The protein-losing enteropathies (PLE) comprise a collection of intestinal, usually small intestinal, diseases typically associated
with weight loss, hypoproteinemia caused by hypoalbuminemia or panhypoproteinemia, and variable signs of vomiting and diarrhea.
In dogs, PLE is most often a consequence of either lymphocytic/plasmacytic enteritis (LPE) or other inflammatory intestinal
infiltrative disease, intestinal lymphangiectasia (IL), or intestinal lymphoma; these disease are the focus of this discussion.
Because the presenting clinical findings and diagnostic features are similar for all 3, they will be considered as a group
with key differences pointed out where relevant. Readers should be aware that other diseases can contribute to the clinical
manifestation of a PLE including gastrointestinal ulcerative disease, other intestinal neoplasms, intestinal histoplasmosis,
gastrointestinal parasites, and chronic intestinal intussusception.
PLE can develop in animals of any age. Dog breeds that seem predisposed to the development of PLE include basenjis, Lundehunds,
soft-coated wheaten terriers, Chinese Shar Peis, Rottweilers, German shepherds and Yorkshire terriers. Dogs are affected with
PLE more often than cats despite the overlap in histological diagnoses of chronic intestinal diseases that exist between the
The clinical signs of PLE can be quite variable. Many dogs with PLE exhibit nonspecific signs, such as anorexia or lethargy;
however, dogs may exhibit polyphagia. Diarrhea is one of the most consistent clinical signs referable to the GI tract but
is not seen in all patients with PLE. When diarrhea is not a presenting complaint, PLE should not necessarily be ruled out
if otherwise compatible signs, such as weight loss, edema, or ascites, are present. Vomiting is also a frequent clinical sign
in dogs with PLE. Dilation of intestinal lymphatics alone in dogs with IL does not seem to cause vomiting, but because many
dogs with IL have intestinal inflammation, vomiting likely results from inflammatory stimuli.
Ascites, subcutaneous dependent edema, and pleural effusion are common in PLE patients. In most cases, fluid accumulates secondary
to decreased colloid oncotic pressure from hypoproteinemia, especially hypoalbuminemia. Effusions or edema may develop when
serum albumin concentrations fall below 1.5 g/dl; effusions in these situations are usually pure transudates (low protein
content, often less than 1 g/dl, and low nucleated cell counts). However, pure transudates in abdominal effusion can sometimes
be seen in the context of serum albumin concentrations higher than 1.5 g/dl, suggesting that other pathophysiological factors
that govern the formation of effusions, such as increased hydrostatic pressure or lymph obstruction, may contribute to fluid
accumulation. Chylothorax can be seen in some patients with PLE secondary to IL. It is important to remember that pure transudates
in the abdomen can also be a consequence of portal hypertension.
In some dogs, clinical signs of thromboembolic disease, such as tachypnea and hyperpnea due to pulmonary thromboemboli, can
develop. The coagulation abnormalities in dogs with PLE are poorly characterized and understood but are attributed to imbalances
between pro- and anti-coagulant factors, or increased platelet aggregability or vascular endothelial injury, both of which
have been documented in humans with inflammatory bowel diseases.
Laboratory abnormalities in dogs with PLE can be quite variable. Anemia of chronic inflammation and neutrophilic leukocytosis
secondary to stress or chronic inflammation) may be observed in some dogs. Some dogs with IL have lymphopenia, but lymphopenia
can also be a component of stress leukograms in such patients. Platelet counts may increase from chronic inflammation. Thrombocytopenia
in a dog with PLE is unusual and suggests a complication of the disease, such as thromboembolism or disseminated intravascular
Hypoalbuminemia is the most consistent laboratory abnormality in canine PLE. Some dogs, however, have normal albumin levels.
Commonly, serum globulin concentration is also low. Globulins can be increased, or remain normal in the face of enteric protein
loss, secondary to increased production associated with the inflammatory process. Total serum calcium level is often decreased
as an artifact of low serum albumin concentration. Occasionally, the total corrected calcium concentration remains abnormally
low, and occasional dogs will have persistently low ionized calcium concentrations.
Other biochemical abnormalities commonly seen in dogs with PLE include hypocholesterolemia (especially with IL) and increased
alanine aminotransferase (ALT) and alkaline phosphatase (AP) activity. Hypocholesterolemia is attributed to GI loss and lipid
malabsorption. Increases in liver enzyme activities could be a reflection of some degree of concurrent hepatobiliary disease.
Vacuolar changes in hepatocytes have been described in dogs with IL and increased liver enzyme activities. Trypsin-like immunoreactivity
(TLI) is expected to be normal in dogs with PLE; TLI testing may be necessary to exclude exocrine pancreatic insufficiency
in dogs with signs of diarrhea and weight loss that do not yet exhibit hypoalbuminemia/hypoproteinemia.