diet may be useful in animals in whichidiopathic IBD is suspected but dietary sensitivity has not yet beenexcluded.



Treatment of idiopathic inflammatory bowel disease should initiallyattempt to eliminate or control an underlying antigenic stimulus thatmay be playing a primary or secondary role in the damage. Treatmentshould first involve the use of a protein hydrolysate diet. The dietshould comprise digestible carbohydrate (preferably rice, which is mostdigestible) and highquality protein. Restriction of fat content may alsobe valuable and can minimize the secretory diarrhea that is aconsequence of bacterial metabolism of fatty acids and bile salts. Oralprednisolone (1 mg/kg, bid for 1 mo, followed by a reducing dose) isindicated in cases of intestinal disease with an obvious inflammatorycomponent, such as lymphocyticplasmacytic enteritis and eosinophilicenteritis. In more severe cases, it may be necessary to addchlorambucil (2–6 mg/m2/day, PO, until remission, followed by drugtapering) in cats or azathioprine (2–2.5 mg/kg/day) in dogs.

Cats are often given adjunctive metronidazole (10 mg/kg, bid); thebeneficial effect of metronidazole may be a result of an inhibition ofcellmediated immune responses as well as anaerobic antibacterialactivity. However, the value of metronidazole in combination withprednisolone in the treatment of IBD in dogs has been questioned.

In lymphangiectasia, a severely fatrestricted, caloriedense, highlydigestible diet reduces diarrhea but tends to exacerbate weight loss.Supplementation with fatsoluble vitamins is advised, and additionalmediumchain triglycerides have been recommended as an easilyabsorbable fat source that bypasses the lymphatics, although thismechanism is now doubted. Prednisone/prednisolone therapy may bebeneficial for its antiinflammatory and immunosuppressive effects,especially if there is associated lipogranulomatous lymphangitis. The



response to treatment is variable; clinical signs may sometimes abatefor months or even years, but the longterm prognosis is grave.

Giardiasis can be treated with metronidazole or fenbendazole, andhistoplasmosis with itraconazole (cats) or ketoconazole (dogs), withor without amphotericin B. In cases of lymphosarcoma, treatmentinvolves an appropriate chemotherapy regimen, but response is poorin dogs and in cats with lymphoblastic forms. In cats, treatment ofsmallcell villous lymphoma with oral prednisone and chlorambucil isassociated with prolonged remission.

PrognosisThe prognosis in cases of malabsorption is good if there is a simplesolution, eg, 85% of cases of EPI respond well to enzyme replacementtherapy. The prognosis is worse the more severe the smallintestinalpathology. A poorer prognosis has been associated with severeintestinal inflammation, neoplastic disease, severe weight loss,hypoalbuminemia and ascites (PLE), anorexia, andhypocobalaminemia.

Last full review/revision February 2015 by Edward J. Hall, MA, VetMB, PhD,DECVIMCA

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