Intestinal villous atrophy

Introduction Intestinal villus atrophy is one of the clinical manifestations of gastrointestinal syndrome with cancer. Gastrointestinal cancer syndrome refers to some syndromes associated with certain cancers of the digestive system. It does not include the general systemic effects of tumors, such as jaundice, fever, weight loss, etc., nor does it refer to the parenteral manifestations of classical digestive tract endocrine tumors.

Cause

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. The half-life of albumin and IgG is long, 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 immunoglobulin 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.

an examination

Related inspection

Gastrointestinal CT examination of gastrointestinal diseases, ultrasound examination, gastrointestinal dysfunction, fiberoptic colonoscopy

Clinical manifestation

First, protein loss gastrointestinal disease

More common in gastric cancer and colon cancer, due to the necrosis of cancer tissue, the permeability of the corresponding gastrointestinal mucosa is increased, and a large amount of plasma protein is lost from the gastrointestinal tract. Carcinoma compresses and blocks lymphatic vessels, causing obstruction of gastrointestinal lymphatic drainage, lymphatic deposition, rupture, and loss of large amounts of protein. Clinically, hypoproteinemia and edema are the main manifestations.

Second, small intestine villi atrophy

Can be seen in colon cancer, rectal cancer, mainly manifested as diarrhea.

Third, diarrhea, dehydration and shock

Mainly found in colonic villus adenomas, occasionally in the digestive tract APUD system tumors, such as VIP tumors, gastrinoma and pancreatic polypeptide tumors. It is characterized by secretory diarrhea, which can lead to loss of water, electrolyte imbalance, and even shock.

diagnosis

A protein-deprived gastrointestinal disorder can be confirmed by a radionuclide-labeled macromolecular substance digestive tract excretion test, or an 1-antitrypsin test.

Differential diagnosis

It should be differentiated from protein loss caused by other causes or pathways.

1. Decompensated cirrhosis: clinical manifestations of liver disease, liver shrinkage, splenomegaly and other portal hypertension, and abnormal liver function. The characteristics of these cirrhosis contribute to their identification.

2. Nephrotic syndrome: nephrotic syndrome has a large amount of plasma protein (especially albumin) lost from the urine, urine protein discharge rate> 3.5g / 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 excessive consumption of hypoproteinemia. 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: mainly seen in most of the stomach resection, chronic pancreatitis and some 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: 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 times of chest pumping, ascites, insufficient protein intake, major bleeding, large-area burns and other hypoproteinemia. According to the unique medical history, clinical manifestations and the lack of evidence that plasma proteins are lost from the gastrointestinal tract are identified.

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