Information on other Diseases
What is Protein Losing Enteropathy:
Excessive loss of plasma and proteins into the gastrointestinal (GI) tract
is called protein-losing enteropathy. It can result from any condition that
damages the lining of the GI tract. Protein-losing enteropathies that are
thought to have an inherited component include intestinal lymhangiectasia,
immunoproliferative enteropathy , and protein-losing enteropathy and
nephropathy in the soft-coated wheaten terrier. The latter condition is thought to be related
to adverse food reactions, and there is also loss of protein from the kidney
(see also familial renal disease).
How is protein-losing enteropathy and nephropathy inherited?
The inheritance may be autosomal recessive.
What breeds are affected by protein-losing enteropathy and nephropathy?
soft-coated wheaten terrier
What does protein-losing enteropathy and nephropathy mean to your dog & you?
Your dog may fail to gain weight or may progressively lose weight. The loss
of protein into the bowel causes loss of fluid from the circulation into the
limbs, the abdomen, or the chest. Your dog's legs and/or abdomen may appear
swollen and he/she may have trouble breathing. There may be a chronic
persistent or intermittent diarrhea due to the loss of protein, fluid and fat into the
bowel. Loss of protein from the kidney will cause increased urination and
drinking in your dog.
How is protein-losing enteropathy and nephropathy diagnosed?
If your dog has the signs described above, your veterinarian will likely
suspect one of the diseases that result in loss of proteins into the gut.
Laboratory tests and an intestinal biopsy are necessary to diagnose the
How is protein-losing enteropathy and nephropathy treated?
This condition can not be cured but it can generally be well-managed by you
and your veterinarian. The major goal of therapy is to reduce the loss of
proteins into the intestine, to restore normal protein levels in your dog.
This is done through diet, and medication to reduce inflammation in the intestinal
wall. An ideal diet for dogs with protein-losing enteropathy contains
minimal fat, and an ample quantity of high-quality protein. There are commercial
prescription diets available which fulfill these requirements, or your
veterinarian can give you information to prepare a low-fat diet at home. In either case,
you will need to supplement your dog's diet with fat-soluble vitamins, due to
the poor absorption of fat that occurs with this condition.
Corticosteroids may help to reduce inflammation, and thereby reduce loss of
protein and associated diarrhea.
Affected dogs should not be used for breeding. Given that the inheritance is
thought to be autosomal recessive, parents (considered carriers) and
siblings (suspect carriers) should not be used for breeding either.
FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.
Burrows, C.F., Batt, R.M., Sherding, R.G. 1995. Diseases of the small
intestine. In S.J. Ettinger and E.C. Feldman (eds.) Textbook of Veterinary
Medicine. p. 1224-1225. W.B. Saunders Co., Toronto.
Williams, D.A. 1998 Protein-losing enteropathy Proc. 16th ACVIM Forum pp
Copyright C 1998 Canine Inherited Disorders Database. All rights reserved.
This database is a joint initiative of the Sir James Dunn Animal Welfare
Centre at the Atlantic Veterinary College, University of Prince Edward
Island, and the Canadian Veterinary Medical Association.
Veterinarians and owners of small breed dogs are on the lookout for signs of a liver problem
that has been recognized by pathologists for some 15 years, but only recently by veterinary
What is MVD?
When the Liver Isn’t Getting Enough Blood
August 07, 2000
Written by: Celeste A. Clements, DVM, Diplomate ACVIM
Hepatoportal microvascular dysplasia, or MVD, is a congenital disorder of the liver’s blood
supply. Dogs that inherit this problem may become quite ill: coma, seizures, and bizarre behavior
are among the more extreme manifestations of the disease. The problem is especially prevalent in
Cairn and Yorkshire terriers.
Dogs that have MVD don’t get an adequate supply of blood to the liver. A healthy liver detoxifies
and purifies blood returning from the abdominal organs. Blood enters the liver through the portal
vein, which branches throughout the liver lobes via seven major tributaries. If blood supply to
the liver is abnormal or insufficient, the liver will not grow properly, and its function will be
affected—and how bad the problem is really depends on the extent of the deformity. Blood that
fails to enter the liver properly is diverted or "shunted" through alternate routes.
An elusive disease
MVD isn’t the only type of congenital liver abnormality resulting from improper blood supply. With
a portosystemic vascular anomaly—or PSVA—the blood supply may be visibly abnormal because it
bypasses all or a portion of the liver. The difference with MVD is that the abnormality is
apparent only at the microscopic level—which is why veterinarians sometimes have a hard time
The disease is so subtle that the veterinarian may not be able to detect it. If the dog does
show signs of illness, they usually include increased thirst and urination, intolerance of food,
or changes in behavior that may reflect the influence of dietary toxins and byproducts of
metabolism on the brain. Hepatic encephalopathy, a condition that results from an excessive
blood level of metabolic byproducts that are normally filtered out by the liver, is observed
in the majority of patients with substantial blood shunting.
Additional signs include depression or confusion, incoordination, apparent blindness, and even
seizures and coma. Dementia or bizarre behavior after eating is a common occurrence in puppies
with "shunts;" however, more subtle signs may be evident in canine patients with MVD.
Bile acid profiles have become a popular noninvasive test for detecting circulatory and other
functional disturbances of the liver. The level of bile acids in the fasting and fed, or
postprandial state, assessed together offer a useful prediction of clinically significant
Bile acids are a component of bile, produced by the liver, and stored in the gallbladder.
When the gallbladder empties, in response to chemical or hormonal signals stimulated by eating,
bile enters the intestinal tract to aid in digestion. Along with other metabolic byproducts, a
significant amount of the bile salts are reabsorbed into the bloodstream at the termination of
the small intestine, the ileum. Subsequently, they pass into the portal circulation, destined for
In dogs with healthy livers, the bile salts are extracted from the blood and recirculated.
However, the level of bile acids will be high if the patient has impaired hepatoportal
circulation, reduced liver mass, or bile retention.
A high level of bile salts doesn’t mean the dog has MVD, though. There is considerable overlap
between different liver diseases, so additional diagnostics are needed to differentiate between
them, to include sonographic imaging, nuclear scintigraphy or dye studies, and, frequently,
When a dog has an abnormal circulation of blood to the liver, the presence of shunting can be
assessed by noninvasive means, including nuclear scintigraphy. With this procedure, a
radioisotope-labeled enema is administered. This radioisotope is taken up by circulation in the
colon and the labeled blood is delivered to the liver in normal dogs and to the heart in dogs
that have shunts. Computer technology allows for the comparison of labeled blood’s entry into the
liver or the heart. Estimates of the shunt fraction are relatively reliable, but the technique
rarely localizes the abnormal circulation. If the shunt fraction is less than or equal to 15
percent, then it’s unlikely that the portosystemic vascular anomaly is surgically correctable.
A dye study can provide a definitive diagnosis of a problem with circulation of blood to the
liver. In the case of MVD, a dye study test will show uneven distribution of contrast within
liver tissue, blunted branches of the portal vein, and persistence of contrast in the liver
tissue. Such procedures are performed on an anesthetized patient, most commonly in connection
with surgery to visualize or sample the liver. However, if an anomalous blood vessel is
identified grossly, contrast studies, termed portography, are rarely performed.
Surgical correction of the shunting vessel, through banding or ligation, is successful in the
majority of dog patients, if performed before two years of age. A more normal pattern of blood
flow is achieved, with improved perfusion of liver tissue and improved liver function, but
microscopic circulatory changes may persist in those patients, preventing establishment of a
completely normal state.
Unlike dogs with PSVA, dogs with MVD cannot enjoy correction of the liver dysfunction. Treatment
of dogs showing signs of disease focuses on feeding diets restricted in dietary protein, using
oral antibiotics to curtail intestinal bacterial growth, and offering lactulose to reduce
intestinal absorption of ammonia, one of the important contributions to hepatic encephalopathy.
Effective control of signs should permit a good quality of life for most dogs. Some will still
develop progressive liver dysfunction, though, with portal hypertension and subsequent
accumulation of abdominal fluid.
No treatment is required for asymptomatic patients, but all dogs with MVD may be at higher risk
for adverse reactions to medications processed by the liver. Discretion is wise when administering
prescription or over-the-counter medications, and when planning for anesthesia. It is unclear
whether MVD predisposes patients to other forms of liver disease, such as inflammatory conditions
Catching it early
Early identification of dogs with MVD is ideal. It’s important to prevent breeding and perpetuation
of the disease and to distinguish the disorder from other diseases that might cause liver
dysfunction in later life. Cairn terriers and Yorkshire terriers may be considered a high-risk
population; MVD also has been documented in other small breeds, such as the miniature schnauzer,
Lhasa apso, dachshund, Maltese, bichon frise, and poodle.
The problem should be suspected in pups or young small breed dogs that have repeatedly elevated
serum bile acids but are otherwise well. Noninvasive scintigraphy makes sense for patients
suspected of MVD or PSVA, although it may not be readily available in all locales. Further, the
test cannot definitively verify or rule out microscopic abnormalities, only gross shunting. Only
a liver biopsy of reasonable size and good quality can definitively diagnose MVD.
Liver biopsies are safely performed in the vast majority of patients, but the risks should be
assessed for each patient and compared to the potential benefits. While a liver biopsy may be
indicated for symptomatic patients with high bile acids, it is much more difficult to justify
this procedure for dogs that have only abnormal test results. If spaying is planned for female
dogs at risk, then a visual inspection of the liver and portal circulation and liver biopsy may
In some cases, MVD remains a tentative diagnosis, which seems reasonable provided no surgically
treatable problem is overlooked. As one of many diseases that are hard to "pin down," MVD
continues to be investigated by veterinary researchers.
Hepatic Microvascular Dysplasia is a condition in which there is mixing of venous blood and
arterial blood at the microscopic levels in the liver. If you search for information on this
condition, it is also called hepatoportal microvascular dysplasia so you may find information
using either name. This condition has been recognized in a number of small dog breeds but seems
especially prevalent in Cairn terriers and Yorkshire terriers.
It is likely that most dogs with this condition have no readily apparent clinical signs
associated with the microvascular dysplasia and are diagnosed when bile acid response testing is
done to rule out liver disease for some reason. Unfortunately, some dogs with this condition do
have clinical signs, which can include seizures or other central nervous system disorders,
gastrointestinal problems or urinary tract disease associated with ammonium biurate cystals in
the urinary tract, which form due to the liver problems.
Abnormal bile acid response testing usually provides the initial suspicion that this disease is
present. High bile acid levels can occur with portosystemic shunts, as well. It is necessary to
rule out that possibility when considering the possibility of hepatic microvascular dysplasia.
Liver biopsy adds further evidence for the presence of this condition, in part by ruling out
other liver diseases.
When dogs have microvascular dysplasia without clinical signs, their prognosis is very good. In
many instances there is not a need for therapy. In dogs that are diagnosed because they have
clinical signs, it is often possible to manage the signs through the use of dietary therapy and
medications. The dietary therapy is aimed at reducing excess protein in the diet and the
medications, including lactulose and antibiotics such as neomycin or metronidazole, which are
used to lower ammonia levels in the digestive tract and thus in the body. The prognosis is
variable for patients who have clinical signs from hepatoportal microvascular dysplasia. Some
dogs do well with therapy and live normal, or nearly normal, life spans. Others have worsening
of the clinical signs over time. I do not know of a method for predicting how well an individual
patient will do.
There are a number of reduced protein diets that might be helpful, including Hills k/d (tm) and
l/d (tm) diets, Purina's NF diet and others. Lactulose dosage is adjusted to individual patient's
needs by using it to obtain a soft but formed stool. Neomycin is usually given at a dosage of
22mg/kg of body weight twice a day and metronidazole at 7.5mg/kg twice a day. This is a lower
metronidazole dosage than is used for many other conditions. I have seen recommendations for
the use of other antibiotics but these two are the most commonly mentioned ones.
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