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 Table of Contents  
CASE REPORT
Year : 2020  |  Volume : 5  |  Issue : 2  |  Page : 86-89

Eosinophilic gastroenteritis presenting as persistent abdominal pain and ascites: A case report


Department of Internal Medicine, College of Medicine, King Khalid University; Department of Internal Medicine, Aseer Central Hospital, Abha, Saudi Arabia

Date of Submission06-Aug-2020
Date of Decision14-Oct-2020
Date of Acceptance30-Oct-2020
Date of Web Publication25-Feb-2021

Correspondence Address:
Dr. Mohammed Attieh S. Alzahrani
Department of Internal Medicine, College of Medicine, King Khalid University, Abha, P. O. Box 641
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/KKUJHS.KKUJHS_3_20

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  Abstract 

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 Jul 28];5:86-9. Available from: https://www.kkujhs.org/text.asp?2020/5/2/86/309608


  Introduction Top


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.[1] 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).[2]

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.[3] 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,[4],[5] or a combination with other autoimmune disorders (ulcerative colitis, celiac disease, and systemic lupus erythematosus.[6],[7]

Kajiser first described EGE in 1937.[8] 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.[9] 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.[10] 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.[11] 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).[12] Many patients develop a relapse after stopping steroid therapy; hence, there is more value on steroid-sparing medication.[2]

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 Top


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

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Figure 2: Magnetic resonance elastography showed thickening of the small bowel

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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 Top


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.[13] 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.[13],[14],[15] 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.[6],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16],[17],[18] 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.[13] 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.[5] 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.[19],[20] 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%).[16] 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.[21]

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.[22] Approximately 50% of patients with the mucosal form were reported to have a food allergy or intolerance.[13] 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.[23] 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

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

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