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ARCH GASTROENTEROHEPATOL 2002; 21 ( No 1 – 2 )

 

 

EOSINOPHILIC ASCITES 

 

Eozinofilni ascites

¹Mira Petrovic¹ Vojislav N. Perisic, ² Miodrag N. Krstic, ³ Dejan Opric, ¹ Sasa Milicevic.

 

^{( accepted May 20th, 2002 )}

 

¹ University Children ^, s Hospital, Belgrade,

² Clinic for Gastroenterohepatology, Institute of Digestive Diseases, Clinical Center of Serbia, Belgrade,

³Institute of Pathology, School of Medicine, University of Belgrade.

 

 

 

Address correspondent to: Professor Dr VN.Perisic

                                               University Children^, s Hospital

                                               10 Tirsova St.

                                               Yu-11000 Belgrade,

                                                Serbia, Yugoslavia

 ………………………………………………………………………………………………

 

A 14-year old by was referred for further evaluation of his tense ascites and dull abdominal pain. This child developed insidious but progressive abdominal distension accompanied with dull abdominal pain few weeks before admission. He had past medical history of well-controlled bronchial asthma. 

 

At admission, beside tense ascitic peritoneal fluid effusion this patient^, s clinical finding was normal. Blood pressure was normal. Immediately performed chest x – ray and ECG were normal as well. Laboratory investigations demonstrated haematological abnormality of pronounced eosinophilia. Total white blood cell count was 17.1 with increased number of eosinophils (20%, total number 3400; normal < 500). ESR, hemoglobin, RBC, and trombocyte counts were within reference range. Urinalysis was negative. Stools for ova and parasites were

 

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Eosinophilic ascites                                            Gastroenteroloska sekcija SLD-

                                                                              01731, 2002.

 

repeatedly negative. Blood biochemistry including blood sugar, BUN, serum creatinine, liver function tests, total serum proteins, albumin, serum electrolytes, serum and urinary amylases, and serum lipase were normal. IgA, IgM, and IgG were within normal limits. Serum IgE was increased 800 u/ml (normal: 0-200). Abdominal ultrasound scan revealed normal liver, spleen, and kidneys. No abdominal masses were detected. Ascitic fluid effusion with floating small bowel loops was seen. FIGURE 1. Diagnostic abdominal

paracentesis was performed. Twenty milliliters of clear ascitic fluid was removed.

Its biochemistry including glucose concentrations and amylase titer was normal except protein concentration of 3.5g/l. After centrifugation, microscopic examination of ascitic fluid sediment was made. Eight thousand cells, exclusively eosinophils per 1 ml of ascitic fluid were found. FIGURE 2.

 

Two weeks of methyl prednisolone treatment (30mg/day) led to quick and full amelioration of peritoneal effusion which almost disappeared, normalisation of peripheral blood eosinophilia, and reduction of serum IgE (350 u/ml). Six-month follow up was uneventful, no peritoneal effusion recurred, and peripheral blood eospnophil count was normal. Abdominal ultrasound examination was normal.

 

Comment:  Eosinophilic gastroenteropathy may be protein sensitive and idiopathic. Protein-sensitive forms of eosinophilic gastroenteropathy occur in infants and children below the age of 2 years and most commonly result from allergic reaction to cow ^, s milk or soy protein or, infrequently, breast milk (1).  The idiopathic form presents with a highly variable clinical picture, depending on the anatomic and histologic distribution of the eosinophilic tissue infiltration. Tissue eosinophilia can be mucosal, muscular, or serosal and has been described to affect the oeosphagus, stomach, intestine, or colon alone or in combination (2).

The most commonly encountered presentation results from mucosal involvement of the small intestine and stomach (1,2,3). This usually presents with chronic diarrhoea weight loss, malabsorption, and protein loosing enteropathy when small intestinal mucosal infiltration with eosinophils occur. Eosinophilic gastritis presents with epigastric pain, nausea, and vomiting.

Patients with predominant muscle layer disease (eosinophilic infiltration of tunica muscularis) manifest with pyloric, intestinal obstruction, or/and achalasia-like picture (1,2,3).

The rarest form is serosal layer disease, which typically present with eosinophilic ascites (4). Serosal eosinophilic infiltration led to weeping of fluid in the peritoneal cavity. An associated pleural effusion may be present. The fluid is usually a sterile exudate that contains a high eosinophil count.

 

In eosinophilic gastroenteropathy laboratory studies usually indicate peripheral eosinophilia and increased serum IgE, particularly in children. In all cases, stool studies must be done to rule out parasitic infestation. The radiographic changes are found in mucosal and muscle layer disease. This are enlarged gastric mucosal folds, pronounced antral and corporal nodularity, small intestinal thickening of the folds with or without nodules (3). The small intestine is dilated. Antro-pyloric obstruction, segmental small intestinal obstruction, and achlasia-like x-ray picture are signs of muscle layer disease. In serosal disease abdominal ultrasound demonstrates peritoneal effusion. Endoscopic mucosal biopsies, laparoscopic muscle layer and serosal biopsies indicating pure tissue eosinophilic infiltration and abdominal paracentesis with cytology are important diagnostic methods. 

Steroids are the mainstay of therapy in particular in obstructive symptoms and eosinophilic ascites. This disease tends to respond quickly. Occasionally low dose maintenance steroids are needed to keep symptoms under control. In severe disease additional immunosuppressive therapy using cyclosporine, azathioprine and cyclophosphamide may be considered

 

 

 

Figure 1. Note Peritoneal effusion. Aspiration needle is visible (arrow).

 

 

Figure 1.  Eosinophilis in the ascitic fluid

 

REFERENCES:

 

1.Proujansky R. Eosinophlic gastroenteritis. In: Pediatric gastrointestinal disease, Wyllie R, Hyams JS, eds. Philadelphia: WB Saunders, 1993;566-71.

 

 

2.Steffen RM, Wylie R, Petras RE, et al. The spectrum of eosinophilic gastroenteritis. Report of six pediatric cases and review of the literature. Clin Ped 1991; 30: 404-11.

 

3.Talley NJ. Eosinophilic gastroenteritis. In: Sleisenger and Fordtran^, s Gastrointestinal and liver disease, Feldman M, Scharschmidt BF, Sleisenger M, eds. Philadelphia: WB Saunders, 1998; 1679-88.

 

4.Talley NJ, Shorter RG, Philips SF, et al. Eosinophilic gastroenteritis. A clinicopathological study of patients with disease of the mucosae, muscle layer, and subserosal tissue. Gut 1990; 299-303.