protein-losing gastroenteropathy
Introduction
Introduction to protein loss gastrointestinal disease Protein-losing gastroenteropathy refers to a group of diseases in which plasma proteins are lost from the gastrointestinal tract and cause hypoproteinemia due to various causes. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: dystrophic edema in children, edema
Cause
Cause of protein loss gastrointestinal disease
(1) Causes of the disease
There are many gastrointestinal diseases that can cause protein loss. Physiological studies have confirmed that only about 10% of the decomposition products of plasma albumin and globulin are excreted from the intestine. Therefore, it is considered that the gastrointestinal protein is lost under normal physiological conditions. Can be ignored.
(two) pathogenesis
There are three main pathogenesis of protein-losing gastrointestinal diseases:
1. Gastrointestinal mucosal erosion or ulceration causes protein to ooze or leak out.
2. Mucosal cells are damaged or missing, and the tight junctions between cells are broadened, resulting in increased mucosal permeability and leakage of plasma proteins into the intestinal lumen.
3. Intestinal lymphatic obstruction, increased intestinal interstitial pressure, so that protein-rich intestinal stroma can not be kept in the interstitial or absorbed into the blood circulation, but it will overflow, enter the intestinal cavity and lose, intestinal inflammation caused The mechanism of protein-losing gastrointestinal disorders is unclear, probably due to exudation of extracellular fluids and inflammatory fluids in the inflammatory zone.
Under normal circumstances, the amount of plasma protein leaking into the gastrointestinal tract is not much. It is estimated that these proteins are less than 6% of circulating albumin, which is equivalent to 10% to 20% of the daily decomposition rate of these plasma proteins, of which more than 90% are Re-absorption after digestion, therefore, gastrointestinal catabolism does not play an important role in the total catabolism of plasma proteins.
In the case of protein-losing gastrointestinal diseases, the loss of plasma protein from the gastrointestinal tract is far beyond the normal loss. The degradation rate of protein in the gastrointestinal tract can be as high as 40% to 60% of the total circulating plasma protein, protein loss. In the gastrointestinal disease, the loss of protein from the gastrointestinal tract is not related to the molecular weight of the protein. A large amount of plasma protein leaks into the gastrointestinal tract, resulting in a shortened half-life of plasma protein and an accelerated turnover rate. Studies have shown that the plasma protein is regardless of its molecular size. Leakage from the gastrointestinal mucosa, so the slower the synthesis rate and/or the longer the half-life, the more obvious the decrease of plasma protein. The half-life of albumin and IgG is longer, even if the body performs compensatory synthesis, its ability is limited, and the liver is synthesized white. The rate of protein can be increased by a factor of at most; while the synthesis of immunoglobulins such as IgG is not stimulated by a decrease in plasma concentration, so the plasma concentrations of albumin and IgG are the most severe in this disease, making patients with this disease often accompanied by Low albuminemia, rapid turnover, and short-lived plasma proteins such as transferrin, ceruloplasmin, IgM, etc. are not easily affected, and the disease is only mild The degree of fibrinogen is the shortest, and the fibrinogen has the shortest half-life and the fastest synthesis rate. Therefore, the plasma concentration is generally normal. The protein lost into the gastrointestinal cavity is decomposed into amino acids in the intestinal lumen, and the peptide is reabsorbed into the blood circulation as a nitrogen source of the body. If the amount of protein lost into the gastrointestinal tract is high, the speed of entering the intestine is faster or the peristalsis is faster, a large amount of protein is excreted from the intestine, and the protein is lost from the intestine due to obstruction of the intestinal lymphatics. At the same time, lymphocytes are lost from the intestinal tract and blood lymphocytes are reduced. In addition, other plasma components such as copper, calcium, iron, lipids, etc. can also be lost from the gastrointestinal tract.
Prevention
Protein loss gastrointestinal disease prevention
Effective treatment of the etiology of protein-losing gastrointestinal diseases is the key to prevention.
Complication
Protein loss gastrointestinal complications Complications, dystrophic edema, edema in children
1. Mainly for the reduction of plasma albumin and IgG, early fatigue, weight loss, fatigue, sexual dysfunction, severe lack of visible dry skin, desquamation, pigmentation, sometimes acne, dry hair, easy to fall off, Insufficient mentality, memory loss, excitement and excitement, and even expression of indifference, some patients, especially children may have growth and development disorders, and even death.
2. Due to the decrease of plasma protein, especially albumin, the plasma colloid osmotic pressure is reduced, the water is transferred from the blood vessel to the interstitial space, and the secondary aldosterone secretion is increased, resulting in the retention of sodium and water, and the lower extremity edema occurs during systemic edema. The most common, but also visible facial, upper limb, or periumpanic edema but systemic edema is rare.
Symptom
Protein Loss Gastrointestinal Symptoms Common Symptoms Hypoproteinemia Vitamin Deficiency in Plant Hemagglutinin... Indigestion Diarrhea
1. Clinical manifestations of primary disease
It varies according to the symptoms and signs of the primary disease.
2. Hypoproteinemia
Plasma albumin, gamma globulin (IgG, IgM, IgA, but often no IgE), reduction of human fibrinogen, transferrin, lipoprotein, serum ceruloplasmin.
3. Lower extremity edema
The decrease in plasma colloid osmotic pressure leads to an increase in fluid exudation from the capillaries. Although systemic edema is very rare, upper extremity or facial edema and/or unilateral edema are visible in lymphatic vessel expansion, and if only serum protein is reduced, albumin is reduced. Not obvious, clinical symptoms are rare.
4. Indigestion
Absorption of fats and/or sugars can cause diarrhea and clinical manifestations of fat-soluble vitamin deficiency.
5. Reduced immune function
Lymphatic obstruction, lymphopenia can reduce the cellular immune function of patients.
Examine
Examination of protein-losing gastrointestinal disorders
1.51Cr-succinylcholine chloride
The diagnosis of protein-loss gastrointestinal disorders in the past relied on the determination of fecal loss of intravascularly injected radioactive macromolecules to determine the diagnosis of protein-loss gastrointestinal disorders. Although this test is more precise, these experiments have radioactive exposure and It is cumbersome, expensive and inconvenient, and therefore does not apply to routine clinical examinations in children.
2.1-antitrypsin test
A glycoprotein synthesized by the liver, a major inhibitor of human serine kinase. This protein has a molecular weight similar to that of albumin and has 5% of total serum protein. Due to its antiproteolytic activity, 1-antitrypsin It is rarely digested by intestinal kinases. Therefore, it is mainly excreted from the feces in its original form. It is discharged, unlike other proteins or fecal nitrogen, and thus can be used as an indirect measurement of albumin lost in the gastrointestinal tract. The concentration of 1-antitrypsin in dried feces was determined by the amount of protein lost in the gastrointestinal tract.
More recently, the researchers quantified 1-antitrypsin in plasma and collected feces for the determination of this protein. The 1-antitrypsin clearance was calculated as ml/d. The literature indicates that 1-antitrypsin is randomized. There was no correlation between stool concentration and clearance rate determination. Plasma alpha 1-antitrypsin clearance is currently considered to be the best method for detecting gastrointestinal protein loss (adults or children), but this method is only suitable for detecting pylorus to colon. Protein loss, because this protein can not be measured when pH < 3 in gastric juice, and because the concentration of 1-antitrypsin in meconium is significantly higher than that in feces, this test cannot be performed in infants under 1 week.
In patients without diarrhea, 1-antitrypsin clearance was >24 ml/d; in patients with diarrhea, 1-antitrypsin clearance was >56 ml/d, indicating abnormal gastrointestinal protein loss, 1-antitrypsin clearance There was a good negative correlation between the rate and serum albumin concentration. When serum albumin <30g/L, 1-antitrypsin>80ml/d, the diagnosis was clear.
Positive fecal occult blood can make the 1-antitrypsin clearance rate abnormal, because intestinal bleeding can significantly increase the intestinal clearance rate, therefore, it is easy to cause misdiagnosis.
The sensitivity of 1-antitrypsin in the diagnosis of intestinal protein loss was 58% and specificity was 80%.
3. X-ray inspection
X-ray examination of the gastrointestinal tract is of great significance for differential diagnosis, especially the following X-ray signs: gastrointestinal mucosal folds are huge hypertrophy (see hypertrophic secretory stomach disease); malabsorption X-ray signs (intestinal dilatation, snowflake or feather) The sputum sputum is deposited, the sputum is distributed in a segmental manner, and is found in various protein-loss gastrointestinal diseases with malabsorption; the intestinal mucosa is generally thickened (lymphoma, Crohn's disease, primary intestinal lymphatics) Dilatation or secondary intestinal lymphatic obstruction; small intestinal mucosa with nodular changes after finger pressure (lymphoma, Crohn's disease), abdominal CT scan helps to find mesenteric lymphadenopathy.
4. Jejunal mucosa biopsy
Multiple jejunal mucosal biopsy is useful for the diagnosis of lymphoma, celiac disease, eosinophilic gastroenteritis, collagen gastroenteritis, intestinal lymphatic dilatation, and Whipple disease.
5. Lymphangiography
Transpedicular lymphangiography is helpful in identifying congenital or secondary intestinal lymphatic dilatation. The former can be seen in peripheral lymphatic dysplasia and thoracic duct lesions. The contrast agent stays in the retroperitoneal lymph nodes, but the mesenteric lymphatic system does not fill. The contrast agent can be refluxed to the dilated mesenteric lymphatics and spilled into the intestinal or peritoneal cavity.
6. Ascites examination
Those with ascites can be used for diagnostic puncture, ascites cells, proteins, chylomicrons, enzymes, malignant cells, etc.
Diagnosis
Diagnosis and differentiation of protein-losing gastrointestinal diseases
Diagnostic criteria
Clinically, hypoproteinemia of unknown origin, such as malnutrition or wasting disease caused by liver and kidney disease, should be suspected and the disease; if accompanied by gastrointestinal disease, it should be considered The diagnosis of this disease should include the following three aspects:
1. There is hypoproteinemia: clinical manifestations of edema, low plasma protein.
2. There is evidence that protein is lost from the gastrointestinal tract: the determination of fecal 51Cr albumin and the determination of 1 antitrypsin clearance have great significance for the diagnosis of protein loss from the gastrointestinal tract, but its detection method is complex and difficult to popularize in clinical practice. There is no simple clinical trial to determine gastrointestinal protein loss.
3. Etiology diagnosis: comprehensive analysis and judgment can be made according to medical history, clinical manifestations and necessary experimental examinations or special examinations.
Differential diagnosis
According to the medical history, clinical manifestations, necessary laboratory tests, special examinations and imaging examinations, most of the primary diseases can be diagnosed, mainly due to the differentiation of hypoproteinemia caused by other causes.
1. Decompensated cirrhosis: clinical manifestations of liver disease, liver shrinkage, splenomegaly and other portal hypertension, and liver dysfunction, etc., the characteristics of these cirrhosis can help identify it.
2. Nephrotic syndrome: nephrotic syndrome has a large amount of plasma protein (especially albumin) lost from the urine, urine protein excretion rate> 3.5g / d, mainly albumin, plasma cholesterol increased, with triacylglycerol and The concentration of low-density lipoprotein is increased, and the urine test has red blood cells, granular casts, and renal function damage and hypertension.
3. Plasma protein hyperactivity disease: long-term fever, hyperthyroidism, malignant tumors, diabetes, etc., can cause excessive consumption of hypoproteinemia, but each has its own disease history and clinical features, there are specific experiments Auxiliary examinations such as the room were abnormal, and no evidence of excessive loss of plasma protein from the gastrointestinal tract was found.
4. Protein digestion and malabsorption: mainly seen in most of the stomach resection, chronic pancreatitis and some intestinal malabsorption diseases, increased protein and its incomplete decomposition products in the feces, often accompanied by increased fecal fat content, pancreatic exocrine function test and corresponding The intestinal absorption function test is abnormal, and there is no evidence that the plasma protein is excessively lost from the gastrointestinal mucosa. However, it should be noted that some diseases causing protein malabsorption can also cause protein-losing gastrointestinal diseases, so it is not excluded. The possibility of simultaneous or sequential existence.
5. Congenital hypoalbuminemia: There is obvious hypoalbuminemia in childhood, serum albumin is often <10g / L, erythrocyte sedimentation rate is high, serum cholesterol is high, globulin is normal or increased.
Sometimes it is necessary to identify with long-term dialysis, multiple chest pumping, ascites, insufficient protein intake, major bleeding, large-area burns, etc., according to the unique medical history, clinical manifestations and no plasma protein found from the stomach. The basis for intestinal loss is identified.
