gastric lost protein
Introduction
Introduction Gastric loss protein, also known as 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. Clinical manifestations vary depending on the symptoms and signs of the primary disease.
Cause
Cause
The cause of gastric loss protein:
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 the protein-rich intestinal stroma can not be kept in the interstitium or absorbed into the blood circulation, but it will overflow and enter the intestinal lumen and be lost. The mechanism by which intestinal inflammation causes protein-losing gastrointestinal disorders is unclear, probably due to exudation of extracellular fluid 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 protein-losing gastrointestinal disorders, plasma protein loss from the gastrointestinal tract far exceeds 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. Loss of protein from the gastrointestinal tract is not related to the molecular weight of the protein in protein-losing gastrointestinal disorders. 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 in this disease, the plasma protein is leaked from the gastrointestinal mucosa regardless of its molecular size, so the slower the synthesis rate and/or the longer the half-life, the more obvious the decrease of plasma protein. Albumin and IgG have a long half-life, and even if the body performs compensatory synthesis, its ability is limited, and the rate of synthesis of albumin in the liver can be increased by a factor of at most; and the synthesis of immunoglobulins such as IgG is not stimulated by a decrease in plasma concentration. Therefore, the plasma concentrations of albumin and IgG are the most severe in this disease, making patients with this disease often accompanied by hypoalbuminemia. Plasma proteins with fast turnover and short half-life, such as transferrin, ceruloplasmin, IgM, etc., are not easily affected, and this disease is only slightly reduced. The fibrinogen has the shortest half-life and the fastest synthesis rate, so the plasma concentration is generally normal. The protein lost into the gastrointestinal cavity is decomposed into amino acids and peptides in the intestinal lumen and reabsorbed into the blood circulation. As a nitrogen source of the body, if the amount of protein lost into the gastrointestinal tract is large, the rate of entering the intestine is faster or The intestinal peristalsis is faster, and a large amount of protein is excreted from the intestine. If the protein is lost from the intestine due to obstruction of the intestinal lymphatics, lymphocytes may be lost from the intestine and blood lymphocytes may be reduced. In addition, other plasma components such as copper, calcium, iron, lipids, and the like can also be lost from the gastrointestinal tract.
Examine
an examination
Related inspection
Gastrointestinal dysfunction test for enzyme tumor markers
Diagnosis of gastric loss proteins:
1. The clinical manifestations of the primary disease vary depending on 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 leakage of fluid from the capillaries increases due to a decrease in plasma colloid osmotic pressure. Although systemic edema is very rare, upper extremity or facial edema and/or unilateral edema are visible in lymphatic vessel expansion. If it is only serum protein and the reduction of albumin is not obvious, clinical symptoms are rarely seen.
4. Indigestion of fat and/or carbohydrate malabsorption can cause clinical manifestations of diarrhea and fat-soluble vitamin deficiency.
5. Immune function reduces lymphatic obstruction, lymphopenia can reduce the cellular immune function of patients.
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 a clinical manifestation of edema and low plasma protein in patients with hypoproteinemia.
2. There is evidence that protein is lost from the gastrointestinal tract. Determination of fecal 51Cr albumin and 1 antitrypsin clearance rate have great significance for the diagnosis of protein loss from the gastrointestinal tract, but its detection method is complex and difficult to popularize clinically. There is currently no simple clinical trial to determine gastrointestinal protein loss.
3. The cause of diagnosis can be comprehensively analyzed and judged according to the medical history, clinical manifestations and necessary experimental examinations or special examinations.
Diagnosis
Differential diagnosis
Differential diagnosis of gastric loss proteins:
According to 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 has a history of liver disease, clinical manifestations of portal hypertension such as liver shrinkage, splenomegaly, and abnormal liver function. The characteristics of these cirrhosis contribute to their identification.
2. Nephrotic syndrome Nephrotic syndrome A large number of plasma proteins (especially albumin) are lost from the urine, and the urinary protein excretion rate is >3.5 g/d, mainly albumin. Increased plasma cholesterol with increased concentrations of triacylglycerol and low density lipoprotein. Urine tests have red blood cells and granules. There may also be manifestations of impaired renal function and hypertension.
3. Plasma protein hyperactivity disease Long-term fever, hyperthyroidism, malignant tumors, diabetes, etc., can cause hyperphagic hyperproteinemia. However, each has its own disease history and clinical features, and there are specific laboratory and other auxiliary examination abnormalities. There is no evidence of excessive loss of plasma proteins from the gastrointestinal tract.
4. Protein digestion and malabsorption is mainly seen in most gastric resection, chronic pancreatitis and certain intestinal malabsorption diseases. The protein in the feces and its incomplete decomposition products increase, often accompanied by increased fecal fat content. The pancreatic exocrine function test and the corresponding small intestinal absorption function test were abnormal, and no evidence of excessive loss of plasma protein from the gastrointestinal mucosa was found. However, it should be noted that some diseases that cause protein malabsorption can also cause protein-losing gastrointestinal diseases, so the possibility that the two can exist simultaneously or sequentially is not excluded.
5. Congenital hypoalbuminemia has obvious hypoalbuminemia in childhood, serum albumin often needs long-term dialysis, multiple times of massive chest pumping, ascites, insufficient protein intake, massive bleeding, large area The diagnosis of hypoproteinemia caused by burns and the like. According to the unique medical history, clinical manifestations and the lack of evidence that plasma proteins are lost from the gastrointestinal tract are identified.
diagnosis:
1. The clinical manifestations of the primary disease vary depending on 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 leakage of fluid from the capillaries increases due to a decrease in plasma colloid osmotic pressure. Although systemic edema is very rare, upper extremity or facial edema and/or unilateral edema are visible in lymphatic vessel expansion. If it is only serum protein and the reduction of albumin is not obvious, clinical symptoms are rarely seen.
4. Indigestion of fat and/or carbohydrate malabsorption can cause clinical manifestations of diarrhea and fat-soluble vitamin deficiency.
5. Immune function reduces lymphatic obstruction, lymphopenia can reduce the cellular immune function of patients.
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 a clinical manifestation of edema and low plasma protein in patients with hypoproteinemia.
2. There is evidence that protein is lost from the gastrointestinal tract. Determination of fecal 51Cr albumin and 1 antitrypsin clearance rate have great significance for the diagnosis of protein loss from the gastrointestinal tract, but its detection method is complex and difficult to popularize clinically. There is currently no simple clinical trial to determine gastrointestinal protein loss.
3. The cause of diagnosis can be comprehensively analyzed and judged according to the medical history, clinical manifestations and necessary experimental examinations or special examinations.
