bubble_chart Overview

Eosinophilic gastroenteritis, also known as eosinophilic gastroenteritis, is a rare disease characterized by diffuse or localized eosinophilic infiltration in certain parts of the gastrointestinal tract. Clinical manifestations include spasmodic pain in the upper abdomen, which may be accompanied by nausea, vomiting, fever, or a history of specific food allergies. Approximately 80% of patients have peripheral blood eosinophils as high as 15-70%. It was first reported by Kaizser in 1937, and to date, there have been about 200 cases reported in the world literature.

bubble_chart Etiology

The etiology of eosinophilic gastritis is not well understood, but it is generally believed to result from an allergic reaction to exogenous or endogenous allergens. Nearly half of the patients have a personal or family history of asthma, allergic rhinitis, eczema, or urticaria. In some patients, symptoms can be triggered by certain foods such as milk, eggs, mutton, or seafood, or by medications like sulfonamides, furazolidone, and indomethacin. In certain cases, consuming specific foods leads to elevated serum IgE levels accompanied by corresponding symptoms, suggesting a link between the disease and specific food allergies.

bubble_chart Pathogenesis

The mechanism by which food allergies cause eosinophilic gastroenteritis may include: 1. Due to the presence of a large number of eosinophilic infiltrations in the lesions, some believe that after food allergens come into contact with sensitive gastrointestinal tissues, an antigen-antibody reaction occurs in the gastrointestinal wall, attracting eosinophils to the sites where antigen-antibody complexes are deposited. This is attributed to the presence of C₃

receptors on the surface of eosinophils. 2. Some suggest it is caused by eosinophil chemotactic factor (ECF) derived from lymphocytes, which attracts eosinophils. 3. Others propose that mast cells in gastrointestinal tissues bind to IgE antibodies induced by food antigens via Fc receptors, and upon encountering the corresponding antigen, this triggers mast cell degranulation, releasing substances such as histamine, ECF, and bradykinin. ECF attracts eosinophils, while histamine further enhances their chemotaxis. However, some hold an antagonistic view, arguing that: 1. Not every patient has a history of allergies; 2. Some individuals do not experience relief in gastrointestinal symptoms even after eliminating suspected allergenic foods; 3. Serum IgE levels are elevated in only a minority of cases, and other immune markers such as IgG, complement, and lymphocyte counts remain normal.

bubble_chart Pathological Changes

Eosinophils extensively infiltrate the gastrointestinal tract, ranging from the pharynx to the rectum, with the stomach and small intestine being the most commonly affected. Based on the extent of infiltration, it can be classified as localized or diffuse. The localized type is most frequently seen in the gastric antrum, presenting as firm or rubbery, smooth, sessile or pedunculated polypoid masses protruding into the lumen, which can lead to pyloric obstruction. The diffuse type often only causes mucosal edema, congestion, and thickening, occasionally accompanied by superficial ulcers and erosions. Intestinal lesions are mostly diffuse, with affected intestinal walls showing edema, thickening, loss of gloss on the serosal surface, and covered by fibrinous exudates.

Histological features include: 1. Submucosal stromal edema composed of fibroblasts and collagen fibers; 2. Massive infiltration of eosinophils and lymphocytes in the stroma, which may also be accompanied by macrophages, giant cells, or histiocytes; 3. Involvement of submucosal blood vessels, lymphatics, muscular layers, serosa, and mesenteric lymph nodes, along with mucosal ulcers and sessile or pedunculated granulomas. Eosinophilic infiltration may be confined to the gastrointestinal wall or may be transmural.

Klein classified eosinophilic infiltration of the gastrointestinal wall into three types based on the degree of involvement: 1. Mucosal type: Massive eosinophilic infiltration within the mucosa, accompanied by significant epithelial abnormalities, with complete loss of intestinal villi, leading to blood loss, iron deficiency, malabsorption, and protein loss; 2. Muscular type: Infiltration primarily in the muscular layer, causing thickening and nodularity of the gastrointestinal wall, leading to stenosis and obstruction; 3. Serosal type: Infiltration mainly in the serosa, with serosal thickening and possible involvement of mesenteric lymph nodes, resulting in ascites formation.

bubble_chart Clinical Manifestations

The disease lacks specific clinical manifestations, and symptoms are related to the location and extent of infiltration. It is generally divided into two types.

(1) Diffuse Type: More common in individuals aged 30–50, with males slightly outnumbering females. The course of the disease can last for decades. 80% of patients experience gastrointestinal symptoms, mainly characterized by spasmodic pain in the upper abdomen, accompanied by nausea, vomiting, and fever. The episodes have no obvious regularity and may be related to certain foods. Antacid and antispasmodic agents do not alleviate the symptoms, but they may resolve spontaneously.

1. Predominantly eosinophilic infiltration of the mucosa: Often presents with upper gastrointestinal bleeding, diarrhea, malabsorption, intestinal protein loss, hypoproteinemia, iron-deficiency anemia, and weight loss. About 50% of patients have asthma or allergic rhinitis, eczema, or urticaria. Fecal occult blood tests are positive, and Charcot-Leyden crystals may be present. 80% of patients show elevated peripheral blood eosinophils. Serum protein levels are reduced, and D-xylose tolerance tests are abnormal. X-ray gastrointestinal barium meal examinations may appear normal or show signs of mucosal edema. Endoscopy may reveal mucosal congestion, edema, or erosion. Biopsy shows eosinophilic infiltration.

2. Predominantly eosinophilic infiltration of the muscular layer: Causes significant thickening and rigidity of the stomach and small intestine walls. Patients often exhibit symptoms and signs of pyloric obstruction or incomplete small intestine obstruction. X-ray gastrointestinal barium meal examinations reveal pyloric stenosis, reduced peristalsis, or multiple polypoid filling defects in the gastric antrum. Diagnosis relies on gastric or small intestine biopsy, showing extensive mature eosinophilic infiltration into the submucosa, extending through the muscular layer to the serosal layer.

3. Predominantly eosinophilic infiltration of the subserosal layer: Often leads to ascites or pleural effusion containing large numbers of eosinophils. Laparotomy commonly reveals thickening of the small intestine serosa and eosinophilic infiltration. Similar changes may also be observed in gastric serosal lesions.

(2) Localized Type: More common in individuals aged 40–60, with no significant gender difference in incidence. The main symptoms are spasmodic pain in the upper abdomen, nausea, and vomiting. The onset is relatively acute, and the course is shorter. Patients typically have no obvious allergy history, and only a minority show elevated peripheral blood eosinophils. X-ray gastrointestinal barium meal examinations may reveal thickening and rigidity of the gastric antrum, antral stenosis, and smooth round, oval, or lobulated filling defects resembling tumors. Endoscopy may show polypoid masses, mucosal congestion, and edema, often misdiagnosed as tumors or Crohn's disease. Tissue biopsy reveals massive eosinophilic infiltration.

bubble_chart Diagnosis

The diagnosis of this disease is not without difficulty, and sometimes surgical exploration is required for confirmation. With the widespread application of endoscopy, it has significant implications for the diagnosis of this disease.

Leinbach proposed the diagnostic criteria as follows: 1. Gastrointestinal symptoms and signs after consuming specific foods; 2. Increased eosinophils in peripheral blood; 3. Histological confirmation of eosinophilia or infiltration in the gastrointestinal tract.

Due to the difficulty in diagnosing many cases, clinically, whenever encountering unresolved gastrointestinal symptoms, a history of allergic diseases, or gastrointestinal symptoms that appear or worsen after consuming certain foods or medications, accompanied by elevated peripheral blood eosinophils, the possibility of this disease should be considered. Gastrointestinal barium meal imaging or endoscopic examination should be performed, with biopsies taken for pathological examination. However, a negative biopsy result does not exclude this disease.

bubble_chart Treatment Measures

The treatment principles for this disease are to remove allergens, suppress allergic reactions, and stabilize mast cells, thereby alleviating symptoms and eliminating lesions.

(1) Medical Treatment

1. Dietary Control: Identified or suspected allergenic foods or medications should be discontinued immediately. For patients with no history of food or drug allergies, a sequential elimination method can be used to exclude potential allergenic foods one by one, such as milk (especially in children), eggs, meat, shrimp, gluten-containing products, and sensitive medications. Many patients experience rapid improvement in abdominal pain and diarrhea after eliminating the causative foods or medications from their diet, particularly those with predominant mucosal lesions, where the effect is more pronounced. Although dietary control may not cure the disease, it should generally be considered a fundamental measure and implemented first when formulating a treatment plan.

2. Use of Glucocorticoids: Hormones are highly effective for this disease, with most cases showing symptom improvement within 1–2 weeks of treatment. This includes rapid relief of abdominal cramping, reduction or cessation of diarrhea, and normalization of peripheral blood eosinophil levels. For patients with serous membrane-type manifestations, ascites typically resolves completely within 7–10 days of hormone therapy. Long-term efficacy is also excellent. In cases where hormone therapy alone does not fully eliminate symptoms, the addition of azathioprine (50–100 mg daily) often yields good results.

The usual regimen is prednisone 20–40 mg/d orally for 7–14 days as one course. An equivalent dose of dexamethasone may also be used.

3. Use of Sodium Cromoglicate: Sodium cromoglicate (cromolyn sodium) is a mast cell stabilizer that inhibits degranulation by stabilizing mast cell membranes, thereby preventing the release of mediators such as histamine, slow-reacting substances, and bradykinin, and exerting its anti-allergic effects. In 1988, Moots reported a case where a patient who failed prednisone treatment achieved good results with sodium cromoglicate. The method was 100 mg orally four times daily. Symptoms gradually improved after 10 days, and complete remission was achieved within one month, with blood eosinophils dropping from 71% to 4%. Full recovery and a 10 kg weight gain were observed after 10 weeks. Di-Gioacchino reported two cases where daily intake of 1200 mg sodium cromoglicate led to symptom resolution, inflammation regression, and normalization of peripheral blood eosinophils after 4–5 months of treatment.

The typical dosage of sodium cromoglicate is 40–60 mg three times daily, though doses up to 800–1200 mg/d have been used. Treatment duration varies from 6 weeks to 5 months. For patients who do not respond to glucocorticoids or experience severe side effects, sodium cromoglicate can be used as an alternative.

(2) Surgical Treatment

For patients with localized lesions primarily involving muscle layer infiltration, often presenting with pyloric obstruction or small intestine obstruction, subtotal gastrectomy, intestinal segment resection, or gastroenterostomy may be considered. If symptoms persist or eosinophil levels remain elevated postoperatively, low-dose prednisone (5 mg or 2.5 mg/d orally) can be used for maintenance therapy for a period.

This disease is a self-limiting allergic disorder. Although it may recur, long-term follow-up has shown no malignant transformation, and the prognosis is generally favorable.

bubble_chart Differentiation

The following diseases should be differentiated from this condition:

(1) Chinese Taxillus Herb infection. Peripheral blood eosinophilia can be seen in Chinese Taxillus Herb diseases caused by hookworms, schistosomes, tapeworms, and Strongyloides stercoralis, each with its own clinical manifestations.

(2) Gastrointestinal cancer and cervical malignancy with cachexia may also present with elevated peripheral blood eosinophils, but these are secondary and should be accompanied by other manifestations of cancer or lymphoma.

(3) Eosinophilic granuloma. This primarily occurs in the stomach, large intestine, and small intestine as localized masses. Pathological examination reveals eosinophilic granulomas mixed within the connective tissue matrix. A history of allergies is rare, and peripheral white blood cell counts and eosinophils often do not increase.

(4) Eosinophilia. In addition to elevated peripheral blood eosinophils, the lesions not only affect the intestines but also extensively involve other solid organs such as the brain, heart, lungs, and kidneys. The disease course is short, the prognosis is poor, and death often occurs within a short period.