Pediatric celiac disease

Introduction to pediatric celiac disease Celiac disease, also known as gluten allergic bowel disease, has been called idiopathic malabsorption syndrome in the past due to unknown etiology. It has been proved that the disease is caused by eating wheat food, including wheat, barley and rye, and the body is allergic to the protein component gluten. Whether oatmeal can cause the disease, there are still different opinions, at least This allergic reaction causes extensive lesions in the upper mucous membrane of the small intestine, clinical manifestations of malabsorption and other malabsorption symptoms, and is a lifelong disease. basic knowledge The proportion of children: the incidence rate of children under 5 years old is about 0.002%-0.003% Susceptible people: children Mode of infection: non-infectious Complications: malnutrition, dehydration, arthritis

Causes of pediatric celiac disease

(1) Causes of the disease

Pathogenic factor

The gluten in wheat (commonly known as gluten) is a complex vegetable protein that can be broken down into four proteins, gliadin, also known as alcohol-soluble bran protein. Glutenin (glutenin). Albumin and globulin, of which gliadin is the causative factor of this disease.

2. Relationship with heredity

The prevalence of the disease in the first-degree relatives of the sick child is about 2% to 3%. For small intestinal mucosal biopsy, 10% of the relative intestinal mucosa has a typical change of the disease, which is significantly higher than that of the general population. About 70%, which indicates that the disease is genetically related. By measuring leukocyte antigen, it is found that the pathogenesis of this disease is related to HLA antigens B8, DR3, DR7, DQ, W2 and DR4, and 80% to 90% of patients are HLA-B8. For those who are positive, the incidence of this disease is higher in areas with more HLA-B8 in the population, such as Southwestern Ireland.

(two) pathogenesis

Pathogenesis

The mechanism of gliadin-induced intestinal mucosal damage is not fully understood. It is believed that the lack of a peptidase in the intestinal mucosa is related to the inability of gliadin to be decomposed and deposited in the intestinal mucosa; however, the peptidase is not long-term deficient. At present, there are many tendencies to think that the pathogenesis is related to immunity, and the immune mechanism is still unknown. It is believed that gliadin acts as an antigen to bind to antibodies to form an immune complex, which can promote the accumulation of T and K (killing) lymphocytes in the intestinal mucosa through cellular immunity. In response to injury to the intestinal mucosa, anti-gliadin IgA antibodies were detected in the serum of untreated patients, indicating that the disease is associated with immunity.

2. Pathology

The mucosal lesions in the small intestine are one of the characteristics of this disease. The mucosa is flattened, and the shallow groove divides it into irregular sulcus. The lens is atrophied and shortened, and it is flattened, which reduces the absorption area of the small intestine. The epithelial hyperplasia of the fossa deepens and distorts the villus, the surface of the villus epithelial cells is not neat, the vacuoles are formed in the cytoplasm, the lymphocytes infiltrate between the epithelial cells, and the lamina propria have chronic inflammatory cells (plasma cells, B lymphocytes, etc.). Infiltration, although the villi shortened, crypt extension can also be seen in other diseases, such as rotavirus enteritis, blue giardiasis and tropical inflammatory diarrhea, but these diseases have no epithelial cell changes, and the mucous membrane is thin, the disease Normal mucosal thickness, milk or legume enteropathy, immunodeficiency disease and other intestinal lesions, mostly patchy, villi only partial atrophy, and the mucosal lesions of this disease are widely different.

Pediatric celiac disease prevention

Mainly for genetic counseling. Eating wheat, including wheat, barley, and rye, the body is allergic to the protein gluten contained in it. Whether oatmeal can cause this disease, there are still different opinions, at least the damage is light, it is recommended to actively prevent not to eat wheat barley and rye, pay attention to do active prevention work. Drugs for gluten allergy in children should be positively symptomatic. Pay attention to early prevention.

Pediatric celiac disease complications Complications, malnutrition, dehydration

Often accompanied by malnutrition, poor growth, diarrhea often accompanied by dehydration, acidosis, and even cause shock (campria syndrome), but also arthritis, chronic unexplained hepatitis and severe enamel dysplasia. Due to extensive malabsorption of the intestine, it is often accompanied by other nutrient absorption disorders such as hypoproteinemia, edema, nutritional anemia, intestinal dermatitis and multiple micronutrient deficiencies.

Symptoms of pediatric celiac disease Common symptoms Deficient watery dehydration, abdominal distension, diarrhea, malabsorption syndrome, pale, stench, abdominal pain, irritability

The baby does not occur before eating the wheat, and can occur in all ages, but the peak incidence is 1 to 2 years old, but different regions may vary in different years. Most of the cases are insidious, often in several months. Only a clear diagnosis is made in the year. The severity of the disease varies greatly. The milder can be completely asymptomatic, and only confirmed by family history and small bowel biopsy. Severe cases of severe intestinal malabsorption, typical cases are as follows:

Gastrointestinal symptoms

Most patients have chronic diarrhea, dysentery and other malabsorption symptoms, such as light stool, oily, foul odor, defecation 2 or 3 times a day, but also once a day, but the amount is large, diarrhea can be intermittently aggravated, become water It is easy to cause dehydration and electrolyte imbalance, but a small number of sick children can have no diarrhea, and even constipation. The sick children have anorexia, but occasionally the appetite increases, other symptoms include vomiting, abdominal pain, abdominal distension and rectal prolapse.

2. Growth and development backwardness

Due to poor absorption height, body weight is often significantly behind, slow growth rate, muscle wasting, especially in the proximal part of the limb. About 30% of the sick children may have enamel dysplasia. After stopping eating gliadin, they can also recover.

3. Other nutritional deficiencies

Commonly due to iron, folic acid malabsorption caused by nutritional anemia, sick children showed pale, due to protein malabsorption and loss of protein bowel disease, can cause hypoproteinemia, severe malnutrition edema, fat malabsorption can cause fat Soluble vitamins are malabsorbed, causing the corresponding symptoms of vitamin A, D, E and K deficiency.

4. Mental symptoms

There may be irritability, personality changes and sleep disorders, etc., especially in patients with malabsorption syndrome, such as increased fecal fat, decreased serum carotene, decreased xylose absorption test, decreased hemoglobin, hypoproteinemia, and The examination of fat-soluble vitamin deficiency can be seen, but these abnormalities can only prove the existence of malabsorption, and it is not certain that malabsorption is caused by this disease.

Examination of pediatric celiac disease

1. Blood routine and biochemical examination

Blood routine examination is often a large cell anemia, can also be positive cell anemia or mixed anemia, serum potassium, sodium, calcium, magnesium, phosphorus, etc. can be reduced, plasma albumin, cholesterol, phospholipids and prothrombin can also Reduced, serum folic acid, carotene and vitamin B12 can be reduced in severe cases.

2. Determination of intestinal malabsorption

The study of fat quantification is the best way to determine lipid malabsorption. The percentage of fat absorption can be calculated by measuring the excretion of fecal fat within 72 hours by taking the same amount of fat at the same interval. Normally greater than 94%, because this experiment requires accurate collection of stool, small infants sometimes have difficulty collecting all the stools, so the application is limited, oral xylose test, that is, 1h serum xylose test is often applied, children under 30kg Oral 5mg xylose or 14.5 ~ 25mg / m2, and then determine the xylose content of serum at 60min, but the false positive and false negative rate of this test is higher, which limits its application.

3. Small intestine permeability test

The permeability test is a non-invasive test based on the permeability of the small intestinal mucosa to sugar. In patients with glioin intestinal disease, small molecules of mannitol and rhamnose (6-deoxy- L-glycolose) absorption is reduced, and the ratio of disaccharide to monosaccharide is decreased due to the increase of intracellular channels or the absorption of macromolecular lactulose and cellobiose due to the lesion of cell membrane, suggesting that the gum is The diagnosis of enteropathy, although this test has a high sensitivity to jejunal mucosal abnormalities, its specificity is low, and the false positive rate mainly occurs in patients with mucosal abnormalities caused by other diseases such as Crohn's disease.

4. Determination of anti-gum antibody

By measuring the anti-gliel antibody in serum, it can help the diagnosis of this disease, the sensitivity is very high, close to 100%, in addition to the anti-reticulin and anti-endometrial antibodies can be detected in the serum, this is beneficial to this Diagnosis of the disease.

5. Small intestinal mucosal biopsy

Use the small intestine biopsy tube to insert mucosal specimens into the small intestine through the oral cavity, perform biopsy or use enteroscopy to visualize and biopsy the upper jejunum and the whole colonoscopy on the ileum end, X-ray barium examination, and the tincture is extended by the small intestine. The jejunum is diffusely dilated, and the mucosal folds are flattened or disappeared. Others should be routinely performed for electrocardiogram and B-ultrasound.

Diagnosis and diagnosis of pediatric celiac disease

The diagnosis of this disease needs to be based on:

1. Biopsy: Small intestinal mucosal biopsy has characteristic pathological changes of celiac disease.

2. Dietary therapy: Dietary therapy means that after removing all the food containing gluten in the diet, the symptoms quickly disappear and the body weight begins to grow. Before the small intestinal mucosa specimens are obtained, diet therapy should not be used first, because once the symptoms are improved, it is difficult to be natural recovery. Or the effect of diet therapy, with the above two to initially diagnose the disease.

3. Induction test: The test is positive, that is, after re-testing the diet containing gliadin, whether the symptoms recur and the pathological changes of the small intestine reappear, the diagnosis of the disease can be confirmed, and whether the child over 2 years old needs to be induced. There is still controversy. Under the age of 2, it is generally advocated, because some other diseases at this age can also cause similar pathological changes in the small intestine. The induction test should be carried out 2 years after the start of diet therapy, and then the pathological changes of the small intestine mucosa should be completely restored. Avoid serious symptoms, can give a small amount of wheat food, such as 1 to 2 pieces of bread per day, most of the sick children can tolerate, often need 2 years or more of intestinal mucosa to re-appear typical pathological changes, found in recent years, untreated The blood C3 complement is low in the sick children, less than half of the IgM is decreased, serum anti-gliadin IgA antibody, anti-reticulin antibody and anti-endomysium antibody can be positive, sensitive and specific. High, combined with small bowel biopsy can be diagnosed, these antibodies can disappear after diet treatment, and the induced test can reappear.

It is differentiated from children with chronic diarrhea, steatorrhea and malnutrition, and can be diagnosed by laboratory tests and clinical features.

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