Protein-losing enteropathy in dogs: PLE symptoms and treatment

Overview

PLE is a syndrome whose shared feature is protein loss through the intestine. It does not automatically mean the same disease as chronic inflammatory enteropathy. Heart disease outside the digestive tract can also disrupt intestinal lymph drainage.

Albumin is a circulating blood protein that helps keep fluid inside blood vessels. Reduced albumin can allow fluid into the abdomen, chest or tissues beneath the skin. Globulins may also decrease alongside albumin in PLE. Normal globulins do not exclude intestinal protein loss.

Small amounts of blood proteins enter even a healthy dog's intestine and are normally broken down and reabsorbed. In PLE, losses exceed the body's ability to produce replacement protein. Protein loss can also occur through the kidneys, a form called protein-losing nephropathy, or PLN.

Causes

Lining damage and lymphatic leakage

In severe intestinal inflammation, protein crosses the damaged lining into the intestine. Dietary protein absorption can also decline. Intestinal lymphoma and other tumours can cause protein loss. Intestinal infections are other possible underlying causes.

Lymphangiectasia means dilation of intestinal lymphatic vessels. Ruptured lymphatic vessels release protein-rich lymph into the intestine. Severe fat malabsorption can accompany this.

Lymphatic disease may be primary or develop when inflammation or a tumour obstructs lymph flow. Inflammation and lymphatic dilation can coexist in one dog. Leaking lymph may sustain intestinal inflammation. Chronic inflammation can in turn impair lymph drainage and cause secondary lymphangiectasia.

After absorption, long-chain dietary fats travel through intestinal lymphatic vessels. Fat type therefore matters as well as total fat quantity. Intestinal ulcers and longstanding foreign body irritation are other possible lining-damaging causes of protein loss.

Risk factors

PLE occurs in many breeds, but Yorkshire Terriers and Soft-Coated Wheaten Terriers, among others, are overrepresented. Primary lymphangiectasia is recognised particularly in Yorkshire Terriers and Norwegian Lundehunds. In Soft-Coated Wheaten Terriers, intestinal protein loss can coexist with renal protein loss.

In one study of 30 Yorkshire Terriers, median age at diagnosis was 7 years, ranging from 1–12 years. Females accounted for 20/30, but this describes the study group rather than sex risk across all breeds. Severe intestinal inflammation, tumours and lymphatic drainage disorders also matter in dogs outside these breeds.

Typical symptoms

Signs may mainly involve digestion or fluid accumulation from protein deficiency.

• Diarrhoea may be continuous, fluctuating or watery.
• Weight may fall despite continued eating.
• Your dog becomes more subdued than usual.
• Intermittent vomiting may occur.
• Appetite may initially increase but decline as disease worsens.
• The abdomen may bulge because fluid accumulates.
• Soft swelling may develop in the limbs or beneath the abdomen.
• Calcium or magnesium deficiency can cause muscle tremors or seizures.

Normal stools do not exclude PLE. Muscle loss and poor nutritional condition have been found in around 2/3 of affected dogs at diagnosis. Fluid accumulation can therefore coexist with obvious muscle wasting.

Complications and consequences

Increased blood clotting tendency has been found in 63–100% of studied dogs with PLE. This predisposes them to thrombotic complications. The figure describes clotting tendency rather than the proportion developing a confirmed clot. Blood calcium, magnesium and cholesterol may decrease.

The underlying cause particularly influences prognosis. In the Yorkshire Terrier study, median survival among responders was 44 months. Non-responders had a median survival of 12 months. These figures do not predict survival for an individual dog of another breed. Across studies totalling 445 dogs with PLE, 54% died or were euthanased because of the disease. Severe back muscle loss was associated with a lower chance of remission within 6 months in inflammatory or lymphangiectasia-associated PLE.

Diagnosis at the vet

Where is protein being lost?

Tests include a blood count, organ biochemistry, electrolytes, urinalysis and faecal parasite examination. Low albumin can also result from renal loss or reduced liver protein production. Renal protein loss is assessed with a urine protein-to-creatinine ratio. Appropriate liver function tests investigate hepatic causes.

Vitamin B12 measurement identifies possible deficiency. Blood TLI investigates pancreatic insufficiency. Addison's disease is a differential diagnosis causing similar intestinal signs. Faecal alpha-1-proteinase inhibitor measurement can demonstrate intestinal protein loss in an adult dog even without low blood albumin.

What do imaging and biopsies show?

Ultrasound assesses intestinal wall structure, lymph nodes and possible tumours. Bright mucosal striations may suggest dilated lymphatic vessels. Fine-needle samples of abnormal lymph nodes or other changes can investigate tumour disease.

Intestinal lining biopsies may establish the cause. Endoscopy may also require samples from the final small intestinal section. Tissue samples help identify infections and tumours as well as inflammation and lymphatic disease underlying protein loss. For suspected inflammatory enteropathy, the aim is good-quality samples, ideally at least 10–15 biopsies from each intestinal site examined. Lymphangiectasia can be patchy and missed by sampling. Identified inflammation therefore does not exclude concurrent lymphatic protein loss.

Severely reduced albumin increases anaesthetic risks. Canine albumin or plasma may be needed to support circulation before endoscopy. Surgery allows full-thickness intestinal biopsies. However, poor healing can increase the risk of wound breakdown.

Treatment

Diet is central to treatment

Treatment depends on the cause of protein loss, and your vet prescribes medication. In lymphangiectasia, a low-fat diet reduces lymphatic dilation and rupture. Low-fat diets used for this contain less than 2 grams of fat per 100 kilocalories.

In lymphangiectasia-associated PLE responding poorly to glucocorticoids or relapsing during medication reduction, fat restriction helped 19/24 dogs, or 79%. This is not a success rate for every dog with PLE. Concurrent inflammatory enteropathy may also prompt selection of a hydrolysed or limited-protein-source diet. During a dietary trial, your dog eats only the agreed food for at least 2 weeks. In inflammatory enteropathy, dietary effects often appear within 10–14 days, but some dogs respond more slowly.

Medicines and hospital care

Inflammatory protein loss may need a glucocorticoid or another immune-modifying medicine if diet is insufficient. Lymphatic dilation alone does not provide the same grounds for broad immunosuppression as uncontrolled inflammatory enteropathy. A poor response also prompts dietary reassessment because a food change may help despite ongoing signs on medication.

Confirmed B12 deficiency is corrected. Vitamin levels are checked after treatment. Antithrombotic medication may be considered because of clot risk. No standard preventive method has been established as suitable for every dog with PLE. Severe protein deficiency may require hospitalisation and plasma transfusion. Fluid impairing breathing can be drained from the chest or abdomen.

Monitoring response

Albumin is generally monitored every 1–2 weeks initially. Once it is normal and your dog is stable, intervals can increase to 2–3 months. Weight, muscle condition, stools and possible medication effects are assessed too. An incomplete response may require new biopsies to investigate intestinal lymphoma missed initially.

Nutritional adequacy and limits of supportive care

An extremely low-fat home-made diet may lack essential fatty acids. Ideally, a home-fed dog's recipe is balanced with help from an animal nutrition specialist. B12 deficiency has been reported in 43–75% of dogs with PLE. Deficiency can itself maintain digestive signs.

Low vitamin D may also correct with successful intestinal disease treatment. One controlled PLE study found no clear clinical benefit from vitamin D supplementation. Levels normalised in 80% of placebo-group dogs in that study. Because supplementation carries an excess-intake risk, additional treatment requires vitamin D and ionised calcium monitoring.

Plasma benefit is limited by potentially large fluid volumes required. Transfused protein may also continue leaking into the diseased intestine. Transfusions are therefore reserved for selected high-risk situations.

Prevention

Different diseases underlie PLE, so preventing recurrence depends on controlling the individual cause. A diet that settles inflammatory enteropathy signs is continued for at least 12 weeks before any transition to another food. Dogs with PLE may benefit from continuing a successful diet long term. In lymphangiectasia, fat restriction reduces lymphatic damage.

Poor dietary adherence has been associated with inflammatory PLE relapse. Some Soft-Coated Wheaten Terrier breeding guidelines advise avoiding dogs with signs suggesting PLE or PLN, or an offspring affected by either. The breed's PLN genetic test screens for the renal form.

Important for dog owners

Record stool consistency, vomiting, appetite and daily food intake. Bring details of every food, treat and supplement, plus previous laboratory results. Follow the agreed diet for treats too. Before discharge, ask for a written plan for refusal to eat or a new diarrhoea episode.

Monitor back and thigh muscles alongside weight, and watch abdominal and limb swelling. Agree albumin checks and medication monitoring from the outset. Do not change medicines yourself according to a good or bad day. Report new vomiting, black stools or clearly increased tiredness. New breathing difficulty or collapse is an emergency.

Frequently asked questions

Can a dog have PLE without diarrhoea?

Yes. Some affected dogs have normal stools. Weight loss, tiredness or swelling of the abdomen and limbs may draw attention instead. This combination needs investigation even without visibly changed stool consistency.

Does low albumin always mean intestinal protein loss?

Reduced albumin may result from the kidneys or impaired liver protein production instead of the intestine. Urine protein tests and liver function tests help distinguish these causes. Low albumin alone therefore does not justify choosing intestinal disease medication without closer investigation.

Is PLE the same as IBD?

PLE describes protein lost into the intestine and may accompany chronic inflammatory enteropathy. Other causes include lymphatic disease, tumours and infections. Investigations distinguish them because treatment does not rely on the same inflammation control for every affected dog.

Is higher-protein food enough to treat it?

Treatment must address why protein is lost into the intestine. In lymphatic protein loss, fat restriction reduces lymphatic dilation and rupture. Food is therefore not selected by protein percentage alone: composition is tailored to the diagnosed disease and previous dietary history.

How long can a dog with PLE live?

The cause and treatment effectiveness influence survival. In a Yorkshire Terrier study, median survival was 44 months in responders and 12 months in non-responders. An individual's condition is assessed through the cause, nutritional status, albumin progress and actual response achieved.