Eosinophilic colitis (EC) is an uncommon inflammatory condition classified under eosinophilic gastrointestinal disorders (EGIDs). It is characterised by a predominance of eosinophilic infiltration in the colonic wall in patients presenting with relevant gastrointestinal (GI) symptoms [1]. Patients often present with abdominal pain and diarrhea, distinguishing EC from primary colonic eosinophilia, a condition in which patients remain asymptomatic [2]. EC can be either primary or secondary, depending on the aetiology of the disease. In most cases, primary EC is associated with an allergic response, either IgE-mediated, leading to an anaphylactic-type food allergy, or non-IgE-mediated, resulting in food enteropathy [3]. There is a slight preponderance among females and Caucasians. In severe cases, when the entire bowel wall is affected, complications such as intestinal obstruction or even perforation may occur [4]. Peripheral eosinophilia is variable, and a definitive diagnosis is established through biopsy. Imaging, laboratory tests, and endoscopy can aid in ruling out other conditions with similar presentations; however, EC remains a diagnosis of exclusion [5]. 

A 42-year-old married female, with no known comorbidities, presented to the outpatient department with a two-year history of intermittent abdominal pain and over one month of loose stools. The abdominal pain was episodic, localised to the epigastric region and the right upper quadrant (RUQ), radiating to the back and shoulder, and associated with nausea. She also reported on-and-off, low-volume diarrhea for more than a month, accompanied by colicky abdominal discomfort. She had no significant past medical history but underwent a cholecystectomy five years ago. Her personal history is notable for disturbed sleep and altered bowel movements. 

On examination, a young female patient was observed sitting comfortably on the bed, oriented to time, place, and person, and was vitally stable. Clinical signs of anaemia were evident, including pallor of the skin, nail beds, and conjunctiva. Koilonychia was noted. There was no evidence of jaundice, clubbing, lymphadenopathy, or peripheral oedema. Jugular venous pressure (JVP) was not elevated. Thyroid examination was unremarkable. On abdominal examination, the abdomen was soft and doughy, with tenderness localised to the right upper quadrant. The liver was palpable 1 cm below the costal margin, while the spleen was not palpable. Bowel sounds were audible. Chest, cardiovascular and neurological examinations were unremarkable. On admission, laboratory investigations revealed haemoglobin (Hb) of 8.3 g/dL (reference range=11.5-16 g/dL), total leukocyte count (TLC) of 14.1 ×10⁹/L (reference range=4.0-11 ×10⁹/L), and marked eosinophilia at 40% (reference range=1-6%). Peripheral blood film supported these findings, indicating hypochromia, anisocytosis, elliptocytes, target cells, leucocytosis, thrombocytosis, and moderate eosinophilia. C-reactive protein (CRP) was elevated at 11.2 mg/L (reference range=<5 mg/L). Renal function tests (urea, creatinine, and electrolytes) and liver function tests (LFTs) were within normal limits. The coagulation profile was also normal. A serum protein analysis revealed elevated total protein at 9.2 g/dL (reference range=6.4-8.3 g/dL) with a normal albumin/globulin (A/G) ratio. Further workup was advised, including stool examination for ova and parasites, serum IgE levels, and iron studies. The stool detailed report (DR), stool culture for sensitivity (CS), and stool occult blood tests were unremarkable. Notably, serum IgE was markedly elevated at 5977 IU/mL (reference range=<100 IU/mL). Table 1.

Table 1: Lab Parameters on Admission.

Echocardiography revealed normal cardiac function with an ejection fraction (EF) of 60%. A whole-abdomen ultrasound showed no abnormalities. Oesophago-gastro-duodenoscopy (OGD) identified fissured duodenal mucosa and mild pangastritis, with biopsies obtained for further evaluation (Fig. 1). Histopathological examination of the duodenal biopsy revealed mildly inflamed fragments of duodenal mucosa. In contrast, the gastric biopsy demonstrated mild focal active Helicobacter pylori-associated gastritis, with no evidence of intestinal metaplasia. A subsequent colonoscopy appeared grossly normal (Fig. 2); however, histopathological examination of colonic biopsies showed eosinophilic microabscesses with more than 100 eosinophils per high-power field (HPF) in the lamina propria and muscularis mucosae, findings consistent with eosinophilic colitis (Fig. 3). A contrast-enhanced CT of the chest, abdomen, and pelvis (CAP) (Fig. 4) was performed to exclude secondary causes of eosinophilic infiltration, such as parasitic infections, lymphoma, and GI malignancies, and to evaluate the extent and pattern of bowel involvement. The findings indicated an enlarged liver, measuring 140 mm with normal parenchymal attenuation. The rest of the scan was unremarkable.

 Figure 1: Upper GI Endoscopy.

Figure 2: Colonoscopy with Biopsy.

Figure 3: Histopathology Report Showing Eosinophilia and Micro-Abcesses.

Figure 4: CT scan of the Whole Abdomen.

The patient was initiated on H. pylori eradication therapy for 14 days following histopathological confirmation of H. pylori-associated gastritis on gastric biopsy. Concurrently, oral corticosteroid therapy was started with prednisolone 1 mg/kg body weight daily to address persistent eosinophilia and associated symptoms. She was advised to obtain a stool antigen test for H. pylori following completion of therapy. At her scheduled follow-up four weeks later, she presented with the test results, which were negative, indicating successful eradication. A repeat CBC showed a reduction in eosinophilia to 8%. The patient remained under outpatient monitoring for further evaluation and management.

Eosinophilic gastrointestinal disorders (EGID) are rare, long-standing conditions affecting the digestive tract and marked by the presence of eosinophilic infiltration within the GI wall. They most frequently involve the stomach and small intestine, with the colon being affected less commonly [6]. Eosinophilic colitis (EC) is the least commonly reported subtype of EGID, with only a limited number of adult cases documented, although its incidence appears to be increasing over the past decade. According to a large retrospective epidemiological study from the United States, the overall incidence of EC was found to be 3.7 per 100,000 individuals, with primary EC accounting for 2.4 per 100,000 population [7]. EGID are generally characterised by three key features: (1) peripheral eosinophilia (commonly ranging between 5% and 35%), (2) segmental infiltration of eosinophils within the GI tract, and (3) associated functional disturbances [8,9]. The clinical presentation of EGID is often non-specific and varies depending on the segment of the GI tract involved. Common symptoms and signs may include abdominal pain, nausea, vomiting, diarrhea, GI bleeding, bowel obstruction, malabsorption, weight loss, and, in some cases, ascites [10].

The clinical presentation of EC often varies depending on the specific layer of the intestinal wall predominantly affected by eosinophilic infiltration. In 1970, Klein et al. [11] proposed a classification system for EGID based on the most extensively infiltrated layer, categorising the disease into mucosa-predominant, muscularis propria–predominant, and serosa-predominant forms. This classification correlates well with both clinical manifestations and histopathological findings and is equally applicable to EC. Mucosal involvement typically results in malabsorption and diarrhea, transmural or muscularis involvement is often associated with signs of intestinal obstruction, and serosal disease is distinguished by the presence of eosinophilic ascites. Histological evaluation of the colonic mucosa of our patient revealed dense eosinophilic infiltration. Although the precise layer involvement was not determined in our case, the clinical presentation was consistent with mucosal-predominant disease as per Klein’s classification [11].

The exact cause of primary EGID remains largely unclear, with the underlying aetiology still not fully understood. In most cases, primary EC is associated with allergic reactions. These may be either IgE-mediated, leading to an anaphylactic-type food allergy, or non-IgE-mediated, resulting in food protein-induced enteropathy. Specific eosinophil chemoattractants, including interleukin-5 (IL-5) and eotaxins, are also believed to contribute to the pathogenesis of eosinophilic colitis by promoting eosinophil recruitment and activation within the GI tract [12]. Our patient had marked peripheral eosinophilia and significantly elevated serum IgE levels, both of which support an allergic or immunological component in disease pathogenesis, despite the absence of an identifiable food allergen or atopic history.

The diagnosis of EC is based on a combination of GI symptoms, peripheral eosinophilia, characteristic endoscopic and histopathological findings, and, in some cases, eosinophilic ascites, while excluding other well-defined causes of eosinophilia through comprehensive evaluation [13]. Laboratory investigations have limited diagnostic value in EGID due to their low sensitivity and specificity. Although peripheral eosinophilia can serve as a useful biological marker, it is not consistently present and may be transient in nature [14]. Endoscopic findings in EGID are often non-specific, and in the majority of cases, the mucosa appears normal on endoscopic examination, as observed in our patient [15], highlighting the importance of obtaining colonic biopsies even in the absence of visible mucosal abnormalities. Moreover, there is currently no established consensus regarding the normal physiological levels of eosinophils in the colonic mucosa. However, some researchers propose that a threshold of more than 40 eosinophils per HPF in at least two distinct colonic segments is required to support the diagnosis of EC [3]. It is important to note that normal eosinophil counts in colonic tissue vary significantly depending on the anatomical segment. Therefore, the location of the biopsy is crucial for accurate interpretation of histological findings [16]. 

Treatment strategies for EC are primarily derived from case reports and small case series. Corticosteroids remain the cornerstone of initial therapy and have demonstrated the highest effectiveness in achieving symptomatic relief and disease control in up to 90% of cases [17]. Our patient showed clinical improvement and a significant reduction in eosinophil count following corticosteroid therapy (prednisolone 40 mg daily), consistent with prior reports showing up to 90% efficacy of corticosteroids in inducing remission [17]. Exclusive elemental diets have been shown to result in both symptomatic and histologic remission in EC and may serve as a steroid-sparing treatment option [18]. In our case, comprehensive evaluation to exclude secondary causes of eosinophilia, including parasitic infection and malignancy, was negative, supporting the diagnosis of primary EC. Budesonide is an effective alternative for managing EC, offering fewer side effects than systemic corticosteroids [19]. Ketotifen, a histamine H1 receptor antagonist, has also shown promise as a steroid-sparing option [20]. The use of montelukast, a leukotriene receptor antagonist, remains controversial and requires further investigation [21]. Furthermore, this case also draws attention to the likely under diagnosis of EC in low-resource settings, where eosinophilia is often attributed solely to parasitic infections. In patients unresponsive to empirical anti-parasitic treatment, a broader diagnostic approach including colonoscopy with biopsies should be pursued. 

Our case underscores the importance of considering EC in the differential diagnosis of chronic diarrhea and abdominal pain, particularly in the presence of peripheral eosinophilia, and especially in low-resource settings, where eosinophilia is often attributed solely to parasitic infections. Normal endoscopic findings should not preclude histologic evaluation, as mucosal biopsies remain critical for diagnosis. Timely recognition and corticosteroid therapy can lead to significant clinical improvement, although relapses may occur.

Acknowledgements:

The authors have no acknowledgements to declare.

Declarations

Funding: No funding was taken for this study

Competing Interests: The authors declare no competing interest in this study

Ethics Approval: Not applicable

Consent to Participate: A written informed consent to participate in this study was obtained from the patient.

Consent to Publication: A written informed consent to publish this study was obtained from the patient.

Availability of Data and Material: Not applicable

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