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It is only for medical professionals to read for reference.
If you encounter abdominal pain or diarrhea of unknown cause, don't miss the cause.
Case profile ■ The main complaint and history of current illness, a 64-year-old male, was admitted to the hospital with recurrent abdominal pain and diarrhea for more than 10 days, and then aggravated for 3 days.
Dissolve yellow and watery stools 5-10 times a day, without mucus, pus, or blood, with intermittent abdominal distension and pain.
■ Past history The patient has not had any abdominal surgery in the past, and denied the history of drug allergy, history of asthma, and history of allergic rhinitis.
■ Physical examination Physical examination has a flat abdomen, slight tenderness around the umbilicus, and normal bowel sounds.
■ Auxiliary examination The absolute value of the patient's eosinophils rose from 0.
92x109/L to 4.
29x109/L within 3 days after admission, and the percentage rose from 6.
7% to 26.
3%.
Gastroscopy: chronic superficial gastritis, duodenal descending segmentitis; colonoscopy: patchy congestion and erosion from the ascending colon to the sigmoid colon, local ulcer formation, covering necrosis, and blurred vascular network.
Figure 1: Shown under the EGE endoscope.
A.
Gastroscopy prompts: duodenal descending flaky congestion; BE enteroscopy prompts: colonic intestinal wall patchy congestion and erosion, local ulcer formation, covering necrosis, vascular network obscured Pathology: moderate chronic mucosal inflammation with ulcers.
Figure 2: Histopathological examination of colonic mucosa (HEx400).
Enhanced CT of the abdomen: the structure of the bowel is not clear.
■ During the diagnosis and treatment, symptomatic treatments such as protection of gastrointestinal mucosa, antidiarrhea, and nutritional support were given, and the patient's diarrhea and abdominal pain were not significantly relieved.
After exclusion of parasitic infections, tumorous diseases, allergic diseases and other diseases that need to be identified, empirical hormone therapy was given on the 6th day after admission.
After oral administration of 40 mg of prednisone acetate once a day, the symptoms of abdominal pain and diarrhea improved significantly, and the absolute value and percentage of eosinophils decreased to normal.
On the 7th day of hormone treatment, the patient suddenly developed continuous pain in the upper right abdomen, unresolved stool, no nausea and vomiting.
Physical examination: whole abdominal tenderness, rebound pain, weak bowel sounds.
Review the abdominal plain film to consider: incomplete intestinal obstruction.
Figure 3: Flat abdominal radiographs, multiple liquid-gas flat intestinal dilatation in the whole abdomen, fasting, conservative treatment in enema.
The patient's family members requested to be discharged automatically and re-admitted one day after discharge.
Abdominal CT showed that the small intestine, ileocecal area and colorectal area were obviously dilated and accumulated fluid, the intestinal wall became thinner, and more gas accumulated.
Intestinal necrosis was not ruled out.
Figure 4: Abdominal CT, the small intestine, ileocecal area and colorectal area are obviously dilated and effusion, the intestinal wall becomes thin, and frequent pneumatosis is treated by emergency surgery.
During the operation, there is 200ml of purulent exudate in the abdominal cavity, starting from the ileocecal area, The small intestine is 50cm from the flexion ligament to 100cm from the ileocecal area.
There is extensive spot necrosis of the jejunum and ileum, partial gangrene; the ascending colon, transverse colon, descending colon to the peritoneal reentry 7cm colon necrosis, surgical removal of necrotic small intestine and colon, and small bowel dissection after resection End anastomosis, ileostomy.
Necrotic small bowel pathology: full-thickness hemorrhage, edema, vasodilation, congestion of the intestinal wall, multiple mucosal ulcers, local areas deep to the submucosa, atrophy and thinning of the submucosa and muscular layer, full-thickness purulent inflammation of the bowel wall, serous Suppurative inflammation, with an increase of about 50 eosinophils/HPF in small focal areas.
Figure 5: Histopathological examination of the small intestine mucosa (HEx400).
After a large number of EOS infiltration in the small focal area of the mucosa, the patient developed a small intestinal anastomotic fistula.
After the second operation, the patient's general condition was poor and eventually died.
■ Case summary This is a case of eosinophilic gastroenteritis (EGE) involving the duodenal mucosa, small intestine, colon mucosa, and muscle layer, and the main manifestation of ulcerative lesions of the intestinal wall of the whole colon.
After empirical hormone therapy, the clinical manifestations and test results improved, but eventually intestinal obstruction and even necrosis still occurred.
Recognizing that EGEEGE is a rare disease, first proposed by Kaijser in 1937 [1], it is characterized by eosinophils infiltrating the intestinal wall, and manifestations of various gastrointestinal symptoms.
EGE manifestations may be affected by location and intestinal wall.
The depth and degree of the disease are different, and the clinical symptoms are different. EGE is a chronic recurrence process, usually involving the stomach and small intestine, and other parts of the infiltration have also been reported.
The most common lesions of eosinophilic small bowel and colitis are diffuse mucosa and submucosal eosinophil infiltration, which typically leads to non-specific thickening of the intestinal wall and folds of the diseased intestinal structure [2,3].
EGE can be divided into mucosal type, muscle type and serosal type according to the degree of involvement [4,5].
Eosinophilic infiltration rarely only affects the muscle layer, mucosa, and submucosa, and may also affect the stomach and duodenum.
■ Clinical manifestations The typical manifestation of EGE is the appearance of non-specific gastrointestinal symptoms and gastrointestinal eosinophil infiltration, without any other verifiable causes of blood eosinophilia, such as parasitic infection or certain blood And autoimmune diseases, there is no specific allergic reaction.
Nevertheless, many patients may have a history of non-specific allergies, such as hay fever, eczema, or drug sensitivity, and up to 72%-90% of patients are found to have abnormally elevated peripheral eosinophils.
Other patients were found to be related to other autoimmune diseases, such as ulcerative colitis, celiac disease, and systemic lupus erythematosus [6].
The clinical manifestations of EGE mainly depend on the site of involvement, including nausea, vomiting, diarrhea, abdominal pain, malabsorption, excess fat, secondary iron deficiency anemia, hypoproteinemia, and intestinal obstruction [7].
■ How to diagnose So far, there is no standard for EGE diagnosis.
At present, the three main diagnostic criteria developed by Talley et al.
[8-9] are the most widely used: (1) gastrointestinal symptoms exist; (2) biopsy shows Eosinophil infiltration in one or more areas of the gastrointestinal tract; (3) No evidence of parasitic diseases or extraintestinal diseases.
An increase in peripheral eosinophils indicates eosinophilic gastroenteritis.
However, the definitive diagnosis of eosinophilic gastroenteritis requires histological evidence of eosinophilic infiltration, that is, 20 eosinophils per high-powered observation under a microscope.
The endoscopic manifestations of EGE are also non-specific, including intestinal mucosal erythema, fragility, nodules and occasional ulcerative changes.
Eosinophil infiltration is usually distributed in patches and can appear in the normal, non-inflammatory bowel wall.
Therefore, multiple biopsies may be required to avoid missed diagnosis.
Several different tests, such as gastroduodenoscopy and colonoscopy, and a variety of deep biopsies may be necessary to confirm the diagnosis.
Even so, due to uneven distribution, the extent and scope of the disease in most patients may be difficult to accurately assess [10-11].
In 1970, Klein et al.
defined three disease manifestations that are related to disease progression and involve the depth of the gastrointestinal tract: (1) The mucosal type of small intestine EGE (25%-100%) is the most common one, and its characteristics are Vomiting, abdominal pain, diarrhea, stool loss, iron deficiency anemia, malabsorption, and protein loss; (2) Muscle type (13%-70%) is dominated by muscle eosinophil infiltration, leading to thickening of the intestinal wall, leading to Gastrointestinal obstructive symptoms; (3) The serosal layer (12%-40%) is the least common, affecting a small number of patients, and is characterized by exudative ascites.
Compared with other types, peripheral blood eosinophils The count goes up [12-13].
■ How to judge the prognosis Under EGE endoscopy, gastric and duodenal mucosal edema is more common.
In this case, the patient has multiple ulcerative lesions in the ascending colon and transverse colon mucosa as the main manifestations.
After hormone treatment, the patient's symptoms of abdominal distension, abdominal pain, and diarrhea were relieved, and the total number and classification of eosinophils also fell to normal, but eventually there were changes in the condition such as intestinal obstruction, and even intestinal necrosis.
It can be considered that in patients with EGE, the more extensive the lesion, the deeper the depth of invasion, the worse the prognosis.
Many previous case reports suggested that the peripheral EOS level may be an effective biomarker for diagnosing relapse and remission in EGE patients [14].
This case is a case of atypical eosinophilic gastroenteritis, and the patient’s peripheral EOS level cannot be used to determine the outcome of the disease during the treatment process, and it cannot be used as a basis for remission.
"Gastroenterology" also clearly pointed out: the degree of increased eosinophils in peripheral blood has nothing to do with the degree of eosinophil infiltration and epithelial damage, and it cannot be used as an indication for efficacy evaluation [15].
References: [1] Yun MY, Cho YU, Park IS, Choi SK, Kim SJ, Shin SH, et al.
Eosinophilic gastroenteritis presenting as small bowel obstruction.
A case report.
World J Gastroenterol 2007;13:1758-60.
[2]Horton KM, Corl FM, Fishman EK: CT of nonneoplastic diseases of the small bowel: spectrum of disease.
Pictorial essay.
J Comput Assist Tomogr, 1999, 23: 417-428.
[3]Vitellas KM, Bennett WF, Bova JG, Johnson JC, Greenson JK, Caldwell JH: Radiographic manifestations of eosinophilic gastroenteritis.
Abdom Imaging, 1995, 20: 406-413[4]Venkataraman S, Ramakrishna BS, Mathan M, Chacko A, Chandy G, Kurian G, Mathan VI.
Eosinophilic gastroenteritis--an Indian experience.
Indian J Gastroenterol 1998; 17: 148-149 [PMID: 9795503][5]Aceves SS, Bastian JF, Newbury RO, Dohil R.
Oral viscous budesonide:a potential new therapy for eosinophilic esophagitis in children.
Am J Gastroenterol 2007; 102: 2271-2279; quiz 2280 [PMID: 17581266 DOI: 10.
1111/ j.
1572-0241.
2007.
01379.
x][6]Eosinophilic gastroenteritis: diagnosis and clinical perspectives[7]Yun MY, Cho YU, Park IS, et al.
Eosinophilic gastroenteritis presenting as small bowel obstruction: A case report and review of the literature[J].
World Journal of Gastroenterology Wjg, 2007, 13(11): 1758 .
[8]Baig MA, Qadir A, Rasheed J.
A review of eosinophilic gastroenteritis.
Journal of Natl Med Assoc 2006;98:1616–9.
[9]Talley NJ, Shorter RG, Phillips SF, Zinsmeister AR.
Eosinophilic gastroenteritis: a clinicopathological study of patients with disease of the mucosa, muscle layer, and subserosal tissues.
Gut 1990;31:54-8.
[10]Chen MJ, Chu CH, Lin SC, Shih SC, Wang TE.
Eosinophilic gastroenteritis:Clinical experience with 15 patients World J Gastroenterol 2003;9:2813-6.
[11]Venkataraman S, Ramakrishna BS, Mathan M, Chacko A, Chandy G, Kurian G, et al.
Eosinophilic gastroenteritis -an Indian experience.
Indian J Gastroenterol 1998;17:148-9.
[12]Jawairia M, Shahzad G, Mustacchia P.
Eosinophilic gastrointestinal Disease,Review and update.
ISRN Gastroenterol 2012;2012:463689.
[13]Ingle SB, Hinge Ingle CR.
Eosinophilic gastroenteritis: An unusual type of gastroenteritis.
World J Gastroenterol 2013;19:5061–6[14]Cheng Yu, Tan Shiyun, Li Ming, et al.
Analysis of 27 cases of eosinophilic gastroenteritis[J].
China Journal of Endoscopy, 2020, 8(26).
[15]Chen Minhu, Yang Yunsheng, Tang Chengwei.
Gastroenterology[M].
People's Medical Publishing House, 2019148-9.
[12]Jawairia M, Shahzad G, Mustacchia P.
Eosinophilic gastrointestinal Disease,Review and update.
ISRN Gastroenterol 2012;2012:463689.
[13]Ingle SB, Hinge Ingle CR.
Eosinophilic gastroenteritis: An unusual type of gastroenteritis .
World J Gastroenterol 2013;19:5061–6[14]Cheng Yu, Tan Shiyun, Li Ming, et al.
Analysis of 27 clinical cases of eosinophilic gastroenteritis[J].
Chinese Journal of Endoscopy, 2020, 8( 26).
[15]Chen Minhu, Yang Yunsheng, Tang Chengwei.
Gastroenterology[M].
People's Medical Publishing House, 2019148-9.
[12]Jawairia M, Shahzad G, Mustacchia P.
Eosinophilic gastrointestinal Disease,Review and update.
ISRN Gastroenterol 2012;2012:463689.
[13]Ingle SB, Hinge Ingle CR.
Eosinophilic gastroenteritis: An unusual type of gastroenteritis .
World J Gastroenterol 2013;19:5061–6[14]Cheng Yu, Tan Shiyun, Li Ming, et al.
Analysis of 27 clinical cases of eosinophilic gastroenteritis[J].
Chinese Journal of Endoscopy, 2020, 8( 26).
[15]Chen Minhu, Yang Yunsheng, Tang Chengwei.
Gastroenterology[M].
People's Medical Publishing House, 2019
If you encounter abdominal pain or diarrhea of unknown cause, don't miss the cause.
Case profile ■ The main complaint and history of current illness, a 64-year-old male, was admitted to the hospital with recurrent abdominal pain and diarrhea for more than 10 days, and then aggravated for 3 days.
Dissolve yellow and watery stools 5-10 times a day, without mucus, pus, or blood, with intermittent abdominal distension and pain.
■ Past history The patient has not had any abdominal surgery in the past, and denied the history of drug allergy, history of asthma, and history of allergic rhinitis.
■ Physical examination Physical examination has a flat abdomen, slight tenderness around the umbilicus, and normal bowel sounds.
■ Auxiliary examination The absolute value of the patient's eosinophils rose from 0.
92x109/L to 4.
29x109/L within 3 days after admission, and the percentage rose from 6.
7% to 26.
3%.
Gastroscopy: chronic superficial gastritis, duodenal descending segmentitis; colonoscopy: patchy congestion and erosion from the ascending colon to the sigmoid colon, local ulcer formation, covering necrosis, and blurred vascular network.
Figure 1: Shown under the EGE endoscope.
A.
Gastroscopy prompts: duodenal descending flaky congestion; BE enteroscopy prompts: colonic intestinal wall patchy congestion and erosion, local ulcer formation, covering necrosis, vascular network obscured Pathology: moderate chronic mucosal inflammation with ulcers.
Figure 2: Histopathological examination of colonic mucosa (HEx400).
Enhanced CT of the abdomen: the structure of the bowel is not clear.
■ During the diagnosis and treatment, symptomatic treatments such as protection of gastrointestinal mucosa, antidiarrhea, and nutritional support were given, and the patient's diarrhea and abdominal pain were not significantly relieved.
After exclusion of parasitic infections, tumorous diseases, allergic diseases and other diseases that need to be identified, empirical hormone therapy was given on the 6th day after admission.
After oral administration of 40 mg of prednisone acetate once a day, the symptoms of abdominal pain and diarrhea improved significantly, and the absolute value and percentage of eosinophils decreased to normal.
On the 7th day of hormone treatment, the patient suddenly developed continuous pain in the upper right abdomen, unresolved stool, no nausea and vomiting.
Physical examination: whole abdominal tenderness, rebound pain, weak bowel sounds.
Review the abdominal plain film to consider: incomplete intestinal obstruction.
Figure 3: Flat abdominal radiographs, multiple liquid-gas flat intestinal dilatation in the whole abdomen, fasting, conservative treatment in enema.
The patient's family members requested to be discharged automatically and re-admitted one day after discharge.
Abdominal CT showed that the small intestine, ileocecal area and colorectal area were obviously dilated and accumulated fluid, the intestinal wall became thinner, and more gas accumulated.
Intestinal necrosis was not ruled out.
Figure 4: Abdominal CT, the small intestine, ileocecal area and colorectal area are obviously dilated and effusion, the intestinal wall becomes thin, and frequent pneumatosis is treated by emergency surgery.
During the operation, there is 200ml of purulent exudate in the abdominal cavity, starting from the ileocecal area, The small intestine is 50cm from the flexion ligament to 100cm from the ileocecal area.
There is extensive spot necrosis of the jejunum and ileum, partial gangrene; the ascending colon, transverse colon, descending colon to the peritoneal reentry 7cm colon necrosis, surgical removal of necrotic small intestine and colon, and small bowel dissection after resection End anastomosis, ileostomy.
Necrotic small bowel pathology: full-thickness hemorrhage, edema, vasodilation, congestion of the intestinal wall, multiple mucosal ulcers, local areas deep to the submucosa, atrophy and thinning of the submucosa and muscular layer, full-thickness purulent inflammation of the bowel wall, serous Suppurative inflammation, with an increase of about 50 eosinophils/HPF in small focal areas.
Figure 5: Histopathological examination of the small intestine mucosa (HEx400).
After a large number of EOS infiltration in the small focal area of the mucosa, the patient developed a small intestinal anastomotic fistula.
After the second operation, the patient's general condition was poor and eventually died.
■ Case summary This is a case of eosinophilic gastroenteritis (EGE) involving the duodenal mucosa, small intestine, colon mucosa, and muscle layer, and the main manifestation of ulcerative lesions of the intestinal wall of the whole colon.
After empirical hormone therapy, the clinical manifestations and test results improved, but eventually intestinal obstruction and even necrosis still occurred.
Recognizing that EGEEGE is a rare disease, first proposed by Kaijser in 1937 [1], it is characterized by eosinophils infiltrating the intestinal wall, and manifestations of various gastrointestinal symptoms.
EGE manifestations may be affected by location and intestinal wall.
The depth and degree of the disease are different, and the clinical symptoms are different. EGE is a chronic recurrence process, usually involving the stomach and small intestine, and other parts of the infiltration have also been reported.
The most common lesions of eosinophilic small bowel and colitis are diffuse mucosa and submucosal eosinophil infiltration, which typically leads to non-specific thickening of the intestinal wall and folds of the diseased intestinal structure [2,3].
EGE can be divided into mucosal type, muscle type and serosal type according to the degree of involvement [4,5].
Eosinophilic infiltration rarely only affects the muscle layer, mucosa, and submucosa, and may also affect the stomach and duodenum.
■ Clinical manifestations The typical manifestation of EGE is the appearance of non-specific gastrointestinal symptoms and gastrointestinal eosinophil infiltration, without any other verifiable causes of blood eosinophilia, such as parasitic infection or certain blood And autoimmune diseases, there is no specific allergic reaction.
Nevertheless, many patients may have a history of non-specific allergies, such as hay fever, eczema, or drug sensitivity, and up to 72%-90% of patients are found to have abnormally elevated peripheral eosinophils.
Other patients were found to be related to other autoimmune diseases, such as ulcerative colitis, celiac disease, and systemic lupus erythematosus [6].
The clinical manifestations of EGE mainly depend on the site of involvement, including nausea, vomiting, diarrhea, abdominal pain, malabsorption, excess fat, secondary iron deficiency anemia, hypoproteinemia, and intestinal obstruction [7].
■ How to diagnose So far, there is no standard for EGE diagnosis.
At present, the three main diagnostic criteria developed by Talley et al.
[8-9] are the most widely used: (1) gastrointestinal symptoms exist; (2) biopsy shows Eosinophil infiltration in one or more areas of the gastrointestinal tract; (3) No evidence of parasitic diseases or extraintestinal diseases.
An increase in peripheral eosinophils indicates eosinophilic gastroenteritis.
However, the definitive diagnosis of eosinophilic gastroenteritis requires histological evidence of eosinophilic infiltration, that is, 20 eosinophils per high-powered observation under a microscope.
The endoscopic manifestations of EGE are also non-specific, including intestinal mucosal erythema, fragility, nodules and occasional ulcerative changes.
Eosinophil infiltration is usually distributed in patches and can appear in the normal, non-inflammatory bowel wall.
Therefore, multiple biopsies may be required to avoid missed diagnosis.
Several different tests, such as gastroduodenoscopy and colonoscopy, and a variety of deep biopsies may be necessary to confirm the diagnosis.
Even so, due to uneven distribution, the extent and scope of the disease in most patients may be difficult to accurately assess [10-11].
In 1970, Klein et al.
defined three disease manifestations that are related to disease progression and involve the depth of the gastrointestinal tract: (1) The mucosal type of small intestine EGE (25%-100%) is the most common one, and its characteristics are Vomiting, abdominal pain, diarrhea, stool loss, iron deficiency anemia, malabsorption, and protein loss; (2) Muscle type (13%-70%) is dominated by muscle eosinophil infiltration, leading to thickening of the intestinal wall, leading to Gastrointestinal obstructive symptoms; (3) The serosal layer (12%-40%) is the least common, affecting a small number of patients, and is characterized by exudative ascites.
Compared with other types, peripheral blood eosinophils The count goes up [12-13].
■ How to judge the prognosis Under EGE endoscopy, gastric and duodenal mucosal edema is more common.
In this case, the patient has multiple ulcerative lesions in the ascending colon and transverse colon mucosa as the main manifestations.
After hormone treatment, the patient's symptoms of abdominal distension, abdominal pain, and diarrhea were relieved, and the total number and classification of eosinophils also fell to normal, but eventually there were changes in the condition such as intestinal obstruction, and even intestinal necrosis.
It can be considered that in patients with EGE, the more extensive the lesion, the deeper the depth of invasion, the worse the prognosis.
Many previous case reports suggested that the peripheral EOS level may be an effective biomarker for diagnosing relapse and remission in EGE patients [14].
This case is a case of atypical eosinophilic gastroenteritis, and the patient’s peripheral EOS level cannot be used to determine the outcome of the disease during the treatment process, and it cannot be used as a basis for remission.
"Gastroenterology" also clearly pointed out: the degree of increased eosinophils in peripheral blood has nothing to do with the degree of eosinophil infiltration and epithelial damage, and it cannot be used as an indication for efficacy evaluation [15].
References: [1] Yun MY, Cho YU, Park IS, Choi SK, Kim SJ, Shin SH, et al.
Eosinophilic gastroenteritis presenting as small bowel obstruction.
A case report.
World J Gastroenterol 2007;13:1758-60.
[2]Horton KM, Corl FM, Fishman EK: CT of nonneoplastic diseases of the small bowel: spectrum of disease.
Pictorial essay.
J Comput Assist Tomogr, 1999, 23: 417-428.
[3]Vitellas KM, Bennett WF, Bova JG, Johnson JC, Greenson JK, Caldwell JH: Radiographic manifestations of eosinophilic gastroenteritis.
Abdom Imaging, 1995, 20: 406-413[4]Venkataraman S, Ramakrishna BS, Mathan M, Chacko A, Chandy G, Kurian G, Mathan VI.
Eosinophilic gastroenteritis--an Indian experience.
Indian J Gastroenterol 1998; 17: 148-149 [PMID: 9795503][5]Aceves SS, Bastian JF, Newbury RO, Dohil R.
Oral viscous budesonide:a potential new therapy for eosinophilic esophagitis in children.
Am J Gastroenterol 2007; 102: 2271-2279; quiz 2280 [PMID: 17581266 DOI: 10.
1111/ j.
1572-0241.
2007.
01379.
x][6]Eosinophilic gastroenteritis: diagnosis and clinical perspectives[7]Yun MY, Cho YU, Park IS, et al.
Eosinophilic gastroenteritis presenting as small bowel obstruction: A case report and review of the literature[J].
World Journal of Gastroenterology Wjg, 2007, 13(11): 1758 .
[8]Baig MA, Qadir A, Rasheed J.
A review of eosinophilic gastroenteritis.
Journal of Natl Med Assoc 2006;98:1616–9.
[9]Talley NJ, Shorter RG, Phillips SF, Zinsmeister AR.
Eosinophilic gastroenteritis: a clinicopathological study of patients with disease of the mucosa, muscle layer, and subserosal tissues.
Gut 1990;31:54-8.
[10]Chen MJ, Chu CH, Lin SC, Shih SC, Wang TE.
Eosinophilic gastroenteritis:Clinical experience with 15 patients World J Gastroenterol 2003;9:2813-6.
[11]Venkataraman S, Ramakrishna BS, Mathan M, Chacko A, Chandy G, Kurian G, et al.
Eosinophilic gastroenteritis -an Indian experience.
Indian J Gastroenterol 1998;17:148-9.
[12]Jawairia M, Shahzad G, Mustacchia P.
Eosinophilic gastrointestinal Disease,Review and update.
ISRN Gastroenterol 2012;2012:463689.
[13]Ingle SB, Hinge Ingle CR.
Eosinophilic gastroenteritis: An unusual type of gastroenteritis.
World J Gastroenterol 2013;19:5061–6[14]Cheng Yu, Tan Shiyun, Li Ming, et al.
Analysis of 27 cases of eosinophilic gastroenteritis[J].
China Journal of Endoscopy, 2020, 8(26).
[15]Chen Minhu, Yang Yunsheng, Tang Chengwei.
Gastroenterology[M].
People's Medical Publishing House, 2019148-9.
[12]Jawairia M, Shahzad G, Mustacchia P.
Eosinophilic gastrointestinal Disease,Review and update.
ISRN Gastroenterol 2012;2012:463689.
[13]Ingle SB, Hinge Ingle CR.
Eosinophilic gastroenteritis: An unusual type of gastroenteritis .
World J Gastroenterol 2013;19:5061–6[14]Cheng Yu, Tan Shiyun, Li Ming, et al.
Analysis of 27 clinical cases of eosinophilic gastroenteritis[J].
Chinese Journal of Endoscopy, 2020, 8( 26).
[15]Chen Minhu, Yang Yunsheng, Tang Chengwei.
Gastroenterology[M].
People's Medical Publishing House, 2019148-9.
[12]Jawairia M, Shahzad G, Mustacchia P.
Eosinophilic gastrointestinal Disease,Review and update.
ISRN Gastroenterol 2012;2012:463689.
[13]Ingle SB, Hinge Ingle CR.
Eosinophilic gastroenteritis: An unusual type of gastroenteritis .
World J Gastroenterol 2013;19:5061–6[14]Cheng Yu, Tan Shiyun, Li Ming, et al.
Analysis of 27 clinical cases of eosinophilic gastroenteritis[J].
Chinese Journal of Endoscopy, 2020, 8( 26).
[15]Chen Minhu, Yang Yunsheng, Tang Chengwei.
Gastroenterology[M].
People's Medical Publishing House, 2019
