Eosinophilic cand Bronchitis: A Case Study
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Mr. Moataz is a 38-year-old Egyptian teacher. He is married & had two children. He is not smoking & had no other special habits of medical importance. He had a history of bronchial asthma for 12 years with occasional use of inhaled B2-agonists for relieve of bronchospasm. He had no known drug or food allergy. He visited the gastrointestinal clinic of our hospital 8 months ago by a complaint of heart burn, odynophagia, repeated vomiting for 25 days earlier. The patient was initially diagnosed as GERD, received proton pump inhibitors (PPI) & prokinetic for one month with only partial improvement. The patient came to the clinic again with severe odynophagia & food impaction along with generalised abdominal pain & enlargement. No diarrhea, bleeding, fever, rash or significant weight loss. He also stated that he had a poorer control of his asthma symptoms through the past 2 months with more frequent use of his reliever inhalers. Chest examination showed bilateral hyper-resonance with prolonged expiration & scattered rhonchi. Abdominal examination revealed generalized tenderness & bilateral shifting dullness with no organomegaly or lower limb edema. Pelvi-abdominal ultrasound & CT confirmed the presence of moderate ascites & mild rightside pleural effusion with normal liver, spleen, portal vessels & mesenteric lymph nodes. Upper GI endoscopy was done showing lower 1/3 esophagitis with white exudate, mild antral & fundal gastritis with four gastric polyps. Colonoscopy also was done with normal findings. Complete blood count (CBC) showed TLC: 14.7 x 103/dl, hemoglobin: 12.4 g/dl, platelets: 312 x 103/dl. Differential count: neutrophils 48%, lymphocytes 13%, monocytes 1%, eosinophils 43%, no blast cells. Serum K: 3.2mEq/ dl & serum Na: 139mEq/dl. Liver & kidney functions, coagulation profile, stool & urine analyses, ESR, LDH & ANA results were normal. Bone marrow biopsy & cytogenetics were normal. Food & drug allergy skin test was normal. Diagnostic paracentesis showed turbid ascitic fluid with protein level 5.2 g/dl, serum ascites-albumin gradient (SAAG): 0.6, TLC: 2710/dl with marked eosinophilia (75%). The ascitic glucose level, LDH and adenosine deaminase (ADA) were all normal. Ascitic fluid bacteriological culture, cytology for malignant cells & PCR for tuberculosis came also normal. Tumor markers (carcinoembryonic antigen (CEA) and CA 19-9) were negative. Biopsy results from esophagus showed non-specific inflammation with marked eosinophilic infiltrate. Gastric biopsy revealed chronic inflammatory changes with excessive eosinophilic infiltrates in mucosa & submucosa (>35/hpf). The patient was diagnosed as eosinophilic esophagitis with eosinophilic ascites. He received initially prednisolone 30 mg orally/day along with empirical 6-food elimination diets. The patient showed only partial improvement of his esophageal symptoms and the amount of ascites after two weeks of treatment. The prednisolone dose was increased to 60 mg/day orally with addition of PPI, Kitotifen & clarithromycin for other two weeks with more effective improvement followed by rapid steroid tapering over 6 weeks. Resolution of ascites & pleural effusion occurred after 13 days while resolution of esophageal symptoms occurred after 23 days of the combined treatment. Follow up endoscopic biopsies & ultrasonography along with laboratory results after 6 months came normal. The asthma symptoms also showed dramatic improvement after resolution of the esophageal symptoms. The patient was scheduled for another follow up evaluation after one year.
With Regards,
Sara Giselle
Associate Managing Editor
Global Journal of Digestive Diseases