Celiac disease
Introduction
Introduction to celiac disease Celiacdisease (celiacsprue) is a primary malabsorption syndrome characterized by small intestinal mucosal lesions caused by gluten (gluten) intolerance. Also known as glutenousenteropathy, nontropical inflammatory celiac disease (nontropicalspure), idiopathic steatorrhea (idiopathicsprue). The incidence of this disease in the western population is about 0.03%, which is rare in China. basic knowledge The proportion of illness: 0.004%-0.007% (this disease is mostly related to fat utilization disorder, the incidence rate is about 0.004%-0.007%) Susceptible people: no special people Mode of infection: non-infectious Complications: esophageal cancer fracture peripheral neuritis
Cause
Causes of celiac disease
(1) Causes of the disease
Dicke first noticed that people with this disease eat more pasta. If they don't get pasta, the symptoms can be alleviated. Therefore, it is suggested that wheat gelatin may be the cause of the disease. Rubin confirmed this view. Rubin injected wheat flour into the stationary phase. In the patient's jejunum, symptoms can be caused and pathological changes in the intestinal mucosa are found.
Wheat flour (barley, wheat, oats, rye) contains 10% to 15% of gluten gluten, which can be decomposed by alcohol into gliadin and glutinen. The former is 30-75kD. The polypeptide can be divided into -, -, - and -4 parts by electrophoresis, and the - part proves to be toxic, while the latter 3 are not certain.
(two) pathogenesis
The pathogenesis of gliadin is unclear. There are several theories:
1. Genetic theory is obvious that the disease is related to heredity, because the incidence rate among relatives is much higher than that of the control population. The consistency of HLA between siblings is 30%, and that between twins can be as high as 90%, HLA-B8 and The positive rate of HLADR3 in the high incidence area of the disease in the United States and northern Europe is 60% to 90%. Recently, the positive rate of HLA DQ2 has reached 90%.
2. Immunology says that the TCD8 lymphocytes in the lamina propria and superficial cells of the small intestinal mucosa are 2 to 6 times more abundant than normal people. These cells can secrete cytotoxins such as interferon to regulate intercellular HLA antigens to damage cells, and immunoglobulins. Increased IgA, increased anti-gliadin IgA and IgG antibodies in plasma, 60% of intestinal secretions can detect anti-alcoholic antibodies, and gliadin contains 8 amino acid sequences and human intestinal adenovirus EIB protein The sequences are the same, so the two have a common antigenicity. Clinical serology also confirms that patients with this disease have a high percentage of adenovirus (Ad-12) infection before the disease, so allergies appear several hours after taking gliadin. The reaction has diarrhea.
3. Enzyme deficiency theory There is a special polypeptide hydrolase in the normal small intestinal mucosa, which can hydrolyze the gliadin to break down into smaller molecules and lose toxicity. When the patient is sick, the enzyme is reduced, but after the treatment is improved, this is improved. The enzymes return to normal and can be reduced when they become sick. Therefore, the causal relationship between the two is still difficult to affirm and needs further study.
The main pathological changes are located in the small intestine mucosa. The duodenum and jejunal mucosa can be obtained by enteroscopy. It can also be obtained by small intestinal mucosa biopsy. The vitreous deformation can be flattened by living microscopy. There is no discriminable villus structure under light microscope, and the crypt is thick and branched. It can be seen that the mitotic image is increased, the basement membrane is flaky thickening, the mucosal inflammatory cells are infiltrated, the epithelial layer is mainly lymphocytes, occasionally eosinophils are seen, and plasma cells are not seen. Unlike normal intestinal mucosa, these cells are located in the nucleus of the absorption. Below the level, it is more dispersed, and the intrinsic layer is mainly the infiltration of plasma cells. As the lesion progresses, it is followed by a decrease in enzyme secretion in intestinal mucosal cells, such as disaccharidase, dipeptidase, lipase and non-special Heterophosphatase and dehydrogenase, intestinal fluid and secretions are also reduced. In addition, intestinal hormones such as cholecystokinin are also reduced. It can be seen from the above that the absorption area and absorption function of the small intestine are reduced, and the activity of the enzyme is low. Digestive function is also reduced, hormone reduction affects exercise and secretion, so patients lose water in addition to losing a lot of fat, protein, sugar every day. And salts (Na, K, Ca, Mg), causing the corresponding clinical symptoms.
Prevention
Celiac disease prevention
Pay attention to rest, work and rest, life in an orderly manner, and maintaining an optimistic, positive and upward attitude towards life can be of great help in preventing diseases.
Complication
Celiac disease complications Complications esophageal cancer fracture peripheral neuritis
Patients with malignant tumors accounted for 15%, male patients with esophageal cancer most common, lymphoma 7% to 10%, jejunum more common than the ileum, it is speculated that intestinal mucosal lesions are easy to cause carcinogen absorption, while mucosal lesions such as ulcerative colitis Precancerous lesion status.
1. Neurological symptoms can be seen in peripheral neuritis and central nervous system changes (large, cerebellum and spinal cord), the cause is still unknown.
2. Ulcer jejunum and ileitis combined with ulcers, the symptoms are more serious, can cause perforation and scarring obstruction, poor prognosis.
3. Bone changes Bone softening is the most common, due to secondary hyperparathyroidism, severe cases can cause fractures.
4. The function of the whole pituitary is low. Because of malnutrition, the pituitary function is low, which is manifested by various endocrine gland dysfunction, and the thyroid, adrenal gland, and gonads are inferior.
Symptom
Symptoms of celiac disease Common symptoms Thin stools, diarrhea, abdominal distension, abdominal pain, nausea, anorexia, lower extremity edema, hypotension, convulsions
Symptom
In infants and young children, the main manifestations of growth retardation, weight loss, vomiting, diarrhea, abdominal pain, bloating and irritability, common symptoms in adults are fatigue, weight loss, nausea, anorexia, bloating, loose stools, some patients except intestinal mucosal pathological changes In addition, there can be no symptoms. After the patient is controlled with the "no wheat gelatin" diet symptoms, if the symptoms appear again after stimulation with the wheat gel, a few patients may experience uncomfortable hours to weeks. In addition, there are often glossitis. Anemia, low calcium convulsions, bone pain, osteoporosis, bleeding and neurological symptoms (depression and peripheral neuritis), female patients can also be characterized by rare menstruation, premature menopause and infertility.
2. Signs
Weight loss is often above 10kg, hair is scarce, color changes, clubbing, lower extremity edema, skin may appear pigmentation, eczema, exfoliation, anemia is also more common, there may also be keratitis, glossitis, hypotension, due to the whole body Spleen atrophy can occur in the dysfunction of the reticuloendothelial system, and sometimes unexplained splenomegaly.
Examine
Celiac examination
1. Blood routine hemoglobin declines, manifested as mild hypopigmentation of large cell anemia, peripheral blood smears can appear target red blood cells, Heinz body and Howell-Jolly body, platelets can be increased or decreased, white blood cells can be reduced.
2. A large amount of fat droplets can be seen by conventional stool Sudan-III staining.
3. Plasma albumin decreased the amyloidemia and intestinal absorption function test, the absorption function was low.
In vivo microscopic examination showed that the villi deformed and flattened; under the light microscope, there was no discriminable villus structure, the crypt was thick, and the branches showed visible mitotic figures, and the basement membrane had flaky thickening.
Diagnosis
Diagnosis and diagnosis of celiac disease
diagnosis
According to the feces, X-ray and small intestinal mucosal biopsy can make a preliminary diagnosis, and then the treatment test can explain the related to the wheat gel, in order to finally determine the diagnosis.
Differential diagnosis
1. The characteristics of patients with refractory steatorrhea are similar to those of celiac disease, but they do not respond well to control diet.
2. Lymphoma and lymphoma can cause lymphatic drainage disorder and cause malabsorption. For example, X-ray examination is suspicious and further laparotomy.
3. History of tropical steatorrhea and different treatment responses, tropical steatorrhea responded well to broad-spectrum antibiotics and folic acid.
4. Although the performance of Crohn's disease can be similar to this disease, but the X-ray shows that there are obvious differences between the two, Crohn's disease can produce longitudinal ulcers, and paving stone-like changes, further can cause ulcer perforation and fistula, lesions It is segmental, and the disease is treated well with a wheat-free diet, and a therapeutic diagnosis can be made.
5. Parasitic diseases Some parasitic diseases such as Giardia lamblia, roundworm, coccidiosis and helminthiasis are also associated with clinical digestive malabsorption. They should be used for examination of fecal eggs or protozoa, and if necessary, feasible treatment tests such as Nitrazole (metidazole) has a remarkable effect.
6. Pancreatic dyspepsia The glucose tolerance test showed a diabetic curve, the xylose absorption test was normal, and the pancreatic function test (spinin and cholecystokinin test) and imaging examination were further performed.
7. Intestinal lymphatic expansion may have diarrhea, hypoproteinemia and edema, but small bowel biopsy has characteristic lymphatic expansion.
8. After gastric excision, the fat diarrhea Bi-type II anastomosis is easy to cause steatorrhea, but the small intestinal mucosa is normal.
9. Blind sputum syndrome occurs after gastrointestinal surgery, Bi-type II gastrointestinal anastomosis, lateral side or end-to-side anastomosis, small bowel diverticulum, or small bowel lesions caused by scleroderma can cause diarrhea, X-ray examination And based on the history of surgery is not difficult to diagnose.
