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Radiol Case Rep
Radiol Case Rep
Radiology Case Reports
1930-0433
Elsevier

S1930-0433(24)00734-9
10.1016/j.radcr.2024.07.152
Case Report
Beyond the norm: Illuminating eosinophilic ascites with 2 rare and intriguing cases
Lamrani Fatima Zahra lamrani.fati12@gmail.com
ab⁎
Amri Fakhrddine ab
Koulali Hajar ab
Mqaddem Ouiam El ab
Zazour Abdelkrim ab
Ismaili Zahi ab
Kharrasse Ghizlane ab
a Department of Hepato-Gastroenterology, Mohammed VI University Hospital, Oujda, Morocco
b Digestive Diseases Research Laboratory (DSRL), Faculty of Medicine and Pharmacy, Mohammed First University, Oujda, Morrocco
⁎ Corresponding author. lamrani.fati12@gmail.com
24 8 2024
11 2024
24 8 2024
19 11 52015205
31 1 2024
24 7 2024
25 7 2024
© 2024 The Authors. Published by Elsevier Inc. on behalf of University of Washington.
2024

https://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Eosinophilic ascites (EA) is a rare and enigmatic disorder characterized by elevated eosinophil counts in peritoneal fluid, commonly associated with eosinophilic gastroenteritis (EGE), hypereosinophilic syndrome (HES), and parasitic infections. Here, we present two cases of EA diagnosed and managed in our gastroenterology department. Case 1: A 45-year-old male presented with diffuse abdominal pain and distension. Imaging revealed septate abdominal ascites, prompting exploratory laparoscopy. Ascitic fluid analysis showed eosinophil predominance, leading to an EA diagnosis. The patient was treated with oral Albendazole, resulting in a favorable outcome. Case 2: A 52-year-old female complained of abdominal pain with alternating diarrhea and constipation. Imaging unveiled moderate ascites, pyloro-duodenal inflammation, and wall thickening. Eosinophilic leukocytosis prompted empirical treatment, yielding a positive response. In conclusion, diagnosing EA involves a combination of histological and laboratory methodologies. Corticosteroids emerge as the primary therapeutic avenue, with the imperative of eradicating parasitic infections before initiation. This study underscores the critical role of education in mitigating the risk of parasitic infections.

Keywords

Eosinophilic ascites
Hypereosinophilia
Eosinophilic gastroenteritis
Atopy
Corticosteroids
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pmcIntroduction

Eosinophilic ascites (EA) is a rare and enigmatic condition characterized by elevated eosinophil counts in the peritoneal fluid, impacting both adult and pediatric populations [1]. The condition is frequently associated with eosinophilic gastroenteritis (EGE), hypereosinophilic syndrome (HES), and various parasitic infections [1]. Diagnosing EA presents significant challenges due to its infrequency, nonspecific clinical manifestations, and often inconclusive endoscopic findings [2]. Accurate diagnosis relies on the identification of peripheral hypereosinophilia and the analysis of ascitic fluid for eosinophil presence via diagnostic paracentesis [2]. Effective management necessitates targeted treatments for underlying parasitic and hematological disorders, with oral corticosteroids commonly serving as the initial therapeutic strategy [1,2]. This report details 2 distinct cases of EA, contributing valuable clinical insights and enhancing the current understanding of this rare condition in the medical literature.

Case 1

A 45-year-old man, with no family history of atopy, recent travel, or medication intake, presented with persistent diffuse abdominal pain and distension lasting 3 months. Physical examination showed no pallor, jaundice, or peripheral edema, but confirmed abdominal distension. Abdominal ultrasonography revealed moderate ascites without portal hypertension, liver, or renal disease. Contrast-enhanced abdominal CT confirmed low abundance ascites, inflammatory mesenteric fat, agglutinated small bowel loops, and low-grade right pleurisy (Fig. 1). Laboratory tests showed peripheral eosinophilic leukocytosis (2500 cells/mm³), elevated IgE (125 IU/mL), normal CRP levels, and positive skin tests for mites, cats, shrimp, almonds, and peanuts. Stool tests indicated polynuclear eosinophils but no isolated parasites. Tumor markers (ACE, CA 19-9) were within normal limits, effectively ruling out hypereosinophilic paraneoplastic syndrome, and tuberculosis tests were negative (Table 2).Fig. 1 Case 1 CT scan, displaying axial and coronal sections of the first case, indicating the presence of ascites with a low volume.

Fig 1:

Table 1 Causes of eosinophilic ascites.

Table 1:Causes of eosinophilic ascites	Percentages	
Eosinophilic gastroenteritis (EGE)	74 %	
Parasitic and fungal infections	10%	
Hypereosinophilic syndrome	7%	
Eosinophilic pancreatitis	9%	
Chronic eosinophilic leukemia	
Myelofibrosis	
T-cell lymphoma	
Churg Strauss Syndrome	
Systemic lupus erythematosus (SLE)	
Familial paroxysmal polyserositis	
Menetrier's disease	

Table 2 Summary of the biological results of the 2 AE cases.

Table 2:	Case 1	Case 2	Normal range	
HB	13	12,1	M 13-18 g/dL
F 12-16 g/dL	
Platelet Count	244000	318000	150000-400 000/uL	
WBC	6860	8630	4000-10 000/uL	
LYM	2620	2468	1500-4000/uL	
Eosinophils	2500	5766		
CRP	7,16	4	0-5mg/L	
				
Creatinine	7,78	9	7-11 mg/L	
Urea	0,14	-	0,15-0,45 g/L	
Albumin	44	-	35-50 g/L	

Pleural puncture revealed exudative, inflammatory citrine yellow fluid without eosinophils and negative tuberculosis PCR. Upper endoscopy and colonoscopy showed congestive duodenitis, jejunitis, and erythematous congestive rectocolic mucosa with punctiform erosions. Histology revealed chronic nonspecific colitis with 30 eosinophils per field. Exploratory laparoscopy showed diffuse peritoneal infiltration with moderate effusion, and fluid analysis revealed high eosinophil concentration and lymphocytic exudate. Mesenteric biopsy indicated reactive lymphadenitis of likely allergic origin.

Due to the daily inaccessibility of ova detection and considering the high prevalence of parasitic origins in our context, the decision was to put the patient on empirical treatment with oral Albendazole for 5 days, repeated twice at 15-day intervals, which ed to a favorable outcome, with resolution of ascites and normalization of eosinophil levels. However, eosinophil levels increased after 2 months, prompting corticosteroid therapy, which resulted in clinical and biological improvement. Follow-up evaluations, including a complete blood count (NFS), were performed 1 month, 3 months, and 6 months after treatment initiation, confirming sustained clinical improvement and eosinophil level normalization. The diagnosis revealed coexisting parasitic infection and hypereosinophilic syndrome (HES).

Case 2

A 52-year-old woman, with no notable medical history, presented with diffuse abdominal pain and alternating diarrhea and constipation for 6 months. Clinical examination showed mild tenderness without fever.

Abdominal ultrasound demonstrated moderate ascites without portal hypertension, confirmed by contrast-enhanced abdominal CT, revealing moderate ascites, diffuse pyloro-duodenal inflammation, and wall thickening (Fig. 2). Abdominal MRI corroborated these findings, showing medium abundance ascites and terminal ileitis (Fig. 3).Fig. 2 Case 2. (A) CT scan, coronal section of the second case indicating the presence of moderate ascites. (B) CT scan, axial section displaying antropyloric thickening. (C) CT scan, axial section revealing small intestine wall thickening.

Fig 2:

Fig. 3 Case 2 (A) MRI, axial LAVA Flex, illustrating thickening of the ileum. (B) MRI indicating a moderate amount of ascites.

Fig 3:

Laboratory tests indicated eosinophilic leukocytosis (5766 cells/mm³), high fecal calprotectin (>1000 µg/g), and normal CRP levels (Table 2). Tuberculosis tests were negative. Tumor markers (ACE, CA 19-9) were within normal limits, ruling out hypereosinophilic paraneoplastic syndrome. Colonoscopy and histology revealed normal colonic and ileal mucosa with few polymorphonuclear eosinophils.

Due to the daily inaccessibility of ova detection and considering the high prevalence of parasitic origins in our context, the decision was to put the patient on empirical treatment with oral Albendazole for 5 days, repeated twice at 15-day intervals, which ed to a favorable outcome, with resolution of ascites and normalization of eosinophil levels, with no relapses observed. Follow-up evaluations, including a complete blood count (NFS), were performed 1 month, 3 months, and 6 months after treatment initiation, confirming sustained clinical improvement and eosinophil level normalization.

Discussion

Eosinophilic ascites (EA) is characterized by elevated eosinophil counts in peritoneal fluid, with an unclear pathophysiology. A strong association with atopy is observed, with about 80% of patients having a history of asthma, eczema, allergic rhinitis, or other allergies [[1], [2], [3]]. Positive skin tests for allergens align with literature findings on the link between EA and atopy. Genetic predisposition is suspected, with 16% of eosinophilic gastroenteritis (EGE) patients having a family history of the condition [[1], [2], [3]].

EA, often occurring within the context of EGE, was first described by Kaijser in 1937 [4]. It predominantly affects individuals aged 20-50 years, with equal gender distribution [1,2]. Both of our cases align with the commonly observed age range in the literature. EGE contributes to 74% of EA cases, involving eosinophilic infiltration in the gastrointestinal tract, leading to ascites [1]. Pathologically, EGE can be classified into mucosal, muscle, or subserosal subtypes, with the subserosal subtype often presenting with ascites [2]. Misdiagnosis is common due to its unusual clinical presentation, emphasizing the need for heightened awareness among healthcare professionals [3]. Common EGE clinical features include abdominal pain (90.4%), nausea and vomiting (57.1%), diarrhea (52.3%), and abdominal distension (38.1%) [5] (Table 3). EA should be considered in patients with abdominal pain, ascites, and peripheral hypereosinophilia. Endoscopy often reveals nonspecific lesions, such as edema, hyperemia, erosions, and mucosal rings [1].Table 3 Clinical signs of EA.

Table 3:Clinical sign	Description	References	
Abdominal Pain	Persistent, diffuse abdominal pain, often with distension.	[5]	
Nausea and Vomiting	Common gastrointestinal symptoms, frequently observed in EA patients.	[5]	
Diarrhea	Alternating with constipation, indicative of gastrointestinal involvement.	[5]	
Abdominal Distension	Notable distension observed upon physical examination.	[5]	
Peripheral Hypereosinophilia	Elevated eosinophil counts in peripheral blood, significant for diagnosis.	[2]	
Allergic Reactions	Positive skin tests for allergens like mites, cats, shrimp, almonds, and peanuts.	[1,3]	

The differential diagnosis of EA is extensive and includes parasitic infections, hypereosinophilic syndrome (HES), eosinophilic pancreatitis, chronic eosinophilic leukemia, myelofibrosis, T-cell lymphoma, Churg-Strauss syndrome, systemic lupus erythematosus, familial paroxysmal polyserositis, and Menetrier's disease [1,8,9]. Parasitic infections, such as those caused by helminths, are a significant consideration and account for 10% of EA cases [1]. It is crucial to exclude these infections through thorough parasitological evaluations, as seen in our cases where stool tests and pleural fluid analysis were conducted. HES is another critical condition to consider, characterized by persistent eosinophilia (>1500/mm³) for at least 6 months and associated with organ damage [1,8]. Diagnostic criteria for HES include gastrointestinal symptoms, biopsies showing eosinophilic infiltration, peripheral eosinophilia or eosinophil-rich ascites, and exclusion of parasitic or extra-intestinal diseases [6,7]. Less common causes of EA, such as eosinophilic pancreatitis and chronic eosinophilic leukemia, should also be considered in the differential diagnosis [1] (Table 1).

The pathophysiological mechanisms underlying EA remain incompletely understood. EGE is thought to be driven by an allergic or immune-mediated response, supported by elevated levels of eosinophils and IgE, as observed in our cases [1,2]. The presence of positive skin tests for various allergens further substantiates this association. Genetic factors may also play a role in the development of EA, with some patients exhibiting a family history of atopic conditions or eosinophilic gastrointestinal disorders [1,2]. Imaging modalities such as abdominal ultrasound, contrast-enhanced CT, and MRI are crucial for diagnosing EA, helping to visualize the extent of ascitic fluid and identify other related findings such as mesenteric fat inflammation, bowel loop agglutination, and intestinal wall thickening [2] (Table 4). Endoscopy and biopsy are essential for confirming the diagnosis by demonstrating eosinophilic infiltration in gastrointestinal tissues [2].Table 4 Role of imaging in diagnosis of EA.

Table 4:Imaging modality	Key Findings	References	
Abdominal Ultrasound	Moderate ascites without portal hypertension, liver, or renal disease.	[2]	
Contrast-enhanced CT	Low abundance ascites, inflammatory mesenteric fat, agglutinated small bowel loops, low-grade pleurisy.	[2]	
MRI	Medium abundance ascites, terminal ileitis, and pyloro-duodenal inflammation.	[2]	
Endoscopy (Upper and Lower)	Congestive duodenitis, jejunitis, erythematous and congestive rectocolic mucosa with punctiform erosions.	[2]	

Empirical treatment with Albendazole, as seen in our cases, aligns with literature recommendations to address parasitic origins before initiating corticosteroid therapy [10]. This approach underscores the importance of considering parasitic infections in EA management. Diagnostic tools also assess allergic diseases and exclude other gastrointestinal conditions, such as food intolerance, infections, inflammatory bowel disease, parasitic infestations, connective tissue disease, systemic mastocytosis, eosinophilic granulomas, and tumors [10]. In allergic or atopic cases, skin prick tests identify implicated agents. Treatment strategies include elimination diets and classical anti-allergic drugs. Steroids are the mainstay of EA treatment, with most patients responding quickly to low-dose maintenance prednisone. Steroid-sparing therapies, such as cell inhibitors, antihistamines, leukotriene receptor antagonists, anti-interleukin agents, or immunosuppressants, should be considered [10]. Coproparasitology challenges in detecting parasitic origins emphasize the necessity of empirical treatment in high-prevalence regions. Specific treatments are required for patients with parasitosis and hematological disorders. Dietary treatment is crucial for patients with food allergies, especially children. Currently, corticosteroids are the primary treatment for EA in patients with EGE and HES [1]. The overall prognosis of EGE is favorable, with an excellent response to oral steroids, which are the first-line therapy [11]. Prednisone at 20-40 mg daily leads to symptomatic remission in 80% of patients within a week and normalization of eosinophil counts within 2 weeks [2]. Preventing parasitic infections through proper dietary and personal hygiene practices is crucial. Education plays a key role in reducing the risk of parasitic infections, including eosinophilic ascites.

Conclusion

Eosinophilic ascites (EA) is a rare and challenging condition that requires a thorough understanding of its clinical features, differential diagnosis, and pathophysiological mechanisms. EA is often associated with eosinophilic gastroenteritis (EGE) and atopic conditions, necessitating careful evaluation of allergic histories and genetic predispositions. Diagnosis relies heavily on imaging modalities, endoscopy, and histological assessments to confirm eosinophilic infiltration and exclude other potential causes such as parasitic infections, hypereosinophilic syndrome (HES), and various hematological and autoimmune disorders. Empirical treatment with Albendazole, followed by corticosteroids, has proven effective in managing EA, particularly in cases with suspected parasitic origins. The favorable prognosis of EGE, with a quick response to oral steroids, highlights the importance of early recognition and appropriate management. Preventative measures, including dietary and personal hygiene practices, are crucial in reducing the risk of parasitic infections associated with EA. Overall, heightened awareness and a multidisciplinary approach are essential for improving outcomes in patients with eosinophilic ascites.

Patient consent

Informed consent was obtained from each patient partaking in the study. The research carried no inherent risks for the participants, and all the information amassed was treated with the utmost confidentiality.

Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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