Chronic gastritis in children

Introduction to chronic gastritis in children Chronic gastritis in children refers to chronic inflammation caused by various causes of repeated action on the gastric mucosa. The causes of chronic gastritis are not known, and various diets, drugs, microorganisms, toxins, and bile reflux may be associated with the onset of chronic gastritis. In recent years, it has been suggested that intragastric infection of Helicobacter pylori is the most important factor causing chronic gastritis. The mechanism it produces is related to the imbalance between mucosal damage and protective factors. basic knowledge Sickness ratio: 0.1% Susceptible people: children Mode of infection: non-infectious Complications: anemia, dystrophy, weight loss

Causes of chronic gastritis in children

Endocrine factors (25%):

Since Australian scholars Warren and Marshall first isolated Hp from gastric mucus in patients with chronic gastritis in 1983, a large number of studies have shown that Hp is closely related to chronic gastritis. In children with primary gastritis, Hp infection rate is as high as 40%, chronic active gastritis is more than 90%, and it is almost impossible to detect Hp in normal gastric mucosa. Therefore, Hp is an important cause of chronic gastritis.

Chemical drugs (10%):

Frequent colds and fever in children, repeated use of non-steroidal drugs, such as aspirin, indomethacin, etc., so that the endogenous protective substance of the gastric mucosa prostaglandin E2 decreased, the gastric mucosal barrier function decreased, resulting in gastric mucosal damage.

Bad eating habits (25%):

Food is too cold, too hot, too acidic, too spicy, too salty or often overeating, eating irregular, etc., can cause chronic inflammation of the gastric mucosa, lack of protein in food, B vitamins also increase the susceptibility of chronic gastritis .

Bacterial virus infection (15%):

Chronic infection of the nasal cavity and oropharynx, such as tonsillitis, sinusitis and other bacteria or their toxins swallowed into the stomach, long-term chronic stimulation can cause chronic gastric mucosal inflammation; 40% of patients with chronic tonsillitis have reported intragastric There is a catarrhal change, gastric mucosal damage after acute gastritis is not cured for a long time, repeated attacks, can also develop into chronic gastritis.

Duodenal reflux (10%):

When the pyloric sphincter dysfunction, the duodenal juice is increased into the stomach. The duodenal juice contains bile, intestinal juice and pancreatic juice. The bile salt can reduce the permeability of the gastric mucosal barrier to hydrogen ions and make the gastric antrum G cells. Releases gastrin and increases gastric acid secretion. Hydrogen ions pass through the damaged mucosal barrier and diffuse into the gastric mucosa, causing inflammatory changes, vasodilation, and increased inflammatory exudation, which causes chronic gastritis to persist.

Pathogenesis

The lamina propria of normal gastric mucosa has only a few mononuclear cells. If most lymphocytes and plasma cells infiltrate, it is a chronic inflammatory activity period. Eosinophils are rare. Chronic superficial gastritis lesions are generally limited to the upper third of the mucosa. In the glandular layer without affecting the glandular part, inflammation affects the epithelial layer to cause degeneration and necrosis, severe exfoliation forms erosion and even hemorrhage, mitotic phase increases significantly, epithelial thickening, most cell infiltration in the lamina propria, white blood cell tour There are various types of casts in the glandular fossa. The inflammatory changes of atrophic gastritis are similar to those of superficial gastritis, but the range extends to the entire mucosal layer. The main feature is the decrease in the number of glands, and the intestinal metaplasia is common in atrophic gastritis. In the light, only a small number of goblet cells are seen. In severe cases, a large number of typical intestinal villus epithelium can be seen. This pathological change is rare in children. According to the results of histological examination of 206 children in the hospital, almost all superficial gastritis. Only 1 case was atrophic gastritis, and 1 case of superficial gastritis with intestinal metaplasia.

Prevention of chronic gastritis in children

1. It is also important to cultivate good eating habits from an early age. Children should be regularly dosed, a small amount of meals, pay attention to nutrition, eat less spicy food; in addition, avoid picky eaters, partial eclipse, do not hunger or fullness; do not eat too much cold drink; do not snack or candy, etc. . Otherwise, it is easy to cause gastrointestinal dysfunction and decreased resistance of the gastric mucosa and suffer from chronic gastritis.

2, to reduce the child's emotional fatigue and other factors, do not give the child too much pressure, pay attention to the child's rest, to ensure that the child has enough sleep, strengthen physical exercise.

Pediatric chronic gastritis complications Complications, anemia, dystrophy, weight loss

Often the child is thin, lack of nutrition, and anemia.

Chronic symptoms of chronic gastritis in children Common symptoms Indigestion, weight loss, abdominal pain, loss of appetite, nausea, dizziness, suffocation, black stool

The symptoms of chronic gastritis in children are not specific, and most of them have different degrees of dyspepsia. The severity of clinical manifestations is not consistent with the degree of gastric mucosal lesions, and the course of disease is prolonged. The main manifestation is repeated abdominal pain, no obvious regularity, usually increased after eating. The location of the pain is not exact, mostly in the umbilical cord.

Abdominal pain in children can only show uneasiness and normal eating behavior changes. Older children have symptoms like adults, often complain of upper abdominal pain, followed by hernia, early satiety, nausea, upper abdominal discomfort, and pantothenic acid. Eating hard, cold, spicy foods, etc., or causing cold, temperature drops, can cause or aggravate symptoms. Some children may have loss of appetite, fatigue, weight loss and dizziness, and those with stomach erosion may have black stools.

Signs are not obvious, the tender part can be in the upper abdomen or umbilical cord, a wide range.

Examination of chronic gastritis in children

1. Determination of gastric acid

Superficial gastritis is normal or low in gastric acid, atrophic gastritis is significantly reduced, and even acid deficiency, the neonatal stomach content is acidic, the newborn baby after the removal of the swallowed alkaline amniotic fluid, the measured pH is less than 4 The concentration of hydrochloric acid reached the highest peak 7 to 10 days after birth, and then gradually decreased. The patient reached the level of 2 to 3 months after birth. In this hospital, 64 children aged 11 to 14 years were examined for fasting stomach acid and gastric mucosa. It was found that the gastric acid results of most children with chronic superficial gastritis were similar to those of normal children. It was consistent with the literature reports that only a small proportion of chronic superficial gastritis had decreased gastric acid, and the cause was unknown. In theory, superficial gastritis lesions did not invade glands. There should be no symptoms of hypoacidity. This phenomenon indicates that some children may have changed their functions before the tissue structure changes, and further discussion is needed.

Pepsinogen

Pepsinogen is secreted by the main cell and activated into a pepsin with digestive function in an acidic environment. Its secretion is consistent with gastric acid, but the number of main cells is more than that of parietal cells, so it is less affected than gastric acid in the pathological state. .

3. Intrinsic factor

The inner factor was present in the fetal stomach for 1 week, and the intra-stomach factor reached the adult level 3 months after birth. The factor secretion in normal adults was 77.00 U/h. The internal factor content was helpful for the diagnosis of atrophic gastritis and pernicious anemia. Some people have found that some children have congenital internal factor secretion defects, 400-600U internal factors in the gastric juice can maintain the normal absorption of vitamin B12, so even patients with atrophic gastritis are not prone to pernicious anemia.

Gastrin

Gastrin is secreted by gastric antrum G cells. The literature reports that serum gastrin is 88pg/ml after birth and increases to 119pg/ml in the second week after birth. The authors report the use of radioimmunoassay for serum gastrin in 148 children. The test was carried out, and the result was 264.92 pg/ml in the first week after birth, 250.07 pg/ml in the second to fourth weeks, and reached the peak at 3 years old, which was 300.7 pg/ml. After 3 years old, it gradually decreased to adult level with age. That is (130.84±8.34) pg/ml, the serum gastrin levels measured by each family are not consistent, and the reasons need to be further explored.

5. Helicobacter pylori detection

Including gastric smear direct smear staining under gastroscope, tissue section staining to find Hp, Hp culture, urease detection, followed by non-invasive method using the biological characteristics of bacteria, especially the ability of Hp urease to hydrolyze urea to form a breath test (13C-urea exhalation) detection of Hp, the determination of serological HpIgG antibody, because it can not provide the basis for the existence of bacteria, it can not be used for the diagnosis of current infection, mainly for screening or epidemiological investigation, in the above methods, The urease method is the easiest, quickest, and often completed, 13C-urea breath test, so the method is expensive and the clinical popularity is limited.

6. Other inspections

In the serum of type A atrophic gastritis (gastric gastritis), parietal cell antibodies, gastrin antibodies and internal factor antibodies may occur, and most of the blood of atrophic gastritis, urinary pepsin secretion is reduced, and superficial gastritis is mostly Normal, serum vitamin B12 levels were significantly reduced during pernicious anemia.

7. X-ray barium meal inspection

The diagnosis of chronic gastritis does not help much. According to foreign data, X-ray examination confirmed by gastroscopy for chronic gastritis shows only 20% to 25% of gastric mucosal inflammation, although most radiologists in the past believe that gastric tension disorder, peristaltic Alteration and gastric juice in the stomach can be used as a basis for the diagnosis of gastritis. However, in recent years, gastroscopy revealed that this phenomenon is caused by abnormal gastric motility and not by gastritis.

8. Gastroscopy

It is the most important diagnostic method for chronic gastritis, and can take mucosal living tissue for pathological examination. Chronic gastritis manifests as hyperemia, edema, reflective enhancement, obvious gastric dimple, mucoid brittle and easy bleeding; mucus increase, tiny nodules Formation, limitation or large flaky accompanied by fresh or old bleeding spots and erosion. When the gastric mucosa has atrophy, the mucous membrane loses its normal orange-red color, the color is gray, the folds become thinner, the mucous membrane becomes thinner, and the submucosal blood vessels are exposed. Histopathological changes, epithelial cell degeneration, epithelial cell proliferation, intrinsic membrane inflammatory cell infiltration, gland atrophy, inflammatory cells are mainly lymphocytes, plasma cells.

Diagnosis and diagnosis of chronic gastritis in children

diagnosis

It is difficult to diagnose with clinical symptoms alone. The diagnosis of children with repeated abdominal pain and dyspepsia depends mainly on gastroscopy and pathological tissue biopsy. According to the diagnosis of glandular atrophy, chronic superficial gastritis or chronic atrophic gastritis, according to inflammation The degree is mild (inflammation infiltration is limited to the superficial 1/3 of mucus), moderate (inflammation involving 1/3 to 2/3 of the superficial mucosa), and severe (inflammation exceeds 2/3 of the superficial mucosa); If there is neutrophil infiltration in the lamina propria, it means "activity". In addition, conventional tissue staining is performed within 5 cm of the antrum or posterior wall from the pylorus, rapid urease test or bacterial culture, or 13C-urea call Gas test for Helicobacter pylori, if positive, diagnosed as "Hp-related gastritis", found pyloric systolic dysfunction, increased reflux, bile retention in the stomach, pathological section showing fibrous tissue hyperplasia, often suggesting gastritis and bile reflux.

Differential diagnosis

In the episode of chronic gastritis, the gastroscope, B-ultrasound, 24h pH monitoring comprehensive examination, exclude liver, gallbladder, pancreas, peptic ulcer, reflux esophagitis, in the episode of gastritis, should pay attention to gastric perforation or early appendicitis Identification.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.