Overview
Protein-losing gastroenteropathies are a group of disorders characterized by hypoproteinemia due to loss of plasma proteins from the gastrointestinal tract from a variety of causes.
Causes
Many gastrointestinal disorders can cause protein loss.
The pathogenesis of protein-losing gastroenteropathy is:
1. erosion or ulceration of the gastrointestinal mucosa leading to protein leakage or exudation;
2. mucosal cell damage or loss, leading to increased mucosal permeability and leakage of plasma proteins into the intestinal lumen;
3. intestinal lymphatic vessel obstruction, so that the protein-rich intestinal interstitium can not be maintained in the interstitium or absorbed into the blood circulation, overflow into the intestinal lumen and loss. The mechanism of protein-losing gastroenteropathy due to intestinal inflammation may be due to leakage of extracellular and inflammatory fluid from the inflamed area.
Symptoms.
Clinical manifestations vary depending on the signs and symptoms of the primary disease.
1. Lower extremity edema
Unilateral edema is seen to arise in lymphatic dilatation due to a decrease in plasma colloid osmolality, resulting in increased fluid exudation from the capillaries.
2. Indigestion
Due to malabsorption of fats and/or sugars, clinical signs of diarrhea and fat-soluble vitamin deficiency may occur.
3. Decreased immune function
Obstruction of lymphatic vessels and lymphopenia result in decreased cellular immunity in patients.
4. Hypoproteinemia
Decrease in plasma albumin, gamma globulin (IgG, IgM, IgA, but often without IgE), human fibrinogen, transferrin, lipoproteins, serum copper blue protein.
Examination
1. Laboratory tests
(1) 51Cr-succinylcholine chloride The diagnosis of protein-losing gastroenteropathy is based on the measurement of fecal loss of intravascularly injected radioactive macromolecules. Because of the exposure to radioactivity and because it is cumbersome, expensive, and inconvenient, it is not indicated for routine clinical examination of children.
(2) α1-antitrypsin test α1-antitrypsin is rarely digested by intestinal kinases and is excreted from the feces primarily in its native form. It can be used as an indirect measurement of albumin lost in the gastrointestinal tract.
2. Other
(1) X-ray examination The following gastrointestinal X-ray signs: huge hypertrophy of the gastrointestinal mucosal folds, X-ray sign of malabsorption, generalized thickening of the mucosal folds of the small intestine, finger-pressure sign of nodular changes in the mucosa of the small intestine, which are significant for differential diagnosis. Abdominal CT scan can help to detect mesenteric lymph node enlargement.
(2) Jejunal mucosal biopsy Multiple pieces of jejunal mucosal biopsy are meaningful in the diagnosis of lymphoma, celiac disease, eosinophilic gastroenteritis, collagenous gastroenteritis, intestinal lymphangiectasia, Whipple’s disease, and so on.
(3) Lymphangiography Congenital or secondary intestinal lymphangiectasia can be differentiated by pedicle lymphangiography. In the former case, peripheral lymphatic dysplasia and thoracic duct lesions can be seen, and the contrast agent is retained in the retroperitoneal lymph nodes, but the mesenteric lymphatic system is not filled; in the latter case, the contrast agent can reflux into the dilated mesenteric lymphatic vessels and overflow into the intestinal or peritoneal cavity.
(4) Ascites examination Diagnostic puncture can be done for those with ascites to check the ascites cells, protein, celiac disease, enzymes, malignant cells, and so on.
Diagnosis
Any unexplained hypoproteinemia with clinical manifestations of gastrointestinal diseases and exclusion of malnutrition or wasting disease caused by liver and kidney diseases should be suspected.
The diagnosis of this disease should include the following three aspects:
1. the presence of hypoproteinemia with clinical manifestations of edema and low plasma protein.
2. Evidence of protein loss from the gastrointestinal tract. Fecal 51Cr albumin measurement and α1 antitrypsin clearance measurement are of great significance in diagnosing protein loss from the gastrointestinal tract.
3. Etiological diagnosis can be based on the history, clinical manifestations and necessary experimental or special examinations for comprehensive analysis and judgment.
Differential diagnosis
This disease should be differentiated from cirrhosis, nephrotic syndrome, hyperthyroidism, malignant tumors, diabetes mellitus, congenital hypoalbuminemia and other conditions.
Complications
This disease may cause the following complications: plasma albumin reduction, IgG reduction, generalized or localized edema due to sodium retention, growth retardation in children, death.
Treatment
Various effective therapeutic measures should be used according to the different causes of the disease. Symptomatic treatment, including low-salt diet, diuretics, etc., static injection of human albumin is effective for a short time.
1. Treatment of etiology
Once the cause of the disease is clear, corresponding treatment should be given. It should be especially pointed out that some causes of this disease need surgical treatment to cure, such as malignant tumors, constrictive pericarditis, giant hypertrophic gastritis and so on. Symptomatic supportive therapy can only be used when the cause of the disease is not yet known, or when the cause of the disease cannot be effectively treated.
2. Symptomatic supportive treatment
(1) Diet A high-protein, high-calorie diet should be given, and a salt-restricted diet should be given to those with high levels of edema; for patients with lymphatic obstructive disease, the diet should be given as a low-fat or medium-chain triacylglycerol (MCT) treatment in order to reduce the load on the intestinal lymphatic vessels.
(2) Diuretics Potassium-preserving and potassium-excreting diuretics, such as spironolactone and thiazides, can be applied in combination, and tachycardia-type strong diuretics can be used to reduce edema and ascites if necessary.
(3) Correcting hypoproteinemia As mentioned before, static injection of human albumin only has temporary effect, generally do not rely on human albumin infusion to correct hypoproteinemia, but through the etiological treatment and dietary regulation to improve plasma protein concentration.
(4) Symptomatic treatment: antibiotics should be applied to those with infection, vitamin supplementation should be applied to those with vitamin deficiency, and calcium and magnesium should be supplemented to those with convulsions. Surgical treatment for limited protein loss gastroenteropathy can be localized lesion excision surgery. If the lymphatic dilatation is limited to a section of small intestine, partial resection of small intestine can be performed.
Questions you may be concerned about
Protein-losing gastroenteropathy, how to treat
Protein-losing gastroenteropathy is a group of diseases characterized by the loss of proteins from the gastrointestinal tract, which is commonly caused by gastric ulcer, giant hypertrophic gastritis, acute enteritis and other diseases. It can be handled by general treatment, drug treatment and other methods.
1. Treatment of the cause
(1) Gastric ulcer: the patient’s gastric mucosa is defective under the attack of high gastric acid and pepsin, resulting in protein exudation. Bismuth potassium citrate and omeprazole can be used.
(2) Giant hypertrophic gastritis: gastritis caused by extensive thickening of the patient’s gastric wall, leading to mucosal damage and protein leakage. Caused by Helicobacter pylori infection usually quadruple drug therapy, as described above. Patients caused by cytomegalovirus infection may be treated with ganciclovir.
(3) Acute enteritis: patients leak extracellular and inflammatory fluid from inflamed areas of the gut, leading to protein-losing gastroenteropathy. Patients may use montelukast to protect the intestinal mucosa. If acute enteritis is caused by bacterial infection, antibiotics such as ofloxacin and cefoperazone can also be used for treatment.
2. Symptomatic treatment
(1) Dietary adjustment: due to the loss of a large amount of protein in the body, a high protein, high calorie diet should be given, such as lean meat, eggs, milk and so on.
(2) Drug therapy: if the patient has hypoproteinemia, it can be temporarily corrected by transfusion of human albumin.
Protein-losing gastrointestinal disease is caused by a variety of factors, and it is recommended that patients actively search for the cause of the disease under the guidance of the doctor and carry out treatment. Medications should be used in accordance with medical advice.