|Year : 2020 | Volume
| Issue : 2 | Page : 86-89
Eosinophilic gastroenteritis presenting as persistent abdominal pain and ascites: A case report
Mohammed Attieh S. Alzahrani
Department of Internal Medicine, College of Medicine, King Khalid University; Department of Internal Medicine, Aseer Central Hospital, Abha, Saudi Arabia
|Date of Submission||06-Aug-2020|
|Date of Decision||14-Oct-2020|
|Date of Acceptance||30-Oct-2020|
|Date of Web Publication||25-Feb-2021|
Dr. Mohammed Attieh S. Alzahrani
Department of Internal Medicine, College of Medicine, King Khalid University, Abha, P. O. Box 641
Source of Support: None, Conflict of Interest: None
Eosinophilic gastroenteritis (EGE) is a rare benign inflammatory disease affecting the infant and adult population. It presents by eosinophilic infiltration of the intestinal tract wall including the stomach, small intestines, and rarely the colon. EGE is divided into three subtypes depending on the layers and extent of bowel involved (mucosal, muscular, and serosal). Accurate diagnosis is still considered a challenge to professionals because of the protean manifestations; it needs a combination of clinical, laboratory, radiological, and histological workup. We report here a case of a 35-year-old male with a 3-month history of abdominal pain and distension. On examination, we found mild-to-moderate ascites and peripheral eosinophilia with markedly elevated eosinophils (85%). The imaging studies showed bowel wall thickening involving the entire small bowel and mild duodenitis. The diagnosis was confirmed by duodenal biopsy. The patient was managed with steroids (prednisolone 40 mg) and had an excellent response to the treatment. There is no single laboratory test or procedure to diagnose EGE; it requires a combination of laboratory, radiologic, and endoscopic findings. This report will guide decision-making for the initial phase of treatment and maintenance therapy in a more consistent way.
Keywords: Endoscopic findings, eosinophilic ascites, eosinophilic gastroenteritis
|How to cite this article:|
Alzahrani MA. Eosinophilic gastroenteritis presenting as persistent abdominal pain and ascites: A case report. King Khalid Univ J Health Sci 2020;5:86-9
|How to cite this URL:|
Alzahrani MA. Eosinophilic gastroenteritis presenting as persistent abdominal pain and ascites: A case report. King Khalid Univ J Health Sci [serial online] 2020 [cited 2021 Sep 27];5:86-9. Available from: https://www.kkujhs.org/text.asp?2020/5/2/86/309608
| Introduction|| |
In ordinary physiological conditions, eosinophils are detected in the whole gastrointestinal tract (GIT) excluding the esophagus and play a major role in the innate immune system of the digestive tract as a defense against several pathogens. Eosinophilic infiltration of the GIT can be observed in several illnesses including infections (parasite or bacteria), inflammatory bowel disease, hypereosinophilic syndrome, connective tissue disorders, myeloproliferative disorders, and drug hypersensitivity. Occasionally, eosinophilic infiltration of the gut is also noted in the deprivation of above causes. The abnormalities with such infiltrations collectively point out to eosinophilic gastrointestinal (GI) disorders that include eosinophilic gastroenteritis (EGE).
EGE is an unusual chronic inflammatory condition that influences both kids and adults and presents with eosinophilic infiltration of the intestinal tract wall usually including the stomach, small intestines, and rarely the colon. The etiology of such infiltration is not yet completely demonstrated. The previous report showed the probability of different pathogenic mechanisms participation including allergen hypersensitivity (asthma, eczema, rhinitis, drug/food allergies,, or a combination with other autoimmune disorders (ulcerative colitis, celiac disease, and systemic lupus erythematosus.,
Kajiser first described EGE in 1937. In 1970, this disease was categorized into three types according to the depth of eosinophilic infiltration: Mucosal, muscular, and subserosal layer disease; mucosal EGE is the most frequent type reported in clinical practice. Signs or manifestations vary from nonspecific GI symptoms such as abdominal discomfort, vomiting, and diarrhea to distinct symptoms such as malabsorption, protein-losing enteropathy, intestinal blockage, eosinophilic ascites, and pleural effusion. EGE can be characterized as primary (associated with inherited connective tissue disorders) or secondary (caused by drug or food allergy).
There is no specific laboratory test or method to diagnose EGE; only the presence of GI manifestations, eosinophilic infiltration of the GIT, and dropout of other intestinal eosinophilia causes are the criteria for diagnosis. Furthermore, there is no ideal treatment for EGE due to the variation in the clinical presentation, gravity, and evolution. Patients with mild disease can be treated symptomatically (dietary and drug treatment), while more symptomatic patients (malabsorption) need more aggressive therapy (corticosteroids). Many patients develop a relapse after stopping steroid therapy; hence, there is more value on steroid-sparing medication.
Most of the collective knowledge about EGE is generated from individual case reports or case series, due to its low prevalence making it hard to demonstrate the decisive findings of its epidemiology. However, recently EGE has gained more popularity because of the broad reconnaissance of eosinophilic esophagitis, the most common subtype of this disorder.
The present study helps in gathering and understanding the most recent, most pertinent reported information about EGE to supply a guide for understanding, diagnosing, and management of this progressively recognized disorder.
| Case Report|| |
A Saudi male patient aged 35 years reached our hospital with a 3-month history of abdominal pain and distension. He did not report any complaints of hematemesis, melena, or change in bowel habits, neither having any weight loss, fever, recurrent mouth ulcers, malar rash or joint pain, nor drug/food allergy. He had visited many hospitals without a clear diagnosis of his abdominal pain. In the emergency room, the patient was overall well with normal vital signs. No lymphadenopathy was noted. Chest, cardiovascular, and central nervous system examinations were normal. Abdominal examination presented positive shifting dullness with no organomegaly. His initial laboratory findings reported a leukocyte count of 17.33 × 103/μL with 35.5% of eosinophils, a hemoglobin count of 15.2 g/dL, and a platelet count of 422 × 103/μL. Coagulation profile, C-reactive protein, erythrocyte sedimentation rate, urea, and electrolytes levels were within the standard range. In the peripheral blood smear, an elevated eosinophilic count (49.1%) was found. The stool microscopy was negative for cyst and ova. Antinuclear antibody, rheumatoid factor, anti-Gliadin IgA, and HIV serology were negative. The diagnostic paracentesis of the ascetic fluid reported low serum/ascites albumin gradient, total white blood cell count was 9.5 × 103/μL, and eosinophilia 85% but no malignant cells. Bone marrow aspirate showed an increase in eosinophils and its precursors and no excess of blast cells. Computed tomography of the abdomen with contrast revealed mild-to-moderate ascites and thickening of the small bowel [Figure 1]. Upper GI endoscopy showed mild duodenitis. Biopsies of the duodenum revealed high eosinophilic infiltration. Magnetic resonant enteroclysis showed thickening of the small bowel [Figure 2].
|Figure 1: Computed tomography abdomen showed thickening of the small bowel|
Click here to view
|Figure 2: Magnetic resonance elastography showed thickening of the small bowel|
Click here to view
After ruling out the probability of parasitic infection, autoimmune disease, and malignancy, EGE was diagnosed based on the combination of symptoms, laboratory, radiological, and histological findings. A steroid, prednisolone 40 mg, was administered daily. Two weeks later, he had improvement from his symptoms. The white blood cell count was 9.9 × 103/μL with 0% eosinophils. One month later, he recovered from EGE, and an ultrasound follow-up of the abdomen revealed the absence of ascites. The treatment was attenuated and then terminated after 6 weeks. We obtained a signed copy of our patient consent permission before publishing personal information.
| Discussion|| |
EGE is a heterogeneous disorder with unexplained GI symptoms and is characterized by the presence of eosinophilic infiltration and degranulation, which can damage the GI wall. A gastroenterologist should be aware of EGE due to the nonspecific nature of the signs and symptoms, specifically in patients with mild manifestations. Studies from the United States have found a higher incidence over the past 50 years. EGE is known to be more frequent among the children and adults aged between 30 and 50 years of life, with a shift from male predominance to female predominance.,, Physicians seldom think of EGE diagnosis unless there is an increased eosinophil count in the peripheral blood. However, not all EGE patients have elevated peripheral blood eosinophilia, which might result in a false-negative diagnosis.,,,,,,,,,,,, The diagnosis can be made by eliminating the different causes of intestinal eosinophilia and relying on laboratory, radiological, and endoscopy findings. It is confirmed by endoscopic biopsy, which should show more of 20–25 eosinophil count per field on microscopic examination. The mucosal form is the most frequent presentation (45% of cases), which includes mucosal and submucosal involvement. Manifestations are characterized by abdominal pain, diarrhea, and malabsorption-related symptoms such as iron deficiency and protein-losing enteropathy. In the muscular form (12% to 30%), the inflammation extends deeper into the muscle coat, causing thickening of the digestive wall and typical symptoms of obstruction; the most frequent affected sites are usually the stomach and duodenum., The diagnosis is generally made after resection of the small bowel for obstruction where it is seen as abnormal luminal narrowing, more precisely in the distal antrum and in the proximal small bowel. In the serosal form or eosinophilic ascites, the rarest (12.5%–39%). The eosinophilic infiltration penetrates all the digestive wall layers including the serosal layer and causing eosinophilic ascites. White blood cell count can vary from a minimum of 10% to more than 80% above normal. Interestingly, this presentation has been detected in pregnant women or after delivery.
This reported case is a good example of reaching the clinical diagnosis and treatment of EGE that can add significant information for clinical practice. EGE should be taken into account when a patient arrives with unexplained GI manifestations and no other causes of intestinal eosinophilia are apparent (parasitic, bacterial, hypersensitivity, etc.). Other findings such as laboratory, radiological, and endoscopy results provide significant information that, when combined with histological findings, will lead to a confirmative diagnosis of EGE.
Food allergy also has a role in causing EGE in some patients. Approximately 50% of patients with the mucosal form were reported to have a food allergy or intolerance. Our patient had recurrent abdominal pain and distension needing upper GI endoscopic intervention. He had ascites and a high eosinophilic count in the ascitic fluid. The CT scan revealed wall thickening involving the entire small bowel [Figure 1]. Bone marrow aspirate showed an increase in eosinophils and its precursors, and biopsies from the duodenum showed eosinophilic infiltration of the intestinal wall.
Regarding that spontaneous remission, it was reported in almost 30%–40% of EGE patients; most of them need chronic treatment. Many treatment suggestions have been proposed including dietary therapy, steroids, leukotrienes inhibitors, and mast cell stabilizers, which have been tried in limited case series, but no prospective or randomized clinical trials have been documented. There is published literature comparing the efficacy and safety profiles of the different treatment options. Treatment with the steroids is the mainstay in the management of EGE; however, the duration of treatment is debatable. Many patients develop a relapse with steroid retraction; hence, there is more added-value on steroid-sparing medication. The long-term prognosis is good. Our patient was managed with steroids and recovered from his symptoms gradually after 2 weeks with an excellent response and 0% eosinophils. One month later, the patient has recovered from EGE with the absence of ascites.
In conclusion, EGE is an uncommon chronic inflammatory disease of the intestinal wall and is commonly underdiagnosed (or underreported), due to protean findings that resemble other GI disorders. Currently, there is still absence of a definite laboratory test or method for EGE diagnosis, which requires a combination of laboratory, radiologic, and endoscopic results. According to the disease gravity at the first presentation, many therapeutic choices can be considered. However, most therapeutic options have been reported in case reports or case series and have shown contradictive efficacy results. Further prospective and randomized clinical trials are necessary to assess the best therapeutic option in terms of efficacy and safety profiles in contrast with other treatment options. It may help in decision-making for the primary period of treatment and maintenance therapy in a more coherent way.
Declaration of patient consent
The author certify that he have obtained all appropriate patient consent forms. In the form, the legal guardian has given his consent for images and other clinical information to be reported in the journal. The guardian understands that names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Rothenberg ME. Eosinophilic gastrointestinal disorders (EGID). J Allergy Clin Immunol 2004;113:11-29.
Uppal V, Kreiger P, Kutsch E. Eosinophilic gastroenteritis and colitis: A comprehensive Review. Clin Rev Allergy Immunol 2016;50:175-88.
Zammit SC, Cachia M, Sapiano K, Gauci J, Montefort S, Ellul P. Eosinophilic gastrointestinal disorder: Is it what it seems to be? Ann Gastroenterol 2018;31:475-9.
Jensen ET, Martin CF, Kappelman MD, Dellon ES. Prevalence of eosinophilic gastritis, gastroenteritis, and colitis: Estimates from a national administrative database. J Pediatr Gastroenterol Nutr 2016;62:36-42.
Chang JY, Choung RS, Lee RM, Locke GR 3rd
, Schleck CD, Zinsmeister AR, et al
. A shift in the clinical spectrum of eosinophilic gastroenteritis toward the mucosal disease type. Clin Gastroenterol Hepatol 2010;8:669-88.
Copeland BH, Aramide OO, Wehbe SA, Fitzgerald SM, Krishnaswamy G. Eosinophilia in a patient with cyclical vomiting: A case report. Clin Mol Allergy 2004;2:7.
Ciccia F, Giardina AR, Alessi N, Rodolico V, Galia M, Ferrante A, et al
. Successful intravenous immunoglobulin treatment for steroid-resistant eosinophilic enteritis in a patient with systemic lupus erythematosus. Clin Exp Rheumatol 2011;29:1018-20.
Sharma H, Wood R, Coppes M. Food Allergy in Children. Pediatric Clinics of North America. 1st
ed., Vol. 58. Saunders; 2011.
Lee M, Hodges WG, Huggins TL, Lee EL. Eosinophilic gastroenteritis. South Med J 1996;89:189-94.
Alzahrani AM, Assiri MA, Alqahtani AS, Nemri NS, Alshehri MA. An unusual presentation of eosinophilic gastroenteritis: Case report and literature review. Open Gastroenterol J 2012;6:31-3.
Cello JP. Eosinophilic gastroenteritis A complex disease entity. Am J Med 1979;67:1097-104.
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.
Tien FM, Wu JF, Jeng YM, Hsu HY, Ni YH, Chang MH, et al
. Clinical features and treatment responses of children with eosinophilic gastroenteritis. Pediatr Neonatol 2011;52:272-8.
Spergel JM, Book WM, Mays E, Song L, Shah SS, Talley NJ, et al
. Variation in prevalence, diagnostic criteria, and initial management options for eosinophilic gastrointestinal diseases in the United States. J Pediatr Gastroenterol Nutr 2011;52:300-6.
Pineton de Chambrun G, Gonzalez F, Canva JY, Gonzalez S, Houssin L, Desreumaux P, et al
. Natural history of eosinophilic gastroenteritis. Clin Gastroenterol Hepatol 2011;9:950-6.e1.
Hurrell JM, Genta RM, Melton SD. Histopathologic diagnosis of eosinophilic conditions in the gastrointestinal tract. Adv Anat Pathol 2011;18:335-48.
Zhang L, Duan L, Ding S, Lu J, Jin Z, Cui R, et al
. Eosinophilic gastroenteritis: Clinical manifestations and morphological characteristics, a retrospective study of 42 patients. Scand J Gastroenterol 2011;46:1074-80.
Lim KC, Tan HK, Rajnakova A, Venkatesh SK. Eosinophilic gastroenteritis presenting with duodenal obstruction and ascites. Ann Acad Med Singap 2011;40:379-81.
Yun MY, Cho YU, Park IS, Choi SK, Kim SJ, Shin SH, et al
. Eosinophilic gastroenteritis presenting as small bowel obstruction: A case report and review of the literature. World J Gastroenterol 2007;13:1758-60.
Park SJ, Kenny PR, Palekar NA. Labor-associated eosinophilic gastroenteritis. Mil Med 2012;177:99-100.
Jaffe JS, James SP, Mullins GE, Braun-Elwert L, Lubensky I, Metcalfe DD. Evidence for an abnormal profile of interleukin-4 (IL-4), IL-5, and gamma-interferon (gamma-IFN) in peripheral blood T cells from patients with allergic eosinophilic gastroenteritis. J Clin Immunol 1994;14:299-309.
Abou Rached A, El Hajj W. Eosinophilic gastroenteritis: Approach to diagnosis and management. World J Gastrointest Pharmacol Ther 2016;7:513-23.
[Figure 1], [Figure 2]