Cases reported "Esophagitis"

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1/4. Synchronous herpes simplex virus and cytomegalovirus esophagitis.

    Infective esophagitis is a rare disease, affecting mostly immunocompromised patients. Very few cases of a multiple viral infection have been reported. We present a case of combined cytomegalovirus (CMV) and herpes simplex virus (HSV) esophagitis in an 81-year-old female with extracapillary sclerosing glomerulonephritis treated for five months with steroids and chemotherapy. She died of septic shock. At autopsy, erosive and ulcerative esophagitis was found in the distal half of the esophagus. Slides were stained by HE, and the immunohistochemical avidin-biotin method was used to detect HSV and CMV infection. On histological examination of the esophagus, epithelial giant cells with intranuclear viral inclusions showing HSV immunopositivity were found at the margin of the ulcerations. giant cells with intranuclear inclusions with CMV immunopositivity were also found in the mesenchymal cells obtained from the ulcer bed. Long-term immunosuppressive therapy provoked an immune deficiency, evidenced by grave leukopenia and depletion of all bone marrow elements. diagnosis of HSV and CMV esophagitis is important to evaluate the risk of hemorrhage and esophageal perforation in esophagitis.
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2/4. Multiple opportunistic infections after high-dose steroid therapy for giant cell arteritis in a patient previously treated with a purine analog.

    We present the case of a 74-y-old hiv-negative female who suffered simultaneously from multiple opportunistic infections and a klebsiella pneumoniae sepsis during high-dose steroids for giant cell arteritis. The patient was treated with a purine analog due to hairy cell leukaemia 10 y previously. Purine analog therapy can lead to long lasting defects in cell-mediated immunity. In these patients, treatment with steroids should be closely monitored with CD4 counts.
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3/4. Staphylococcal esophagitis causing giant ulcers.

    A 29-year-old woman with hodgkin disease developed odynophagia while receiving chemotherapy. Large esophageal ulcers due to staphylococcal infection of the mucosa were visualized by endoscopy and radiography. This unusual bacterial esophagitis represents another potential cause of giant esophageal ulcerations.
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4/4. Multinucleated epithelial giant cell changes in esophagitis: a clinicopathologic study of 14 cases.

    We describe the clinical and pathologic features of a hitherto unreported finding in patients with esophagitis: the presence of multinucleated squamous epithelial giant cells simulating viral cytopathic effect and/or dysplasia. Routinely processed hematoxylin and eosin (H&E)-stained slides of esophageal mucosal biopsies from 14 patients with both active esophagitis and multinucleated epithelial giant cells were evaluated for a variety of inflammatory and epithelial features. Clinical, endoscopic, and follow-up data were collected and correlated with the histologic findings. Immunostaining (ABC method) for cytokeratin AE1/AE3, S-100, MIB-1, herpes simplex virus 1 and 2 (HSV), cytomegalovirus (CMV), as well as dna in situ hybridization for human papilloma virus (HPV-ISH) was performed in all cases. Electron microscopic evaluation for viral particles was performed in three cases. The study group consisted of nine men and five women (mean age 59 years; range 23-87 years; 12 white, one black, one Hispanic). patients presented with dysphagia or odynophagia (n = 5), upper gastrointestinal bleeding (n = 5), heartburn (n = 2), or abdominal pain (n = 2). The etiology of esophagitis was attributed to gastroesophageal reflux in 10, radiotherapy in one, candida infection in one, drug-induced (alendronate) in one, and unknown in 1. Endoscopically, seven patients had an ulcer or erosion, four erythema, two stricture formation, and one white mucosal plaques. Microscopically, all cases showed multiple multinucleated (mean three nuclei per cell, range two to nine) squamous epithelial cells (range 2 to 11 cells per biopsy) confined to the basal zone in nine of 14 cases and involving the basal and superficial epithelium in the remainder. The nuclei contained a single or multiple eosinophilic nucleoli with a perinucleolar halo, but no inclusions, hyperchromaticity, or atypical mitoses. All cases showed associated nonspecific features of active esophagitis such as ulceration, neutrophilic and eosinophilic inflammation, basal cell hyperplasia, and elongation of the lamina propria papillae. The multinucleated giant cells, in all cases, were strongly positive for cytokeratin AE1/AE3 and were negative for S-100, HSV I and II, CMV, and HPV-ISH. MIB-1 positivity was observed in all basally located multinucleated giant cells, whereas those in the more superficial layers were negative. Electron microscopy failed to show viral particles in three of three cases. After treatment, all patients demonstrated clinical improvement. Three patients in whom follow-up biopsies were performed showed no evidence of esophagitis, epithelial cell multinucleation, or dysplasia. Multinucleated epithelial giant cell changes may rarely be seen in patients with esophagitis of varying etiology and probably represent a regenerative response to injury. This feature is important to distinguish from either viral cytopathic effect or dysplasia.
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