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An enigma of eosinophilic esophagitis.
Introduction: Eosinophilic esophagitis is a chronic immunogenic-antigen mediated disease of the esophagus, characterized by symptoms related to esophagus dysfunction, histologically defined by over 15 eosinophil counts seen in high-power microscopic field, without gastroesophageal reflux disease. In adults, the most common clinical manifestations are dysphagia, reflux, chest pain, regurgitation and bolus impaction.
Case report: We presented the case of a female patient, hospitalized for a serious form of pancreatitis with complications, which required artificial ventilation and enteral feeding, after the initial esophagoscopy verified reflux esophagitis. Further treatment cured the primary illness, and peroral feeding was reintroduced. However, dysphagia with regurgitation occurred, and endoscopic and radiological tests verified esophagus stenosis, which histopathologically corresponded to erosive esophagitis. Two months of treatment by a double dosage of proton pump inhibitors led to no regression of disorders, and the repeated biopsies from the stenotic segments resulted in over 30 eosinophil counts in the high-power microscopic field, which histologically corresponds to eosinophilic esophagitis. Subsequent therapy included fluticasone 880 μg/day orally for a period of eight weeks, which led to complete regression of disorders, and endoscopic and histopathologic remission.
Conclusion: In case of irresponsiveness to the conventional therapy by proton pump inhibitors, repeated esophagoscopy and histopathological analyses of esophagus mucosa biopsy can point to the diagnosis of eosinophilic esophagitis, and a good therapeutic response to topical corticosteroids can be regarded as the clinical confirmation of the diagnosis.
Case report: We presented the case of a female patient, hospitalized for a serious form of pancreatitis with complications, which required artificial ventilation and enteral feeding, after the initial esophagoscopy verified reflux esophagitis. Further treatment cured the primary illness, and peroral feeding was reintroduced. However, dysphagia with regurgitation occurred, and endoscopic and radiological tests verified esophagus stenosis, which histopathologically corresponded to erosive esophagitis. Two months of treatment by a double dosage of proton pump inhibitors led to no regression of disorders, and the repeated biopsies from the stenotic segments resulted in over 30 eosinophil counts in the high-power microscopic field, which histologically corresponds to eosinophilic esophagitis. Subsequent therapy included fluticasone 880 μg/day orally for a period of eight weeks, which led to complete regression of disorders, and endoscopic and histopathologic remission.
Conclusion: In case of irresponsiveness to the conventional therapy by proton pump inhibitors, repeated esophagoscopy and histopathological analyses of esophagus mucosa biopsy can point to the diagnosis of eosinophilic esophagitis, and a good therapeutic response to topical corticosteroids can be regarded as the clinical confirmation of the diagnosis.
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