Occurs when the intestinal mucosa fails to function as a barrier separating the body from the outside world.
The two main pathological mechanisms that compromise epithelial retention of interstitial, contents are direct damage to the mucosa and failed lymph drainage, causing backflow through the epithelium into the lumen.
Some diseases involve other mechanisms, in addition to the above
PLE, is an uncompensated loss of plasma proteins in the intestine, indicated by elevated alpha 1 antitrypsin levels in the stool, which leads to panhypoproteinemia in the absence of liver or kidney disease.
Results in the leakage of serum fluids and proteins into the stool with diarrhea, and hypoalbuminemia..
May be related to loss of heparin sulfate proteins normally expressed on intestinal cells.
Refers to any condition of the gastrointestinal tract that results in a net loss of protein from the body.
PLE is manifested, as non-selective depletion of all plasma proteins includes albumin, immunoglobulins, and acute phase reactants.
Mucosal erosion, occurs in inflammatory bowel disease, peptic, ulcer, infections, and carcinoma and cause loss of plasma proteins into the gut lumen.
This is commonly seen in Crohn’s disease, ulcerative, colitis, erosive, gastritis, and pseudomembranous colitis.
Other inflammatory conditions with erosive, PLE include: sarcoidosis, graft versus host disease, G.I. amyloidosis.
Infections can precipitate inflammatory mucosal damage as well.
Uncommonly malignancies involving epithelial tumors of the esophagus, stomach and intestine and mucosal metastatic disease can lead to mucosal drainage and PLE.
Where really, PLE is seen in AIDS who have Kaposi’s sarcoma and patients with organ transplantation.
A selective protein deficiency indicates conditions, other than PLE: hypoalbuminemia with normal immunoglobulin levels may reflect liver disease, or reduced low molecular weight proteins, indicate the nephrotic syndrome, or other kidney diseases, and low immunoglobulin level suggest immunodeficiency.
PLE, involves the wasting of all other intestinal fluid components.
The pressure of each heartbeat drives fluid with albumin, immunoglobulins, and other serum components from peripheral blood vessels into the interstitium.
Inflammation permits capillary permeability, and interstitial influx.
Interstitial fluid is recirculated by the lymphatics, which are tributaries to the arterial venous circulation that start as opened vessels in the interstitium.
Lymphatics have valves for one-way flow down the shallow pressure gradient to the thoracic duct, which returns to the subclavian vein.
Lymph flow is screened for pathogenic agents through lymph nodes.
Food, stuffs, nutrients, and micro nutrients, such as calcium, magnesium, zinc, iron, and copper, or absorbed in the gut interstitium of the villus, which contains a central intestinal, lymphatic or lacteal.
Other blood constituents, including hematopoietic cells, fats, and vitamins can also enter the lymph.
Epithelial cells connected by tight junctions guard the integrity and composition of the gut interstitium.
Proteins losing enteropathy occurs when the intestinal epithelium is breached and the intestitial fluid leaks into the gut lumen.
Interstitial fluid is recirculated by lymphatics, which are tributaries to the arterial venous circulation.
PLE involves the wasting of interstitial fluid compartments.
Each heartbeat drives fluid, containing albumin, immunoglobulins, and other serum components from peripheral blood vessels into the interstitium.
The signs/symptoms are consistent with diarrhea, fever, and general abdominal discomfort.
Presenting features of PLE include: hypoproteinemia, edema, nutritional deficiencies, infections, G.I. symptoms of diarrhea, steatorrhea, abdominal pain, and vomiting.
Hypoproteinemia is nonselective with decreased albumin and immunoglobulin levels.
Facial edema, and edema of the arms and legs, and effusions of the peritoneum, pleura and pericardium caused by reduced oncotic pressure in the blood.
Infections can result from hypogammaglobulinemia and lymphopenia.
In children, malabsorption and malnutrition may be severe, resulting in retarded growth and development.
Swelling of the legs can occur.
The causes of protein-losing enteropathy include GI conditions:
Inflammatory bowel disease.
Idiopathic ulcerative jejunoileitis.
Systemic lupus erythematosus (SLE)
Common variable immunodeficiency
Primary intestinal lymphangectasia
The process is a result of plasma proteins loss, which enters GI tract.
It is a complication of a disorder, be it lymphatic obstruction or mucosal disease.
Diagnosis is made by excluding other causes of protein loss, and endoscopy can be used to localize its cause.
Fecal excretion of alpha 1-antitrypsin is a marker of protein losing enteropathy,
Treatment depends upon the underlying process.