Journals / Turkish Journal of Gastroenterology / 2014 / Cilt: 25 - Sayı: 5

Is it possible to diagnose infectious oesophagitis without seeing the causative organism? A histopathological study

Pages
481–487
DOI
—
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AI Summary & Key Takeaways

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⚡ TL;DR(Too Long; Didn't Read)

Clinicopathological correlation and control with repeat targeted biopsies are essential for diagnosis.

📌 3 Key Takeaways

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Objective & Hypothesis:Background/Aims: We investigated the utility of using histological changes to diagnose infectious oesophagitis when causative organisms cannot be seen.Materials and Methods: Sixty-seven endoscopic biopsy specimens (51 Candida, 9 herpes simplex virus, 4 tuberculosis, and 3 cytomegalovirus oesophagitis) collected from 2000-2010 that matched the investigative criteria were included in the study.
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Key Findings & Data:Results: Thirty-nine cases occurred in male patients, and 28 occurred in female patients; the mean age of the patients was 51±20.1 years (range, 5-94 years).
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Conclusion & Impact:Clinicopathological correlation and control with repeat targeted biopsies are essential for diagnosis.
🔬Design:Research Article
📍Scope:2000-2010 Verileri
⚙️Variables:Domain Parameters

Özet

Background/Aims: We investigated the utility of using histological changes to diagnose infectious oesophagitis when causative organisms cannot be seen.Materials and Methods: Sixty-seven endoscopic biopsy specimens (51 Candida, 9 herpes simplex virus, 4 tuberculosis, and 3 cytomegalovirus oesophagitis) collected from 2000-2010 that matched the investigative criteria were included in the study. Cases were re-evaluated for histological changes observed in oesophagitis, and the findings were statistically compared using nonparametric tests. Results: Thirty-nine cases occurred in male patients, and 28 occurred in female patients; the mean age of the patients was 51±20.1 years (range, 5-94 years). All cases showed lymphocytic and neutrophilic infiltration; while 27 (40.3%) showed eosinophilic infiltration. The density of lymphocytes and eosinophils were 8.43±6 and 1.07±1.62 per high power field, respectively, and these rates were higher in tuberculosis oesophagitis cases. Lamina propria infiltration was present in herpes simplex virus and Candida oesophagitis. Dense neutrophilic infiltration (>50/high power field) was noted in herpes simplex virus oesophagitis. Candida colonization was observed in 82% of cases with eosinophilic infiltration, and 80% of cases with erosion. Ulceration was present in all tuberculosis oesophagitis cases (p<0.001). Basal cell hyperplasia, papillary elongation, and dilated intercellular spaces were seen in all cases except for 2 Candida oesophagitis cases. Lamina propria fibrosis was especially noted in cytomegalovirus oesophagitis cases. Conclusion: It is not possible to distinguish infectious oesophagitis from other subtypes, especially reflux oesophagitis, if the causative organism is not detected. Clinicopathological correlation and control with repeat targeted biopsies are essential for diagnosis.

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Cite This Article

DEMİR, D., YAKUT, B. D., KUMBARACI, B. S., SEZAK, M., TUNÇYÜREK, M. (2014). Is it possible to diagnose infectious oesophagitis without seeing the causative organism? A histopathological study. Turkish Journal of Gastroenterology, Cilt: 25 - Sayı: 5, 481–487. https://ajindex.com/articles/409535

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References (9)

  1. Mills ES. Sternberg's diagnostic surgical pathology. Philadelphia: Lippincott Williams and Wilkins; 2004.
  2. Kumar V, AHPFS AK, Fausto N. In: Robbins and Cotran, ed. Patho- logic basis of disease. Philadelphia: Saunders Press; 2010. Fenoglio-Preiser CM. The nonneoplastic esophagus. In: Fenoglio- Preiser CM, Noffsinger AE, Stemmermann GN, Lantz PE, Listrom MB, Rilke FO, eds. Gastrointestinal Pathology: An Atlas and Text- book. Philadelphia: Lippincott Williams and Wilkins; 2008.
  3. Ismail-Beigi F, Horton PF, Pope CE 2nd. Histological consequences of gastroesophageal reflux in man. Gastroenterology 1970; 58: 163-74.
  4. Takubo K, Honma N, Aryal G, et al. Is there a set of histological changes that are invariably reflux associated? Arch Pathol Lab Med 2005; 129: 159-63.
  5. Geboes K, Desmet V, Vantrappen G, Mebis J. Vascular changes in the esophageal mucosa. An early histological sign of esophagitis. Gastrointest Endosc 1980; 26: 29-32. Dent J. Microscopic esophageal mucosal injury in nonerosive re- flux disease. Clin Gastroenterol Hepatol 2007; 5: 4-16.
  6. Vieth M, Fiocca R, Haringsma J, et al. Radial distribution of dilated intercellular spaces of the esophageal squamus epithelium in pa- tients with reflux disease exhibiting discrete endoscopic lesions. Dig Dis 2004; 22: 208-12. Rothenberg ME. Eosinophilic gastrointestinal disorders (EGID). J Allergy Clin Immunol 2004; 113: 11. Parfitt JR, Gregor JC, Suskin NG, Jawa HA, Driman DK. Eosinophilic esophagitis in adults; distinguishing features from gastroeospha- geal reflux disease: a study of 41 patients. Mod Pathol 2006; 19: 90-6.
  7. Sonnenberg A, El-Serag HB. Clinical epidemiology and natural history of gastroesophageal reflux disease. Yale J Biol Med 1999; 72: 81-92. Greenson JK. Macrophage aggregates in cytomegalovirus esoph- agitis. Hum Pathol 1997; 28: 375-8.
  8. Greenson JK, Beschorner WE, Boitnott JK, Yardley JH. Prominent mononuclear cell infiltrate is characteristic of herpes esophagitis. Hum Pathol 1991; 22: 541-9.
  9. Fujiwara T, Yoshida Y, Yamada S, Kawamata H, Fujimori T, Imawari M. A case of primary esophageal tuberculosis diagnosed by identification of mycobacteria in paraffin-embedded esophageal biopsy speci- mens by polymerase chain reaction. J Gastroenrerol 2003; 38: 74. Takubo K. Pathology of the esophagus: An atlas and textbook. Springer; 2007.