Journal of Regional Section of Serbian Medical Association in Zajecar
Year 2005     Volumen 30     Number 2
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UDK: 616.33/.34-002 ISSN 0350-2899, 30(2005) 2 p.82-85
Case report

Eosinophilic gastroenteritis - case review

Zoran Joksimović(1), Dušan Bastać(2)
(1) Private doctor's office of Internal medicine "Joskimović", Bor;
(2) Private doctor's office of Internal medicine "Dr Bastać", Zaječar



  Summary: Base Eosinophilic gastroenteritis (EGE) is a rare disease of unknown etiology characterised by eosinophilic infiltration of gastrointestinal tract wall. The symptoms and physical findings depend on the place seized by eosinophilic infiltration and on the depth of infiltration in the organ wall.
Patient and method: This is a case of a female patient with abdominal pain and diarrhea as the leading symptoms. Eosinophilic Le-s were increased in the leukocyte formula. The upper digestive endoscopy showed a hyperemia of duodenum mucosa and a positive ureasa test for Helicobacter pylori. The helicobacter infection eradication therapy resulted in no improvement. After some diagnostic uncertainties, the esophagogastroduodenoscopy with duodenum mucosa biopsy was repeated. The pathohistological findings of eosinophilic infiltration of mucosa and persistent peripheral eosinophilia directed the differential diagnostics at the EGE.
Results: Upon therapy with glucocorticoides, all subjective discomforts were removed and laboratory parameters were normalised.
Conclusion: The EGE is a rare entity that can easily be left undiagnosed. We suspect this disease when we have patients with gastrointestinal discomforts whereby diagnosis cannot be established by standard checkups. Pathohistological findings are necessary for diagnosis confirmation.
Key words: eosinophilia, gastroenteritis, infiltration, glucocorticoides

Note: full text in Serbian
Napomena: kompletan tekst rada na srpskom jeziku



Eosinophilic gastroenteritis (EGE) is a rare disease characterized by gastrointenstinal symptoms, eosinophilic infiltration of one or many areas of gastrointenstinal tract, absence of other known causes of eosinophilia and exclusion of eosinophilia connection with organs out of gastrointenstinal tract(GIT). Etiology of EGE is unknown, and pathophysiological mechanisms of disease are insufficiently explained (1, 2).

This nosologic unit was first time described by Kaiser in 1937. He defined EGE as eosinophilic
infiltration in gastrointenstinal tract with percent increase of eosinophile in periphery blood (3).
Disease is described in all parts of the world and all age groups. It is the most often in an age group from 20 – 60 years. Mortality is rare and result of complications : malnutrition, intestinal opstruction, perforation or bleeding (4).

Clinical picture of EGE depends on the seized region of GIT or depth of wall infiltration.
Disease hits most often stomach and small intestine (antrum in 63% and approx. part of small intestine in 75% of cases). Regarding to the prevailed infiltration of eosiphile in organ wall, the following types of disease are: mucous, muscle, subserous and mixed (1, 4, 5).

The following possible symptoms are: pains in epigastrium and/or lower part of stomach,
appetite loss, difficulty in swallowing, nausea, emesis, growling and pouring in intenstines, body weight loss, endem of shanks. When a muscle layer of intenstine is also seized, the signs of subileus and leus are developed, that is obstructive icterus. When a subserous is seized, an ascites appears with high concentration of eosinophile in it (5, 6).

Laboratory findings : erythrocyte sedimentation is usually moderately rapid. Number of leucocytes is easily increased. Eosinophilia of 20 – 80% is present in differential blood picture. Patients with EGE have increased IgE in serum. Sideropenial anemia is present very often. Increased alpha 1-antitrypsin in stool means loss of albumin, what would result into hypoalbuminemia (1, 7, 8).
Contrast X-ray examinations GIT, Ultra saund examination and CT, that is NMR, could possibly show some changes as the result disease complication (symptoms of pseudoachalasia, ileus, ascites) (4, 9).
Treatment of patients with EGE depends on disease flow and clinical symptoms. Glucocorticoiodes are basic therapy (1, 2, 4).



Female patient J.D., born in 1953, came to medical examination on 23rd November 2003 due to
paints in stomach, nausea and diarrhea. Discomforts have started two and a half months ago. Patient lost about 5 kg of body weight since discomforts appeared. Objective findings during medical examination: apherbile, eupnoic, cardiopulmonary compensated, good bled skin and visible mucous membranes. Body height 159 cm, body weight 62 kg. Abdomen light meteoristic on palpation painful sensitive periumbilicaly without palpatory findings with increased aabdominal organs and resistances. Ultra sound examination of upper abdomen normal.
Laboratory parameters SE 23,Le 9,8x109 /l (Eo 14%),Eri 4,1x1012 /l,Hb 11,8 g/l . Values of basic biochemical analyses (glycemia, urea, creatinine, AST, ALT, bilirubines, amylase in serum, alkali phosphatase and gama GT) in normal limits. Coprocultures (three times) without increase of pathogenic bacterium. Stool negative (three times) on intestinal parasite. Colonoscopy : findings regular. Eosophagogasstroduodenoscopy : light hyperemic mucose membrane of duodenal bulbus. Positive ureasic test on Helicobaster pilori. Diagnosis making : Duodenitis,Helicobacteriosis. Patient has obtained a tripartite eradication therapy. Then, the therapy was continued with inhibitors of protonic pump. However, subjective discomforts are persistent. Even though, diarhea continued and patient lost another 4 kg of weight for the next thirty days. Upper digestive endoscopy was repeated (28th January 2004) and showed completely normal endoscopic findings. In spite of that, biopsy of the most distal part of duodenum was done due to differential diagnostics of malabsorption syndrom. Pathohystological findings showed light atrophy of villus, mucose infiltration of with cells of chronic immflamation and eosinophilic leucocites.
Control laboratory analyses showed again eosinophilia (23 %) with normal values of other parameters. Then, diagnosis for EGE was at first place in differential diagnostics.
Patient has obtained a therapy with glucocorticoides since 1st February 2004 : Pronison tablets 40 mg in one morning dosage, then 10 days the dosage was gradually decreased to dosage of 10 mg that was maintained for 10 days. (Total duration of therapy was six weeks). After a week since therapy introduction, the pains sopped. Stool was normalised on tenth day. Patient got her weight. Eosinophilia was decreased such as after a month and half the percent of eosinophile was 5 %, and 2 % on 25th March 2004. On control check up, 18th August 2004, patient haad no subjective discomforts, physical findings were regular (body weight 65 kg). Laboratory findings were within lilmits of reference values.



Although the EGE etiology was not explained, it was noticed that there is a connection between disease and some allergic reactions. About 50 % of patients with EGE have one or more allergic manifestation in anamnesis (bronchial asthma, eczema or aathopic dermatitis). The all patients have good reactions on therapy with glucocorticoides (10, 11).

According to this, a hypothesis for specific intolerantion on food was developed, although the exact allergens were not identified (2, 11, 12). Inflammatory stimulants could be a trigger of eosinophilic infiltration GIT including allergy on food, immunological disordeers, possible infections (1, 2). Inflammation results into tissued lesion with degranulation with liberation of cytokine and proteine that could directly destroy a wall of some GIT parts. The basic protein was identified from IgE class – eosinophilic cationic protein liberated by eosinophile. It seams that interlukin 5 (IL-5) from activated T lymphocytes presents a responsible factor for eosinophilic colonization (2, 7).

There is a suspicion that Helicobacter pylori infection could have some connections with EGE was not confirmed although this microorganism could induce reaction of histamine libereration from basophile with IgE as reaction mediator (13).

We suspects on EGE of patients with gastrointenstinal discomforts and eosinophilia in leucocyte formula, that is increased IgE in serum (14, 15).

Diagnosis is made by endoscopy and pathohystological verification of disease. Endoscopic changes are ulceration, haemorrhage and nodular thickenings. Histopathological changes show eoasinophilic infiltration of mucose, specially lamine proprie.Disease penetration of muscle layer the hollow organ GIT is confirmed by endoscopic ultrasonography (2, 16).

Differential diagnosis EGE includes malignant diseases, GIT, CrohnĘs disease, ulcus disease, system diseases, amyloidosis, MenetrierĘs disease, tuberculosis, sarcoidosis, allergy on food, parasitic diseases, hypereosinophilic syndrom and eosinophilic granuloma (1, 2, 17).

Patient treatment with EGE depends on disease flow and clinical symptoms. Glucocorticoides are basic therapy, specially for patients with obstructive gastrointenstinal symptoms and eosinophilic ascites. Prednisolon 0.5 - 0.75 mg/kg body weight (usually in daily dosage of 40-60 mg) is often used orally or parenterally Metilprednisolon 0.25 – 0.5 mg/kg body weight (the most often 32 mg daily).

Answer on therapy is obtained upon 1 – 2 weeks. Therapy is carried out for 4 – 8 weeks. Some patients need longer therapy, but some of them need permanent treatment with small dosage of glucocorticoides (18, 19).

In some cases, the antiinflammatory medicines were successful as well as modifyers of leucotriene (monteleucast), stabilizers of mast cells (chromoglicate) and antagonist of 5-HT2 receptor (ketotiphene) (4, 20). In cases where diarrhea is the main symptom, very careful use of antidiuretic is required (for exp. Loperamid). When anemia is expressed, iron has to be compensated. Clinical investigations have not confirmed a connection between allergy on food and EGE, therefore the elimination diets even have no influence on disease flow (21).
Surgical treatment is required for patients with symptoms of gastrointenstinal opstruction (2, 4, 22).



A case of female patient with EGE was presented in this work where a diagnosis could be easily missed. Disease is masked with number of often gastrointenstinal symptoms and signs and very often it is discovered on operating table. We suspect on this disease when patients have gastrointenstinal discomforts and where standard examinations could give the explanation of those discomforts. Early diagnosis enables successful treatment, decreases unnecessary surgical operations and mortality. Pathohystological findings of eosinophilic infiltration are required for diagnosis confirmation.



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  Corresponding Address:
Zoran Joksimović
Cara Lazara 12, 19210 Bor
Tel. +381 30/439-606
e-mail: joksaz@ptt.yu
  Paper received: 30. 06. 2005.
Paper accepted: 26. 07. 2005.
Published online: 20. 08. 2005.
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