EGE is a rare, heterogeneous disorder of unknown etiology. There have been no large studies, but hundreds of cases and small case series have been reported. The epidemiology of EGE is unclear. It affects all age groups, from infants to adults, but it is the most common in patients in their 30s and 40s had has a slight male predominance [2, 7, 8].
The symptoms of EGE are nonspecific and varied; however, the most common symptoms are abdominal pain, nausea, and vomiting [9, 10]. EGE is classified into three types depending on the clinical manifestations and depth of eosinophilic infiltration of the gastrointestinal tract wall-mucosal, muscular, and serosal . Mucosal EGE is the most common type of EGE. It manifests with abdominal pain, nausea, vomiting, diarrhea, bleeding, anemia, and protein-losing enteropathy, which may lead to malabsorption, and weight loss. Muscularis involvement results in gut wall thickening and may lead to obstruction. Serosal EGE is the rarest type of EGE. In serosal EGE, eosinophil-rich inflammatory infiltrate permeates all layers of the gastrointestinal wall and lead to eosinophilic ascites; this type of EGE responds well to steroid treatment [2, 11]. Serosal EGE presenting with eosinophilic ascites is more common in females than in males [12, 13], occasionally occurring during pregnancy or delivery [3, 5, 6, 14, 15]. A French study  reported the natural history and long-term outcomes of 43 adult patients with EGE during a median follow-up of 13 years. Most cases of serosal EGE presented as single flare-ups and did not follow a continuous chronic course, whereas most cases of mucosal EGE followed a continuous course.
There are no strict or standardized diagnostic criteria for EGE. Definitive diagnosis is based on typical gastrointestinal symptoms along with histological evidence of eosinophilic infiltration of the gastrointestinal tract wall. In addition, other causes of hypereosinophilia, such as drug reactions, malignancy, parasites, infection, or systemic disease, should be excluded. The endoscopic appearance of EGE is nonspecific. However, diffuse or local mucosal hyperemia and thickened gastric folds are common manifestations . Moreover, mucosal biopsies may show no eosinophils in serosal EGE because the serosal layer is predominantly involved . On computed tomography, the hallmark of EGE is nodular and irregular thickening of the folds in the distal stomach and proximal small bowel [8, 16]. Although mesenteric inflammation and ascites are not uncommon findings, they are usually nonspecific.
Laparoscopic serosal biopsies may be required for a definite diagnosis. However, our patient was in early pregnancy, and similar to computed tomography findings, magnetic resonance imaging findings were suggestive of EGE, and also responded well to steroid therapy, as observed in other previous cases [3, 17, 18]. There was no evidence of other causes of blood eosinophilia. Hence, EGE was diagnosed without a biopsy.
Eosinophils are normally present in the lamina propria of the mucosa, except esophagus, along the gastrointestinal tract. It is involved in the mucosal immune system , and the number of eosinophils increases in numerous inflammatory processes, including parasitic infections and allergic diseases. Activated eosinophils produce and release inflammatory mediators that lead to tissue damage through their proinflammatory functions.
The Th2 immune response may be involved in EGE [20-23]. Th2 cytokines, such as interleukin (IL)-4, IL-5, and IL-13, and chemokines, such as eotaxin, play a central role in the recruitment of eosinophils from the circulating blood into the tissues  related to the pathogenesis of EGE. The expression of these Th2 cytokines and eotaxin tend to be upregulated in the tissues of patients with EGE compared to that in tissues of patients without EGE. Moreover, the blood eosinophil count correlated with tissue pathology . EGE is defined as a systemic Th2-associated disorder with profound blood and gastrointestinal track eosinophilia.
There have been no reports on the prevalence of EGE during pregnancy, but only a few cases have reported pregnancies in patients with EGE. A switch from Th1 immunity to Th2 immunity has been reported during pregnancy; it contributes to the maintenance of pregnancy [25-27]. Both Th2 cell migration and Th2 cell differentiation induce Th2 immunity at the feto-maternal interface. This may be associated with EGE in pregnant women. Amadori et al.  described that EGE may be connected with late preterm delivery after reviewing a total of 12 cases of EGE in pregnant women; 5 cases were antepartum EGE, and 5 were postpartum EGE. The other 2 cases occurred in one patient . A 27-year-old woman developed hypereosinophilia with pericardial effusion, pleural effusion, and ascites at 10 weeks of gestation. However, intrauterine fetal death occurred, and there was no eosinophil infiltration in the tissues obtained by uterine curettage. The patients may be associated with hypereosinophlia with hyperpermeability symptoms rather than EGE. Moreover, they described that it is unclear the relationship between the fetal death and the eosinophilia.
Dietary treatment such as elimination or elemental diet has been used for the treatment of EGE. Our patient had no history of food allergy. Furthermore, skin prick tests for food allergens revealed negative results. Therefore, dietary treatment was not administered to our patient. Corticosteroids are mainly used for the treatment of EGE as they have shown good therapeutic efficacy. However, prenatal exposure to immunosuppressive medications is associated with potentially adverse effects on the fetus. No complications have been reported in newborns of mothers treated with corticosteroids for EGE , including in our case.
The serosal EGE is very rare type of EG. However, it can occur during pregnancy. Further studies are needed to clarify the relationship between EGE and pregnancy. To our knowledge, this is the first reported case of EGE with eosinophilic ascites that developed during pregnancy, which was successfully treated with corticosteroids.