Malabsorption is the defective uptake of a dietary constituent resulting from interference with its digestion or absorption, due to either exocrine pancreatic insufficiency (EPI) or small-intestinal disease. Malabsorption typically results in diarrhea, altered appetite, and weight loss.

The primary function of the small intestine is digestion and absorption of nutrients, occurring in sequential phases: intraluminal digestion, mucosal digestion and absorption, and delivery of nutrients to the circulation. Many chronic small-intestinal diseases cause malabsorption by interfering with these processes. Malabsorptive syndromes have been studied in most detail in dogs, but basic diagnostic and therapeutic principles are relevant to other species.

Physiology

The normal digestive processes convert polymeric dietary nutrients into forms (monomers) that can cross the luminal surface or the brush border of intestinal absorptive epithelial cells (ie, the enterocytes). Most digestive enzymes are secreted by the pancreas; EPI is thus a major cause of malabsorption. Some terminal digestion before absorption is performed by brush border enzymes.

The main dietary carbohydrates are starch, glycogen, sucrose, and lactose. Starch and glycogen are first hydrolyzed by pancreatic amylase to the oligosaccharides maltose, maltotriose, and α-limit dextrins. Oligosaccharides and ingested disaccharides (sucrose, lactose) are further hydrolyzed to monosaccharides by enzymes located on the brush border of the enterocytes. Brush border lactase activity declines after weaning, especially in cats, and animals may become lactose-intolerant, especially if the brush border has been damaged by another disease. The final products of mucosal hydrolysis (glucose, galactose, and fructose) are actively transported into the enterocyte by a protein-carrier-mediated process. Once in the cell, glucose is not used by the glycolytic pathway but is passed by facilitated diffusion down a concentration gradient into the lamina propria and then by diffusion into the portal venous circulation.

Protein digestion and absorption follow a similar pattern. Proteolytic enzymes from the stomach and pancreas degrade protein into a mixture of short-chain oligopeptides, dipeptides, and amino acids. Oligopeptides are further hydrolyzed by brush-border peptidases to dipeptides and amino acids that cross the brush-border membrane on specific carrier proteins.

Fat-soluble molecules do not need specific carriers to cross the phospholipid barrier of the brush border. However, intraluminal degradation of large lipids is essential. Fat in the duodenum stimulates release of cholecystokinin, which, in turn, stimulates secretion of pancreatic lipase. After solubilization by bile salt micelles, triglycerides are digested by pancreatic lipase to monoglycerides and free fatty acids. At the cell membrane, the monoglycerides and free fatty acids disaggregate from the micelle and are passively absorbed into the cell. Released bile acids remain within the lumen and are ultimately reabsorbed by the ileum and recycled. Once inside the cell, the monoglycerides and free fatty acids are reesterified to triglycerides and incorporated into chylomicrons, which subsequently enter the central lacteals of the villus, being delivered to the venous circulation via the thoracic duct. Medium-chain triglycerides (C₈–C₁₀) may be absorbed directly into the portal blood, providing an alternative route for fat uptake in case of lymphatic obstruction, but some do normally enter the circulation via the thoracic duct.

Etiology and Pathophysiology

Malabsorption is a consequence of interference with mechanisms responsible for either the degradation or absorption of dietary constituents (see Diseases of the Stomach and Intestines in Small Animals: Mechanisms of Malabsorption).

Table 1
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Mechanisms of Malabsorption Location Disease Mechanism Luminal Exocrine pancreatic insufficiency Lack of pancreatic enzymes (maldigestion) Luminal Small intestinal bacterial overgrowth (antibiotic-responsive diarrhea) Bacterial activity: bile salt deconjugation, fatty acid hydroxylation, competition for cobalamin and nutrients Mucosal Inflammatory bowel disease, infectious enteropathies, dietary sensitivities, neoplastic infiltration Mucosal damage: inflammation, brush border defects, disturbed enterocyte function, reduction of surface area Mucosal Villous atrophy Reduction in surface area Mucosal Brush border enzyme deficiencies Lactase deficiency, diffuse small-intestinal disease Postmucosal Lymphangiectasia Lymphatic obstruction Postmucosal Vasculitis, portal hypertension Impaired delivery

Diseases that disrupt the synthesis or secretion of digestive pancreatic enzymes cause maldigestion with subsequent malabsorption, so that the end result is the same. An important cause is EPI (p 368), which occurs if there is a loss of ~85–90% of exocrine pancreatic mass. EPI is characterized by severe maldigestion-malabsorption of starch, protein, and most notably, fat. In dogs, EPI is most commonly due to acinar atrophy; chronic pancreatitis is less common and is seen in older animals, and pancreatic hypoplasia is a rare congenital cause. EPI in dogs is often complicated by secondary small-intestinal bacterial overgrowth (SIBO), which further disrupts nutrient digestion and absorption. EPI is relatively uncommon in 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 and hydroxy fatty acids exacerbate diarrhea by stimulating colonic secretion. True SIBO can be secondary to defective gastric acid secretion, interference with normal motility or mechanical obstruction of the intestine, interference with the function of the ileocecal valve, and local immunodeficiency. In other cases, there is no defined SIBO, but a positive response to antibiotic therapy and lack of overt mucosal damage indicates that the malabsorption is being caused by bacterial activity. Originally called idiopathic SIBO, this syndrome is better termed antibiotic-responsive diarrhea (ARD).

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

Small-intestinal disease can cause malabsorption by reduction of the number or function of individual enterocytes. Diffuse diseases of the mucosa can result in reduced activities of brush border enzymes, decreased carrier-protein function, decreased mucosal absorptive surface area, and interference with final transport of nutrients into the circulation. Weight loss may be compounded by reduced nutrient intake due to inappetence. In addition, malabsorbed nutrients exert strong intraluminal osmotic effects that diminish intestinal and colonic absorption of water and electrolytes, resulting in diarrhea. This may be exacerbated if mucosal damage is accompanied by intestinal inflammation, which can cause secretory and permeability diarrhea.

Potential causes of mucosal damage include inflammatory bowel disease, enteric pathogens (eg, enteric viruses, pathogenic bacteria, Giardia, Histoplasma, Pythium), dietary sensitivity, SIBO, and intestinal neoplasia (eg, lymphosarcoma). Histologic changes such as villous atrophy and infiltration with inflammatory cells indicate intestinal disease but do not identify the underlying cause. For example, lymphocytic-plasmacytic enteritis may be a common response of the intestinal mucosa to more than one provocative agent, particularly microbial and dietary antigens. Definite associations with parasites, pathogenic bacteria, and dietary sensitivity have been demonstrated in dogs, but often the underlying cause cannot be identified.

Mucosal damage may also occur without obvious changes under light microscopy. This is typified by infection with enteropathogenic Escherichia coli (which specifically cause ultrastructural damage to microvilli in an attaching-effacing lesion) and sometimes also by ARD in the proximal small intestine (which in dogs can cause biochemical damage to the intestinal brush border interfering with enterocyte function).

The main brush border enzyme deficiency reported is a relative lactase deficiency, leading to milk intolerance in adult dogs and cats. Acquired brush border defects also may be seen in the course of generalized small-intestinal disease.

Postmucosal obstruction may be seen with lymphatic obstruction (especially lymph-angiectasia) and vascular compromise (portal hypertension, vasculitis). Intestinal lymphangiectasia causes intestinal protein loss as well as severe fat malabsorption.

Usually there is malabsorption of a number of ingredients with consequent diarrhea; malabsorption of a single ingredient without GI signs is rare (eg, selective cobalamin malabsorption in Giant Schnauzers and Border Collies). Furthermore, the large absorptive capacity of the colon may prevent overt diarrhea despite significant malabsorption and weight loss.

Clinical Findings

Clinical signs of malabsorption are mainly the result of lack of nutrient uptake and losses in the feces. The duration, severity, and primary cause determine the severity of signs, which typically include chronic diarrhea, weight loss, and altered appetite (anorexia or polyphagia). The absence of diarrhea does not exclude the possibility of severe GI disease. Weight loss may be substantial despite a ravenous appetite, sometimes characterized by coprophagia and pica. Typically, animals with malabsorption are systemically well unless there is severe inflammation or neoplasia. Nonspecific signs may include dehydration, anemia, and ascites or edema in cases of hypoproteinemia. Thickened bowel loops or enlarged mesenteric lymph nodes may be palpable, especially in cats.

Diagnosis

Chronic diarrhea and weight loss are nonspecific signs common to a variety of systemic and metabolic diseases, as well as malabsorption. A thorough diagnostic approach in dogs and cats with signs suggestive of malabsorption is therefore needed to help exclude association with possible underlying systemic or metabolic disease. A precise diagnosis is also important for determining treatment and prognosis.

The history is particularly important because it may suggest specific dietary intolerance, indiscretion, or sensitivity. Weight loss may indicate malabsorption or protein-losing enteropathy but may also be due to anorexia, vomiting, or extra-GI disease. Small- and large-intestinal diarrhea may be distinguished by a number of features (see Digestive System Introduction: Differentiation of Small-Intestinal from Large-Intestinal Diarrhea). This distinction is more helpful in dogs than in cats, which rarely have exclusively large-intestinal disease. Suspected large-intestinal disease in dogs may be further evaluated by colonoscopic biopsy of the large intestine. However, if signs of large-intestinal disease are accompanied by weight loss or large volumes of feces, then the small intestine is probably also diseased concurrently.

A thorough physical examination should be performed. Abdominal palpation is essential to identify abnormalities, and rectal examination is required even when no large-intestinal disease is suspected to provide a fecal sample and possibly reveal previously unreported melena. In older cats, the thyroid should be palpated carefully and serum T₄ assayed, because signs of hyperthyroidism can closely mimic those of malabsorption.

Initial evaluation should include a CBC, biochemical profile, urinalysis, fecal examination, abdominal ultrasonography and, when indicated by clinical signs or abnormal abdominal palpation, plain radiography. Hematologic correlates in small-intestinal diseases sometimes include anemia of chronic blood loss (microcytic, hypochromic) or chronic inflammation (normocytic, normochromic); neutrophilia and/or monocytosis associated with inflammatory bowel diseases, infectious enteropathies, or neoplasia; eosinophilia associated with parasitism, eosinophilic enteritis, or hypoadrenocorticism; and lymphopenia that may be associated with intestinal lymphan-giectasia in dogs.

Biochemical tests and urinalysis help to exclude systemic diseases that cause chronic diarrhea, most notably hypoadrenocorticism, protein-losing nephropathies and renal failure, and liver disease. Hypoproteinemia frequently is secondary to a protein-losing enteropathy. In most cases, serum albumin and globulin are both low, but a low albumin alone does not rule it out; inflammatory bowel disease and neoplasia are occasionally associated with hyperglobulinemia as well as hypoalbuminemia. Liver enzymes (ALT, AST) may be elevated as a consequence of increased intestinal permeability, allowing more antigens to reach the liver; in such cases, a bile acid stimulation test as well as ultrasonography should be performed to exclude primary liver disease. Hypocholesterolemia may develop with fat malabsorption and is notable in lymphangiectasia. Urinalysis is important to exclude renal causes of hypoalbuminemia and/or renal disease. However, sometimes both may be seen together (eg, the familial protein-losing enteropathy and nephropathy of Soft-coated Wheaten Terriers). In cats, serologic tests for feline leukemia and feline immunodeficiency viruses should be performed, not only because both may be associated with secondary chronic diarrhea but also because they are important prognostic factors. Feline infectious peritonitis and toxoplasmosis have also been described as occasional causes of chronic diarrhea in cats. Feline hyperthyroidism can be excluded by measuring serum T₄ concentrations.

Feces should be examined for parasites (especially hookworms and Giardia) and potentially pathogenic bacteria (including Salmonella and Campylobacter). Pathogenic Escherichia coli are emerging as a potentially important problem in dogs, but molecular techniques to identify genes encoding pathogenicity determinants are required for diagnosis. Giardia can be detected using serial zinc sulfate fecal flotations or with commercially available ELISA; the latter are easier to perform and their sensitivity is better than fecal flotation performed by inexperienced personnel. The presence of fat, undigested muscle fibers, or starch in feces may provide indirect evidence for malabsorption, but these are unreliable. Detection of excessive leukocytes on fecal cytology may indicate chronic inflammatory bowel disease or presence of enteric pathogens. Cytology of rectal scrapings may reveal Histoplasma organisms.

Abdominal radiography is more useful when vomiting is present or palpable abnormalities are detected. Ultrasonography is an important part of the investigation of most small-intestinal diseases. It can be used to measure intestinal wall thickness, layering, and luminal diameter, and to detect other intestinal lesions (eg, masses, intussusception), mesenteric lymphadenopathy (in neoplasia and inflammatory bowel disease), and abnormalities in other organs.

Once obvious dietary, systemic, parasitic, and infectious causes of chronic small-intestinal diarrhea have been eliminated, the next step is differentiation of EPI from intestinal malabsorption; the diagnosis of EPI is relatively straightforward, while that of small-intestinal disease is more complex. Numerous tests have been recommended for dogs and cats with suspected EPI, but they are too inaccurate or impractical to be recommended. Assay of serum trypsin-like immunoreactivity (TLI) is a highly sensitive and specific test and should be used for the diagnosis of EPI. This assay measures trypsinogen, some of which normally leaks from the pancreas into the blood, thereby providing an indirect assessment of functional pancreatic tissue. In EPI, functional exocrine tissue is severely depleted and serum TLI concentrations are extremely low, clearly distinguishing EPI from other causes of malabsorption. This test requires a fasted serum sample. Species-specific canine and feline TLI tests are available.

Diagnosis of small-intestinal disease is difficult due to limitations of routine screening procedures, the need for biopsy, and frequently the absence of diagnostic histologic changes.

Simultaneous assay of serum folate and cobalamin (vitamin B₁₂) concentrations can be a helpful initial test in the assessment of small-intestinal disease. Folate is absorbed primarily by the proximal small intestine (jejunum), whereas cobalamin is absorbed by the distal small intestine (ileum). As a result, serum folate concentrations can be decreased in proximal small-intestinal diseases, serum cobalamin concentrations can be decreased in distal diseases, and both can be decreased in diffuse enteropathies. Other factors such as the severity, extent, and duration of a mucosal abnormality; dietary intake; and vitamin supplementation also influence these concentrations. In addition, EPI can affect serum folate and cobalamin concentrations, and changes in serum folate are unreliable for the diagnosis of ARD and secondary SIBO. The validity of serum folate and cobalamin assays for the investigation of small-intestinal disease in cats is less clear, but low serum cobalamin concentrations may be found with both small-intestinal disease and EPI and are an indication of parenteral supplementation. A further indirect approach to the detection of small-intestinal disease is the assessment of intestinal function and permeability by oral administration of test substances that are subsequently measured in blood or urine samples. Historically, the xylose absorption test was used to assess intestinal function, but it is insensitive, especially in cats. Measurement of d-xylose/3- o-methyl-d-glucose differential absorption appears to be a more effective approach but is technically demanding and not suited to general practice. Similarly, measurement of intestinal permeability, to provide information about the physical integrity rather than the functional capacity of the mucosa, is not generally used. This test involves measurement of urinary or blood concentrations of orally administered probes that cross the intestinal mucosa by unmediated permeation through 2 possible pathways (intercellular and transcellular).

Calculation of the ratio of the urinary excretion of a mixture of 2 probes of different sizes, such as lactulose and rhamnose, has been used successfully not only for the diagnosis of small-intestinal disease in dogs but also to monitor response to treatment (eg, to document dietary sensitivity or SIBO). Unfortunately, this approach does not appear to be useful in cats because intestinal permeability in healthy cats is high.

IV administration of ⁵¹Cr-labeled albumin (or ⁵¹CrCl₃ to label endogenous albumin) has been used historically to document protein-losing enteropathy in dogs. Measurement of 3-day fecal excretion of this radioactive marker provides an estimation of labeled albumin and hence protein loss into the intestinal lumen. However, its use is very limited because of the use of radioactive markers. An alternative approach is the measurement of α-1 protease inhibitor in the feces. This plasma protein is lost into the intestinal lumen together with albumin, but unlike albumin it is an antiprotease and is excreted in the feces essentially intact. Species-specific assays have been developed. Three fresh fecal samples passed by spontaneous evacuation are required; any GI bleeding invalidates the result.

Hydrogen breath testing after oral administration of individual sugars has been used extensively in people to assess bacterial colonization of the small intestine and carbohydrate malabsorption. The test works on the principle that intestinal bacteria ferment intraluminal carbohydrate and produce hydrogen gas, some of which is absorbed into the blood and excreted by the lungs. Increased breath hydrogen concentrations after oral carbohydrate may therefore reflect either bacterial colonization in the proximal small intestine or malabsorption of carbohydrate (which then reaches the flora normally present in the large intestine). This is a simple procedure to detect malabsorption and to assess transit time, but is likely to be available only at specialist centers.

Attempts to detect SIBO by breath hydrogen or measurement of serum unconjugated bile acids are unreliable because bacterial numbers may not actually be increased in ARD.

Definitive diagnosis of chronic small-intestinal disease typically includes histologic examination of intestinal biopsies taken by endoscopy or at laparotomy. Endoscopy is minimally invasive and allows visualization of the mucosa and targeted biopsy sampling. However, endoscopic mucosal biopsies may not always give an adequate representation of deeper disease and are limited to the parts of the small intestine (duodenum and sometimes proximal jejunum and ileum [via colonoscopy]) that can be visualized. Endoscopic biopsy is preferred initially because the risk of intestinal wound dehiscence can exceed 10% in debilitated, malnourished, or hypoproteinemic animals. However, surgery is the preferred option when there is a concern about deeper and extraintestinal disease or a focal lesion. If a laparotomy is performed, multiple elliptical, longitudinal biopsy samples should be collected from at least the duodenum, jejunum, and ileum; mesenteric lymph nodes should be biopsied and other organs examined.

Histologic examination of intestinal biopsy specimens can identify morphologic changes in inflammatory bowel diseases, including lymphocytic-plasmacytic enteritis and eosinophilic enteritis, intestinal lymphangiectasia, villous atrophy, and intestinal neoplasia. The description of morphologic abnormalities can provide a baseline to evaluate response to treatment if sequential small-intestinal biopsies are possible. Morphologic abnormalities may also provide prognostic information, because more severe enteropathies tend to be more difficult to manage. However, there may be minimal or no obvious abnormalities in certain disorders (eg, ARD) despite considerable interference with intestinal function. Histologic descriptions alone provide little information on possible etiology or underlying mechanisms of damage, which would clearly assist effective management. Furthermore, inconsistencies in histologic descriptions between pathologists is a recognized problem. However, the World Small Animal Veterinary Association GI Standardization Group has published a descriptive template as a basis for concordance.

Bacteriologic culture of duodenal fluid obtained endoscopically or at laparotomy has been used to confirm a diagnosis of SIBO. However, the exact cut-off point at which small-intestinal bacterial numbers are considered excessive is still a matter of debate, because numbers >10⁵ total or >10⁴ obligate anaerobic colony-forming units (CFU)/mL may be found in apparently clinically healthy dogs, depending on circumstances, including environment, diet, scavenging, and coprophagia.

Treatment

Treatment of malabsorption involves dietary therapy, management of complications, and treatment of the primary cause (if identified). Management of EPI in dogs is relatively straightforward (see p 369). It should include feeding a low-fiber diet that contains moderate levels of fat or highly digestible fat, very digestible carbohydrate, and high-quality protein. Specific treatment involves lifelong supplementation of each meal with pancreatic extract. Powdered extracts (1 tsp/10 kg body wt) are preferable to tablets, capsules, and enteric-coated preparations. Fresh or frozen pancreas can be used as an alternative (100 g/meal for an adult German Shepherd). If response to pancreatic replacement therapy is poor, secondary SIBO may be suspected, and the animal treated with oral antibiotics for ≥1 mo (see below). H₂-receptor blockers, such as cimetidine or ranitidine, may be given 20 min before a meal to inhibit acid secretion and to minimize degradation of enzymes in the pancreatic extract, but they are expensive and their efficacy is questionable. Oral multivitamin supplementation should be considered as supportive therapy, but cobalamin (500–1,000 μg/wk until normalized) should be given parenterally. Dietary requirements of cats with EPI can generally be met by conventional commercial diets, but pancreatic replacement therapy is still needed, as well as parenteral cobalamin supplementation in cats with low serum cobalamin concentrations.

Effective treatment of small-intestinal disease depends on the nature of the disorder, but therapy may be empirical when a specific diagnosis cannot be made. In dogs with ARD, a low-fat diet may help by minimizing secretory diarrhea due to bacterial metabolism of fatty acids and bile salts. Oral broad-spectrum antibiotic therapy with oxy-tetracycline (10–20 mg/kg, tid for 28 days) has been successful. Metronidazole (10–20 mg/kg, bid) and tylosin (20 mg/kg, tid) are effective alternatives. Repeated or longterm treatment may be necessary in dogs with idiopathic ARD. Vitamin supplementation may be helpful, particularly for animals with cobalamin deficiency. Secondary SIBO usually resolves with appropriate management of the underlying disease, but idiopathic SIBO can be difficult to control, especially in young German Shepherds, which are predisposed to developing the condition.

Dietary modification is an important aspect of the management of small intestinal disease in both dogs and cats. Diets generally contain moderate levels of limited protein sources and highly digestible carbohydrates (to reduce protein antigenicity, reduce osmolar effects, and improve nutrient availability), and low to moderate levels of fat. In addition, they are lactose and gluten free; may be fiber-restricted; and may contain increased levels of antioxidants, prebiotics (eg, fructo-oligosaccharides), or omega-3 fatty acids. These additives are thought to modulate the inflammatory response and increase the health of the bacterial gut flora and enterocytes. Treatment with an exclusion diet consisting of a single novel protein source should be used as trial therapy when dietary sensitivity is suspected. In addition, intestinal inflammation is sometimes a manifestation of dietary sensitivity, and an initial exclusion food trial is indicated in mild cases of inflammatory bowel disease before other treatments. Boiled white rice and potato are suitable carbohydrate sources, while lamb or chicken are often used as a protein source, depending on the dietary history. Cottage cheese, horsemeat, rabbit, venison, or fish may be acceptable alternatives. Commercial exclusion diets are not necessary for diagnosing food hypersensitivity; however, they are preferred for maintenance to reduce dietary imbalances. Protein hydrolysate diets may be most effective in detecting dietary sensitivity. The exclusion diet generally does not need to be fed for >3 wk. Oral prednisolone (1 mg/kg, bid for 2–4 wk, followed by a reducing dose) in combination with an exclusion diet may be useful in animals in which idiopathic inflammatory bowel disease is suspected but dietary sensitivity has not yet been ruled out.

Treatment of idiopathic inflammatory bowel disease should initially attempt to eliminate or control an underlying antigenic stimulus that may be playing a primary or secondary role in the damage. Treatment should first involve the use of an exclusion or protein hydrolysate diet for suspected dietary sensitivity as described above. The diet should comprise digestible carbohydrate (preferably rice, which is most digestible) and high-quality protein. Restriction of fat content may also be valuable and can minimize the secretory diarrhea that is a consequence of bacterial metabolism of fatty acids and bile salts. Oral prednisolone (1 mg/kg, bid for 1 mo, followed by a reducing dose) is indicated in cases of intestinal disease with an obvious inflammatory component, such as lymphocytic-plasmacytic enteritis and eosinophilic enteritis. In more severe cases, it may be necessary to add chlorambucil (2–6 mg/m², PO, sid until remission, followed by drug tapering) in cats or azathioprine (2–2.5 mg/kg, sid) in dogs.

Cats are often given adjunctive metronidazole (10 mg/kg, bid); the beneficial effect of metronidazole may be a result of an inhibition of cell-mediated immune responses as well as anaerobic antibacterial activity.

In lymphangiectasia, a severely fat-restricted, calorie-dense, highly digestible diet reduces diarrhea but tends to exacerbate weight loss. Supplementation with fat-soluble vitamins is advised, and additional medium-chain triglycerides have been recommended as an easily absorbable fat source that bypasses the lymphatics, although this mechanism is now doubted. Prednisone therapy may be beneficial for its anti-inflammatory and immunosuppressive effects, especially if there is associated lipo-granulomatous lymphangitis. The response to treatment is variable; clinical signs may sometimes abate for months or even years, but the longterm prognosis is grave.

Giardiasis can be treated with metronidazole or fenbendazole, and histoplasmosis with itraconazole (cats) or ketoconazole (dogs), with or without amphotericin B. In cases of lymphosarcoma, treatment involves an appropriate chemotherapy regimen, but response is poor in dogs and cats with lymphoblastic forms. In cats, treatment of small-cell villous lymphoma with oral prednisone and chlorambucil is associated with prolonged remission.

Last full review/revision March 2012 by Edward J. Hall