gluten enteropathy
Introduction
Introduction to glucan enteropathy Gluten-induced enteropathy (also known as coeliacdisease), nontropical rosacea (nontropicsprue), has a high incidence in North America, Northern Europe, and Australia, and is rare in China. The ratio of male to female is 1:1.3 to 2.0. More women than men can be affected at any age. The peak age of the disease is mainly children and young people, but the number of elderly people in this disease has increased in recent years. basic knowledge The proportion of illness: 0.03% Susceptible people: children and youth Mode of infection: non-infectious Complications: male infertility stomatitis keratitis beriberi anemia
Cause
Cause of glucan enteropathy
The disease is closely related to the consumption of wheat flour. A large number of studies have confirmed that gluten may be the causative factor of this disease. Therefore, the disease name has recently been directly changed to glucan enteropathy, and the pathogenesis is genetic, immune and The result of the interaction of the wheat gelatin diet.
Eating wheat flour (30%):
The patient is extremely sensitive to wheat flour food containing wheat gum (commonly known as gluten). The wheat gelatin in barley, wheat, rye and oats can be decomposed by ethanol into gliadin (ie, gliadin), which may be the disease. Pathogenic factors, wheat glutamate is rich in glutamic acid and proline, and can be separated into , , and 4 kinds of methicin by electrophoresis. is toxic to small intestinal mucosa, and gliadin is on intestinal mucosa. Toxicity disappears after continued hydrolysis. Normal human intestinal mucosa cells have polypeptide degrading enzymes that can be broken down into smaller molecules of non-toxic substances. However, in patients with active celiac disease, intestinal mucosal cells have insufficient enzyme activity and cannot be decomposed. And cause illness.
The immunopathological study of this disease found that alcohol-soluble glutenin antibodies can be detected in blood, small intestine secretions and feces of patients with active celiac disease, and IgA antibodies of endomysial and reticular proteins can also be detected recently. After eating the wheat gelatin for a period of time, when the wheat gelatin food was added, the hemolytic complement and C3 in the serum of the patient decreased sharply, and the immune complex was detected. The intestinal mucosal biopsy showed epithelial lymphocytosis and in situ proliferation, among which It is a sensitized T cell. In vitro organ culture experiments show that T cell activation can cause intestinal villus atrophy and gland crypt hyperplasia. All of the above may suggest that the disease is an immune disease caused by wheat gelatin.
Genetics (20%):
The disease has a genetic predisposition and is closely related to the MHC gene. It has been observed that many people in the family of the patient are sick. In the asymptomatic family, the alcohol-soluble wheat protein, the reticular protein and the endothelin antibody carrier can be detected. .
Pathological changes: The main pathological changes are in the small intestine mucosa. The extent and extent of the lesions are very different. The small intestine mucosa is atrophied, flattened, deformed, or even disappeared. The surface ring cells are reduced, and the subepithelial layer has inflammatory cells and glands. Hyperplasia, mucosal columnar epithelial cells become flat, cytoplasm has vacuoles, nuclear size is different, microvilli are unclear, and in some cases the mucosa is thick and thick, showing chronic inflammation, villi still exist, but disordered, intestinal lumen can be different The degree is expanded.
Reduced enzyme secretion of intestinal mucosal cells, such as disaccharidase, dipeptidase, lipase, phosphatase and dehydrogenase, intestinal secretion and intestinal hormone secretion are also reduced, therefore, not only the intestinal mucosal absorption area is reduced, absorption function is reduced, enzyme The activity is also reduced, and the function of digesting food is also reduced. The patient loses a lot of fat, protein, sugar, water and salt every day, causing various clinical symptoms.
Prevention
Glucose enteropathy prevention
The disease is closely related to eating wheat flour, so people who are susceptible to the disease should avoid eating a wheat-containing diet (such as various wheat), such as removing the gluten from the flour, and the remaining starch can be eaten. In principle, it is based on high protein, high calorie, low fat, non-irritating and digestible diet.
Complication
Glucose enteropathy complications Complications male infertility stomatitis keratitis beriberi anemia
Patients with IgA nephropathy, infertility, stomatitis, angular cheilitis, beriberi, night blindness, anemia, and even cachexia.
Symptom
Glucose enteropathy symptoms Common symptoms Bone pain, abdominal pain, bleeding tendency, osteomalacia, osteoporosis, constipation, night blind muscle tenderness, bloating, diarrhea
The clinical manifestations of this disease are essentially the malnutrition syndrome caused by the digestion and absorption of nutrients. The clinical manifestations vary greatly. A considerable number of patients have mild symptoms and are not easy to detect. The performance of adult patients can be atypical, common symptoms. And signs are as follows:
(1) diarrhea, abdominal pain 80% to 97% of patients have diarrhea, typical of fatty diarrhea, fecal light, a large amount, oily or foamy, often floating on the surface of the water, more stench, daily stools from the number More than ten times, most patients have recurrent or intermittent diarrhea; a few early or mild cases can have no diarrhea, and even constipation, often missed diagnosis, abdominal pain is less common than diarrhea, mostly abdominal pain, often appear before defecation Mild tenderness in the abdomen, and some cases have obvious abdominal distension, nausea and vomiting.
(2) Weight loss, fatigue and fatigue are not the same, almost necessarily performance, weight loss, fatigue mainly due to protein, fat and other absorption disorders, and other dehydration, lack of potassium, loss of appetite is also an important factor, serious cases can be cachexia.
(3) Vitamin deficiency and electrolyte imbalance The lack of calcium and vitamin D can cause hand and foot spasm, abnormal feeling, osteoporosis, bone softening and can cause bone pain, vitamin K deficiency can cause bleeding tendency, vitamin B deficiency can cause tongue coating , stomatitis, angular cheilitis, beriberi, pella-like pigmentation, vitamin A deficiency can cause follicular keratosis, corneal dryness, night blindness, etc. More than half of patients have anemia, accompanied by concave nails, a few patients can have muscles Tenderness and clubbing (toe).
(D) edema, fever and nocturia edema are common, fever is caused by concomitant infection, the amount of nocturnal urine is more than the amount of urine in the onset, may have IgA nephropathy, infertility, bleeding tendency.
Examine
Examination of gummy enteropathy
(1) Most of the blood tests are macrocytic anemia, normal red blood cell or mixed anemia, serum potassium, calcium, sodium, magnesium can be reduced, plasma albumin, cholesterol and phospholipids and prothrombin can also be reduced, serious The serum folate, carotene and vitamin B12 levels were also reduced in the case.
(2) Quantitative measurement of fecal fat and fat absorption test generally adopt Van de kamer assay. When normal people consume 50-100g of fat per day, the amount of fecal fat is <5g/d, fat absorption rate is >95%, fat absorption rate The calculation method is:
Fat absorption rate = intake of fat - amount of fecal fat × 100 intake of fat
Test method: Continuously eat the standard test meal (containing fat amount 60-100g/d) for 3 days, and measure the amount of fecal fat for 3 days at the same time, and take the daily average value, such as the fecal fat quantitative>6g/d, or the fat absorption rate. <95%, can be considered to have fat malabsorption.
The method of quantification of fecal fat is simple. Most patients with steatorrhea can make a diagnosis based on this, but they are not sensitive enough. In patients with mild or fat intake <60g/d, the amount of fecal fat does not necessarily increase, and the fat absorption test can be accurate. The ground reflects the fat absorption.
(C) 131 iodine-triglyceride and 131 iodine-oleic acid absorption test before oral test compound iodine solution (Lugol solution) to block the thyroid absorption of 131 iodine function, taking 131 iodine-triglyceride (or 131 iodine-oleic acid ) and peanut oil and water each 0.5ml / kg, leave the stool within 72 hours, and calculate the amount of radiation discharged from the feces as a percentage of the amount of radiation, fecal 131 iodine - triglyceride discharge rate > 5%, or 131 Iodine-oleic acid >3%, all suggest lipid absorption, the test method is simple, but the accuracy is not as good as the chemical method of fecal lipid.
(D) Determination of serum carotene concentration is a valuable screening test, the normal value is greater than 100IU / dl, often lower than normal in malabsorption caused by intestinal diseases, normal or slightly reduced pancreatic dyspepsia, malnutrition Insufficient food intake, high fever or certain liver diseases can also be reduced.
(5) Other intestinal absorption function tests Water-soluble substances such as xylose, glucose, lactose, and folic acid can be used to determine the absorption function of the upper small intestine. In patients with primary malabsorption syndrome, there may be typical impairment, but in pancreatic or Secondary steatorrhea can be normal.
1. D-xylose absorption test D-xylose is passively absorbed in the jejunum after oral administration, and is not metabolized in the body but mainly excreted by the kidney. When the kidney function is normal, the dextrose test can best reflect the jejunum. Absorption function, the method is fasting oral d-xylose 25g (dissolved in 250ml water), and then drinking water 250ml to promote urination, normal, 5 hours after serving, the urine can be discharged from the dextrose 4.5 ~ 5g, such as the discharge 3 to 4.5g is suspicious and abnormal, <3g is definitely poor absorption of the small intestine; or 2 hours after oral administration, the blood concentration is measured, normal >20mg/dl, when renal insufficiency, the release of dextrose in the urine is reduced. False negative, but the blood concentration is normal, there is a large number of bacteria in the intestines, gastric retention and ascites patients, xylose can also be reduced by renal excretion and affect the test results. Due to the ingestion of 25g of dextrose, a few patients have upper abdominal discomfort. , vomiting, diarrhea and other adverse reactions, so some people switched to oral d-xylose 5g method, the normal person's 5-hour urine discharge should be >1.0 ~ 1.2g, the diagnostic value is similar to the oral 25g method, but the adverse reactions are reduced, in recent years Dextrose hydrogen breath test , Not on renal function, urinary xylose excretion test as effective.
2. Vitamin B12 absorption test The radioactive cobalt labeled vitamin B12 can be used to measure the absorption function of the lower ileum. The vitamin B121 is injected intramuscularly to saturate the body's stock, and then oral cobalt or cobalt-cobalt-labeled vitamin B 122g is used to measure the radioactivity of urine in 48 hours. Normal should be >8~10%. In the case of ileal dysfunction or resection, when the intestinal bacteria overproduce (such as blind sputum syndrome), the urinary discharge is lower than normal.
3.14C-glycocholate-breathing test Oral 14C glycocholic acid 10 microcuries, most of the normal people are absorbed in the ileum, circulated to the liver and then discharged into the biliary tract, only a very small part of the colon is discharged from the feces. Discharged; the other part is metabolized into 14CO2 and discharged through the lungs. After oral administration of 14C-glycocholic acid in normal people, the discharge of 14CO2 in the feces within 4 hours <1% of the total amount, 24 hours of discharge <8%, in the small intestine When there is a large amount of bacterial reproduction, ileal resection or dysfunction, the discharge of 14CO2 from the lungs and 14C in the feces is significantly increased, up to 10 times that of normal people.
(6) Pancreatic function test In the case of chronic pancreatitis, pancreatic cancer and pancreatic cystic fibrosis, abnormalities can be shown to aid in the diagnosis of pancreatic absorption.
(7) Gastrointestinal X-ray examination The small intestine often has functional changes, which are more common in the middle and distal jejunum. The main manifestations are enlargement of the intestine, accumulation of effusion and expectorant; the distribution of intestinal tract is snow-like; Thickening or smoothing of the intestinal wall is a "wax tube" sign; the time delay of the expectorant is delayed, and the gastrointestinal X-ray examination can also exclude other organic diseases of the gastrointestinal tract.
(8) Endoscopy examination The insertion enterocoloscopy can reach 60~100cm below the flexor ligament, the probe type enteroscopy is 256cm long, and the head end diameter is about 5mm. After insertion into the jejunum, it is slowly moved into the distal ileum by means of peristalsis. Even reaching the colon, the operation takes 6-8 hours, generally can see 50% ~ 70% of the small intestine mucosa, can be used for direct biopsy, improve the diagnosis of small bowel lesions, basically replace the blind aspiration biopsy, Colonoscopy can sometimes be used to observe lesions at the end of the ileum through the ileocecal valve.
The appearance of the normal small intestine mucosa is similar to that of the duodenal mucosa. The upper jejunal mucosa is a ring-shaped fold, the mucosal surface is fluffy, and the folds of the mucosa gradually disappear from the bottom to the end of the ileum. The villi are short and blunt. When the small intestine is malabsorbed, the basic characteristics of the mucosa are The villi become shorter, thicker, lodging and exfoliation and other atrophy.
In addition, the detection of alcohol-soluble gliadin antibodies, endothelium proteins and reticular IgA antibodies may contribute to the diagnosis of this disease.
Diagnosis
Diagnosis and identification of glucan enteropathy
For cases of long-term diarrhea and weight loss, the small intestine malabsorption should be guarded against. The diagnosis of glucan enteropathy should first be differentiated from other intestinal organic diseases and malabsorption caused by pancreatic diseases. According to fecal fat, gastrointestinal X-ray examination, various small intestine absorption test, alcohol-soluble gliadin and other antibodies, endoscopy and small intestinal mucosal biopsy can be initially diagnosed, and then the treatment test can be related to the wheat gel, in order to finally determine the diagnosis.
It should be differentiated from other intestinal diseases and malabsorption caused by pancreatic diseases.
