Protein-Losing Enteropathy (PLE)

Outline

Overview
Signalment
Signs
Causes and Risk Factors

BASICS

Overview

GI protein loss may result from mucosal ulceration and plasma exudation, lymphatic obstruction with leakage and rupture of dilated lacteals, passive diffusion through intracellular spaces, active secretion by mucosal cells, intracellular loss, increased permeability of capillaries and venules, and disordered cell metabolism
Excessive loss of proteins into the GI tract causes hypoproteinemia. The early intestinal protein loss in PLE involves relatively larger quantities of albumin than globulins. If severe, hypoalbuminemia may result in the development of subcutaneous edema. In the later stages of the disease, all protein fractions may be lost. If large colon function is not impaired, feces frequently normal
PLE usually a progressive condition; however, accelerated protein leakage can occur in acute GI diseases

Signalment

Eosinophilic gastroenteritis and GE most common in young adult horses. GE more common in Standardbreds
Intestinal lymphosarcoma and intestinal parasitism occur in horses of all ages
Lawsonia intracellularis in weanling foals
Ponies and young animals are reportedly more susceptible to NSAID toxicity

Signs

Affected animals show some of the following:

Chronic, progressive weight loss
Dependent edema
Depression
Anorexia
Reduced performance
Lethargy
Intermittent or chronic colic
Diarrhea not present in PLE cases with lesions primarily in the small intestine
±Skin lesions
±Enlarged peripheral lymph nodes
Acute colic and endotoxemia may occur in horses with intestinal parasitism or NSAID toxicity
Per rectum examination—may palpate enlarged mesenteric lymph nodes; thickened bowel wall

Causes and Risk Factors

Chronic inflammatory bowel diseases (lymphocytic–plasmacytic enterocolitis, GE, idiopathic eosinophilic enterocolitis, multisystemic eosinophilic epitheliotropic disease), GI neoplasia, parasitic thrombosis of cranial mesenteric artery (Strongylus vulgaris), cyathostomiasis, NSAID toxicity, acute salmonellosis, other causes of acute enterocolitis, proliferative enteropathy due to L. intracellularis, congestive heart failure, amyloidosis.

Diagnosis ⬆ ⬇

Outline

Differential Diagnosis
CBC/Biochemistry/Urinalysis
Other Laboratory Tests
Diagnostic Procedures

DIAGNOSIS

Differential Diagnosis

Diagnosis of PLE usually made after protein loss through other routes and inability to synthesize protein ruled out.

CBC/Biochemistry/Urinalysis

Hypoalbuminemia
Decreased, normal, or increased plasma globulin concentrations
Serum protein electrophoresis—preferred test for quantifying protein fractions
Panhypoproteinemia
Hypocalcemia may occur in conjunction with hypoalbuminemia because a large portion of serum calcium is protein bound
Anemia

Other Laboratory Tests

Coprology for parasitic ova and larvae
Fecal PCR test for L. intracellularis in young foals and weanlings
Ultrasonography—to determine intestinal wall thickness
Oral d-xylose absorption test—preferable to oral glucose tolerance test
Abdominocentesis—cytology to detect neoplasia. Normal abdominal fluid does not rule out neoplasia

Diagnostic Procedures

Immunoelectrophoresis
Gastroduodenoscopy
Rectal mucosal biopsy—histopathologic examination
Exploratory laparotomy and intestinal biopsy—often necessary for definitive diagnosis

Treatment ⬆ ⬇

TREATMENT

Treatment depends on the primary disease causing PLE or treating the hypoproteinemia
Treatment frequently unrewarding
Prognosis for recovery generally guarded to very poor
Dietary management—provide palatable, easily assimilated, high-energy and -protein sources; electrolyte mixtures; zinc, copper, iron, fat- and water-soluble vitamins

Medications ⬆ ⬇

MEDICATIONS

Drug(s) of Choice

Plasma transfusion is usually indicated when total plasma protein concentration is or falls below 40 g/L (4 g/dL). The effect may be minimal owing to the continued protein losses
If horse is receiving NSAIDs, therapy should be discontinued
When internal parasites are suspected as the cause, administer larvicidal anthelmintics (moxidectin 0.4 mg/kg PO, ivermectin 0.2 mg/kg PO, or fenbendazole 10 mg/kg daily PO for 5 days)
For L. intracellularis proliferative enteropathy—oral macrolides (azithromycin, clarithromycin, erythromycin) alone or in combination with or rifampin (rifampicin), or oral doxycycline for minimum of 21 days
±Total parenteral nutrition—in valuable horses
Corticosteroid therapy often ineffective in treating chronic inflammatory bowel disease