However, some cases may relapse after the discontinuation of steroid treatment. a dramatic response to the steroid treatment. This case indicates that we L-Octanoylcarnitine should be highly aware of MSSE as the first clinical manifestation of eosinophilic gastroenteritis. and em Toxocara /em . Moreover, as listed in Table 1, all other laboratory data were unremarkable (including serum electrolytes, coagulation parameters, tuberculin purified protein derivative, and thyroid, kidney, and liver test results). Antinuclear antibody was negative and bone marrow biopsy showed no abnormalities. Ultrasonography showed a large amount of ascites and a moderate amount of bilateral pleural effusion. In addition, echocardiography showed only a small amount of pericardial effusion without cardiac disease. Chest and abdominal computed tomography (CT) showed diffuse thickening of the gastric antrum and duodenum, mild edema of the small bowel loops, and large amounts of abdominal ascites, bilateral pleural effusion, and pericardial effusion (Figure 1); however, no ovarian masses were present. Esophagogastroduodenoscopy showed extensive congestion and edema in the duodenum and antrum. Colonoscopy revealed no abnormalities (Figure 2). Biopsies demonstrated significant eosinophilic infiltration in the duodenum and rectum (Figure 3). In addition, gastric mucosal biopsies displayed mucosal eosinophilic infiltration (18C20 cells/mm2), but there was no evidence of em Helicobacter pylori /em -associated gastritis. The patient was treated with 30 mg of prednisolone, and seafood was excluded from her diet for 4 weeks. She was also treated with 600 mg of calciumCvitamin D3 chewable tablets and 40 mg of oral omeprazole to prevent the occurrence of prednisolone-induced osteoporosis and upper GI bleeding. Her symptoms improved immediately, and her eosinophil count normalized within 3 weeks. Prednisolone was tapered over 8 weeks and continued at 5 mg prednisolone daily. The serum level of CA125 dropped to the normal range, and her MSSE was in complete remission throughout the 2-month follow-up period. Follow-up esophagogastroduodenoscopy after 3 months showed normal mucosa of the gastric antrum and duodenum. Table 1. Laboratory parameters upon admission thead valign=”top” th rowspan=”1″ colspan=”1″ Parameters /th th rowspan=”1″ colspan=”1″ Index /th th rowspan=”1″ colspan=”1″ Reference range /th /thead Blood?WBC (109/L)8.744.0C10.0?EO (109/L)1.310.02C0.52?EO (%)15.00.4C8.0?RBC (1012/L)4.653.5C5.5?Hb (g/L)144120C155?PLT (109/L)478100C300?TP (g/L)55.360C82?ALB (g/L)24.635C55?cTnI (ng/mL)0.00780C0.04?AFP (ng/mL)3.560C8?CEA (ng/mL)0.70C5?CA199 (U/mL)11.80C37?CA125 (U/mL)193.30C35?ESR (mm/h)20 38?CRP (U/L)3030C110?IgE (kU/L)868 60?IgG (g/L)11.27.23C16.8?IgM (g/L)2.780.63C2.77?IgA (g/L)1.350.69C3.82?Anti-ANA(?)C?T-spot(?)CPeritoneal fluid?WBC (106/L)597C?EO (%)82.7C?TP (g/L)40.063C82?LDH (U/L)274313C618?ADA (U/L)10.8C?CRP (mg/L)9.6C?CEA (ng/mL)0.2C?CA125 (U/mL)1108.0C Open in a separate window WBC, white blood cells; EO, eosinophils; RBC, red blood cells; Hb, hemoglobin; PLT, platelets; TP, total protein; ALB, albumin; cTnI, cardiac troponin I; AFP, alpha-fetoprotein; CEA, carcinoembryonic antigen; ESR, erythrocyte sedimentation rate; CRP, C-reactive protein; Ig, immunoglobulin; ANA, antinuclear antibodies; T-spot, T-SPOT.TB test; LDH, lactate dehydrogenase; ADA, adenosine aminohydrolase. Open in a separate window Figure 1. Conventional and enhanced computed tomography images. (a) Chest and abdominal computed tomography demonstrated a large amount of ascites and a moderate amount of L-Octanoylcarnitine pleural effusion and pericardial effusion (red arrowhead). (b) Imaging study shows multiple segments of small bowel wall thickening (yellow arrowhead). Open in a separate window Figure 2. Endoscopic appearance. Endoscopy showed extensive congestion and edema in the (a) duodenum and (b) antrum. (c) Colonoscopy revealed no abnormality. Open in a separate window Figure 3. Histological examination. Histological sections of the (a, b) duodenum and (c, d) antrum demonstrated eosinophilic infiltration within inflammatory cells in the lamina propria and submucosa (hematoxylin and eosin stain). (a, c) Magnification, 20. (b, d) Magnification, 40. Discussion EGE is a rare disease characterized by eosinophil-rich inflammation of the GI tract that affects both the pediatric and adult populations.3,4 However, the precise process of the development of EGE remains obscure. The current hypothesis of an immunoglobulin E-mediated immune response to various food allergens has long L-Octanoylcarnitine been widely accepted.5,6 Food allergens may stimulate the transformation of lymphocytes in the GI lymphoid tissue to cytokine-secreting T helper type 2 effector cells, which produce interleukin 5.7,8 Interleukin 5 functions as a key L-Octanoylcarnitine mediator, activating the expansion of eosinophils and their migration from bone Rabbit polyclonal to Cannabinoid R2 marrow.8 Therefore, eosinophils are considered an important hallmark of the pathology of EGE. The patient in the current case had peripheral blood eosinophilia at presentation and a history of asthma. Clinical manifestations of EGE are diverse depending on the affected layers of the GI tract and range from barely perceptible symptoms to intestinal obstruction or ascites.2,9 Mucosal involvement, the most common manifestation, may result in abdominal pain, vomiting, nausea, and weight loss. Muscularis involvement results in gut.