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

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

INTRODUCTION

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).

REVIEW OF CASE

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.

DISCUSSION

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, Crohn¨s disease, ulcus disease, system diseases, amyloidosis, Menetrier¨s 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).

CONCLUSION

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.

REFERENCES

1. MyNgoc T Nguyen, MD Jean-Luc Szpakowski, MD Eosinophilic Gastroenteritis Last Updated: June 27, 2004 http://www.emedicine.com/med/topic688.htm
2. Štabuc B, Stevanović Ž et all: Eozinofilni gastroenteritis Zdrav. vestn. 2003; 72: 443-5:
3. Kaijser R. Zur Kenntnis der Allergischen Affectionen des Verdauungskannals vom Štandpunkt des Chirurgen aus. Arch Klin Chir 188: 36–64, 1937.
4. Jovan Teodorović et all: Gastroenterologija II Excelsior Beograd 1998 212-213
5. Chou CH, Shin JS, Wu MH, Chow NH, Lin XZ. Eosinophilic Gastroenteritis with Oesophageal Involvement. J Formos Med Assoc 1996; 95: 403-405.
6. Katz JA, Goldman H, Grand JR. Gastric mucosal biopsy in eosinophilic (allergic) gastroenteritis.Gastroenterology 1977; 73: 705.
7. Britto M.R.C. Thomas L. Eosinophilic Gastroenteritis - A Cause of Gastric Outlet Obstruction,Dyspepsia and Ascites Journal Gastroenterology, Hepatology & Nutrition, 2000; Volume3 No 3: 104-105
8. Santos J, Junquera F, Torres I, Molero X, Vilaseca J, Malagelada J. Eosinophilic gastroenteritispresenting as ascites and splenomegaly. European Journal of Gastroenterology &Hepatology 1995; 7: 675-678.
9. Gay et al. Gastrointestinal Case of the Day: Eosinophilic Gastroenteritis. American Journalof Roentgenology 1996; 167: 244.
10. Talley NJ, Shorter RG, Phillips SF, Zinsmeister AR. Eosinophilic gastroenteritis: a clinicopathological study of patients with disease of the mucosa, muscle layer, and submucosal tissues. Gut 1990; 31: 54-58.
11. Kalantar SJ, Marks R, Lambert JR, Badov D, Talley NJ. Dyspepsia due to Eosinophilic Gastroenteritis. Digestive Diseases and Sciences 1997; 42(11): 2327-2332.
12. Hogan SP, Mishra A, Brandt EB et al. A critical role for eotaxin in experimental oral antigen-induced eosinophilic gastrointestinal allergy. Proc Natl Acad Sci USA 2000; 97: 6681-93.
    Murakami K, Fujioka T, Nishizono A, Nagai J, Tokieda M, Kodama R, Kubota T, Nasu M.Atopic dermatitis successfully treated by eradication of Helicobacter pylori. Journal of Gastroenterology 1996; 31(supp IX): 77-82.
13. Takahashi T, Nakamura K, Nishikawa S, Tsuyuoka R, Suzuki A, Murakami M, Amenomori M,Okuno Y, Imura H: Interleukin 5 in eosinophilic gastroenteritis. Am J Haematol 1992; 40: 295-298.
14. Landres RT, Kuster GGR, Strum WB. Eosinophilic eosophagitis in a patient with vigorous achalasia. Gastroenterology 1978; 74: 1298-303.
15. Lee KJ, Hahm KB, Kim YS, Kim JH, Cho SW, Jie H et al. The Usefulness of Tc-99m HMPAO LabelledWBC SPECT in Eosinophilic Gastroenteritis. Clinical Nuclear Medicine 1997; 22(8): 536-541.
16. Lee CM, Changchien CS, Chen PC et al. Eosinophilic gastroenteritis: 10 years experience. Am J Gastroenterol 1993; 88: 70-4.
17. Lee M, Hodges WG, Huggins TL, Lee EL. Eosinophilic gastroenteritis. South Med J 1996; 89: 189-93.
18. Cello JP. Eosinophilic gastroenteritis - a complex disease entity. Am J Med 1979; 67: 1097-104.
19. Farmakologija Humprey.P.Rang et et all 5.izdanje 1. srpsko izdanje Data Status Novi Sad 2005 str 188
20. Talley N: Eosinophilic Gastroenteritis. In: Feldman M, Scharschmidt BF, Sleisenger M, Zorab R, eds. Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/ Management. 6th ed. Philadelphia, Pa: WB Saunders; 1998: 1679-86.
21. Matsushita M, Hajiro K, Morita Y, Takakuwa H, Suzaki T. Eosinophilic Gastroenteritis Involving the Entire Digestive Tract. American Journal of Gastroenterology 1995; 90(10): 1868-1870.