Cases reported "Esophagitis"

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1/41. Esophageal candidoma in a patient with acquired immunodeficiency syndrome.

    Oral thrush and esophagitis caused by candida are common in patients infected with the human immunodeficiency virus. We present the case of a 33-year-old man with acquired immunodeficiency syndrome who developed dysphagia during a hospitalization for pneumonia. signs and symptoms were consistent with candida esophagitis. Despite therapy with fluconazole, the patient's symptoms persisted. At upper endoscopy, a 1-cm, polypoid esophageal mass at 30 cm from the incisors and several other nodular lesions were observed; white plaques were noted throughout the esophagus. biopsy specimens of the mass contained hyphal forms consistent with candida species. Therapy with amphotericin b improved the patient's symptoms, and resolution of the mass was confirmed by repeat upper endoscopy. We believe this is the first case in the medical literature of a candida mass (candidoma) causing dysphagia in a patient with acquired immunodeficiency syndrome. Candidoma should be considered in the differential diagnosis of dysphagia in patients with human immunodeficiency virus infection or immunosuppression due to other causes.
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2/41. Esophageal ulcer caused by cytomegalovirus: resolution during combination antiretroviral therapy for acquired immunodeficiency syndrome.

    A 36-year-old man with a 5-year history of untreated human immunodeficiency virus (hiv) infection had odynophagia for 14 days. Fifteen days earlier, he had begun taking trimethoprim-sulphamethoxazole and combination antiretroviral therapy that included lamivudine, zidovudine, and nelfinavir. He had no history of opportunistic infection. The cd4 lymphocyte count was 67/microL and hiv-rna level was 359,396 copies/mL. Esophagogastroduodenoscopy revealed a large, well-circumscribed esophageal ulceration 31 cm from the incisors. Histopathologic examination of esophageal biopsy specimens showed cytopathic changes diagnostic of cytomegalovirus (CMV). In situ dna hybridization was positive for CMV. While combination antiretroviral therapy was continued, the esophageal symptoms resolved within 4 days of endoscopy without specific therapy for CMV. Follow-up endoscopy 4 weeks later revealed a normal-appearing esophagus, and the patient has remained symptom-free for 10 months.
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3/41. Transmission of Trichosporon asahii oesophagitis by a contaminated endoscope.

    Two cases of oesophageal trichosporonosis due to a suspected nosocomial infection are reported. Both the patients were immunocompetent and had undergone an endoscopic examination on the same day. Six strains of Trichosporon were isolated: three strains from the oesophageal biopsy of the first patient, one strain from the endoscopic forceps, one from the air in the endoscopy room, and one from the oesophageal biopsy of the second patient. The nosocomial nature of the infection and the role of the endoscopic forceps in transporting the micro-organism was suspected, but the morphology and physiology of the isolated strains did not confirm such hypothesis. To elucidate the nature of the infection and the genetic similarities of the strains isolated, all strains were typed with RFLPs of the rDNA fragment and with RAPD. The results of RAPD using primer (GTG)5 (GACA)4, M13 core sequence, and the 15-mer oligonucleotide GAGGGTGGXGGXTCT indicated the molecular identity of three strains supporting the hypothesis concerning a transport of the aetiological agent from the first patient to the second and that the carrier was the forceps of the endoscopic device.
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4/41. Alkaline esophagitis evaluated by endoscopic ultrasound.

    Case Report: Two patients with corrosive esophagitis caused by alkaline household agents were examined with endoscopic ultrasound using a 20-MHz probe. In the first case, endoscopic ultrasound revealed circumferentially thickened mucosa and muscularis propria, and lack of differentiation between the mucosa and submucosa. However, esophageal stricture did not develop during 3 months of follow-up, suggesting that the deep lesion may have involved a narrow section of esophagus only. In the second case, a markedly thickened mucosa was seen, resulting in no sequelae. Endoscopic ultrasound offers a more accurate evaluation of the depth of the lesions in alkaline esophagitis compared to standard endoscopy or computed tomography. longitudinal studies are needed to identify lesions at greatest risk for progression to stricture.
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5/41. Acute necrotizing esophagitis: a case report.

    Acute necrotizing esophagitis is rare. The exact etiology is unknown in most cases. The esophagus appears black, necrotic and ulcerated on the upper endoscopy, thus the term "black esophagus" is used. Histologically, there is necrosis of the esophageal mucosa and submucosa. Here, we present a patient with cholangiocarcinoma who had upper gastrointestinal bleeding and was found to have acute necrotizing esophagitis on the upper endoscopy.
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6/41. Dysphagia in Crohn's disease: a diagnostic challenge.

    Dysphagia is a rare manifestation in a patient with Crohn's disease. We report on the case of a patient with long-standing Crohn's disease who developed progressive dysphagia over 3 years. endoscopy showed minimal distal oesophagitis with non-specific histological findings. Further investigation with cinematography, barium swallow and manometry established an achalasia-like motility disorder. Biopsies obtained from the oesophagus were non-specific. Balloon dilatation was performed. Initial success was followed by recurrent dysphagia. At repeat endoscopy, an oesophageal fistula was detected. An attempt at conservative medical management failed and oesophagectomy was successfully performed. pathology results of the resected specimen confirmed the suspected diagnosis of oesophageal Crohn's disease. Even if achalasia is suspected in a Crohn's patient, it should be taken into consideration that the motility disorder could be the result of a transmural inflammation with or without fibrosis caused by Crohn's disease.
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7/41. Fragility of the esophageal mucosa: a pathognomonic endoscopic sign of primary eosinophilic esophagitis?

    BACKGROUND: Primary eosinophilic esophagitis, a chronic inflammatory disorder of the esophagus, evokes recurrent dysphagia. endoscopy is often unremarkable, and no consensus exists regarding management of resultant dysphagia. The response of a series of patients with primary eosinophilic esophagitis to dilation is reported together with a description of a possibly pathognomonic sign: fragile esophageal mucosa, for which the term "crepe-paper" mucosa is introduced. methods: Five men underwent endoscopy because of dysphagia confirmed (clinically, endoscopically, and histologically) to be caused by primary eosinophilic esophagitis and were treated by bouginage. OBSERVATIONS: All patients had extremely fragile, inelastic, and delicate mucosa, which tore easily even with minor trauma. After the procedure, patients remained asymptomatic for 3 to 24 months. CONCLUSIONS: Primary eosinophilic esophagitis is characterized by fragile esophageal mucosa that readily tears in response to minor trauma during otherwise uneventful diagnostic endoscopy. This "crepe-paper" sign may alert endoscopists to the presence of the disease when other mucosal alterations are lacking. Dilation is effective for patients with symptoms with minimal morbidity, despite development of disquieting lesions in response to the procedure.
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8/41. Celecoxib associated esophagitis: review of gastrointestinal side effects from cox-2 inhibitors.

    BACKGROUND: With the extensive use of COX-2 inhibitors to treat inflammatory and pain syndromes, gastrointestinal adverse effects are being increasingly observed. CASE REPORT: An 87-year-old white man with chronic peptic esophageal stricture presented to us with dysphagia and odynophagia. The patient was taking Celecoxib for 5 months for trigeminal neuralgia. An upper endoscopy revealed severe desquamative esophagitis. Celecoxib was discontinued and the patient was started on esomeprazole. The patient's symptoms improved in 1 month. Three months later, EGD revealed complete healing of the esophageal mucosa. DISCUSSION: Because recent studies have shown that COX-2 inhibitors are similar to NSAIDs with regards to absorption, in contrast to premarketing trials, extensive use of COX-2 inhibitors is likely to demonstrate gastrointestinal adverse effects similar to those caused by traditional NSAIDs. Our patient had severe esophagitis caused by Celecoxib and aggravated by reflux of achlorhydric gastric contents after dilatation of the stricture. SUMMARY: We report for the first time severe esophagitis caused by the COX-2 inhibitor Celecoxib.
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9/41. candida oesophagitis with hepatitis C virus: an uncommon association.

    candida oesophagitis is an acquired immune deficiency syndrome (AIDS)-defining illness. We report a 28-year-old woman who presented with candida oesophagitis with underlying chronic hepatitis C. The patient presented with anorexia and weakness and was noted to have raised serum transaminases. Upper-gastrointestinal endoscopy revealed candida oesophagitis involving the whole oesophagus. Oesophageal biopsy demonstrated changes consistent with candida oesophagitis. serology was positive for hepatitis c antibodies, and polymerase chain reaction (PCR) genotyped hepatitis C virus (HCV) as genotype 3. liver biopsy revealed chronic hepatitis with moderately active portal inflammation. A human immunodeficiency virus (hiv) test was non-reactive for types 1 and 2. The development of candida oesophagitis in a patient with chronic HCV infection demands prompt consideration of general debility and immunosuppression as effects of HCV that led to an occurrence of opportunistic infection. Evaluation of this case provides insight into various mechanisms of immune suppression associated with HCV infection.
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10/41. Isolated oesophageal involvement of Crohn's disease.

    A 31-year-old male was admitted with complaints of dysphagia and odynophagia. An upper gastrointestinal tract series revealed inflammatory changes in the mid and distal oesophagus with intramural extravasation of the barium. An upper endoscopy showed multiple ulcerations and inflammation. The patient developed a large stricture with no response to serial endoscopic dilations and a surgical resection of the oesophagus was required. Gross examination of the surgical specimen revealed transmural inflammation, deep ulcerations and non-necrotizing epithelioid cell granuloma. All these pathological findings were characteristic of Crohn's disease of the oesophagus. After 36 months of follow-up there has been no recurrence of symptoms or of other sites of involvement.
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